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Background: Excessive submental fat under the chin is a known aesthetic concern because of its negative impact on facial appearance and psychological well-being. AYP-101 is a newly developed injectable agent containing 93% soybean phosphatidylcholine (SPC) designed to reduce submental fat. We conducted a phase 1 study to evaluate the safety, pharmacokinetic (PK), and lipid profile effects of AYP-101. Methods: This study was a randomized, double-blind, placebo-controlled, single-dose, two-cohort trial. Participants were randomized into groups receiving 250 mg of AYP-101, 500 mg of AYP-101, or placebo at a 9:9:8 ratio across both cohorts. Safety was assessed through standard clinical evaluations. Blood samples were collected up to 144 h postdose in cohort 1 and up to 48 h postdose in cohort 2. The PK parameters were calculated via noncompartmental analysis. Results: All 26 randomized subjects completed the study. A total of 72 solicited adverse drug reactions (ADRs) were reported by 24 subjects, all of which were mild. The most common ADRs were injection site pain and bruising. There were 29 ADR cases in the 250 mg group; 26 cases in the 500 mg group; and 18 cases in the placebo group, indicating that there were no clinically significant differences in the safety profiles between the groups. All the dose groups presented similar PK profiles, with Cmax values of 12.86, 13.44, and 13.61 µg/L and AUC0−24 h values of 278.06, 274.79, and 267.63 µg*h/L, respectively. No clinically significant differences in PK or lipid profiles were observed between the postdose group and the baseline group for any of the dose groups. Conclusions: AYP-101 appears to be a safe candidate for treating submental fat, with localized reactions and no systemic exposure at single subcutaneous doses of up to 500 mg. Trial registration: ClinicalTrials.gov NCT05476094. [ABSTRACT FROM AUTHOR]

Background: Familial hypercholesterolemia (FH) is an inherited disorder mainly marked by increased low-density lipoprotein cholesterol (LDL-C) concentrations and a heightened risk of early-onset arteriosclerotic cardiovascular disease (ASCVD). This study seeks to characterize the genetic spectrum and genotype‒phenotype correlations of FH in Chinese pediatric individuals. Methods: Data were gathered from individuals diagnosed with FH either clinically or genetically at multiple hospitals across mainland China from January 2016 to June 2024. Results: In total, 140 children and adolescents (mean age of 6.00 years) with clinically and genetically diagnosed FH were enrolled in the study, with 87 distinct variants identified in the LDLR, APOB and PCSK9 genes. Among the variants, 11 variants were newly identified worldwide, with 9 classified as "pathogenic" or "likely pathogenic", and 2 classified as "variants of uncertain significance". Additionally, the 5 most common variants in the study were c.1448G > A (p.W483*), c.1879G > A (p.A627T), c.1216C > A (p.R406R), and c.1747C > T (p.H583Y) in the LDLR gene, as well as c.10579C > T (p.R3527W) in the APOB gene, accounting for 49.29% (69/140) of all patients. These variants are primarily observed in the Asian or Chinese population and are distinct from those present in Caucasian groups. In this cohort, 105 patients were diagnosed with heterozygous FH (HeFH), while 35 were diagnosed with homozygous FH (HoFH). Finally, only 28.57% of the patients (40/140) were using lipid-lowering medications with 33.33% of HoFH patients initiating treatment after the age of 8. Additionally, only 3 compound heterozygous patients (2.14%) underwent liver transplantation because of significantly high lipid levels. Conclusion: This study reveals the variable genotypes and phenotypes of children with FH in China and illustrates that the genotypes in the Chinese population differ from those in Caucasians, providing a valuable dataset for the clinical genetic screening of FH in China. Furthermore, the older age at diagnosis and treatment highlights the underdiagnosis and undertreatment of Chinese FH pediatric patients, suggesting that early identification should be improved through lipid or genetic screening, and that more timely and regular pharmacological treatments should be implemented. [ABSTRACT FROM AUTHOR]

Background: Point-of-care testing (POCT) is commonly used in epidemiological surveys due to its various advantages, such as portability and immediate test results. The CardioChek® PA analyser 3-in-1 lipid panel measures total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol. This study tested the reliability and diagnostic accuracy of the CardioChek® PA analyser using a 3-in-1 lipid panel. Methods: A cross-sectional study design with quota sampling was used. A total of 203 respondents aged 18 years and above from a research centre in the Ministry of Health, Malaysia, were recruited. Venous blood was sent to the laboratory and tested with Siemens Atellica CH, while a POCT analyser was used for capillary blood measurements. Intraclass coefficient correlation (ICC) analysis was employed to determine the agreement between capillary and venous blood parameters. The diagnostic performance of the evaluated tests was evaluated using STATA version 12. Results: The agreement between capillary and laboratory venous blood was moderate (0.64–0.67) for TC and HDL, good (0.75) for LDL and excellent (0.91) for TG). The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were as follows: TC, 57.1%, 94.3%, 92.3% and 64.8%; TG, 76.0%, 100%, 100%, and 96.6%; HDL, 96.2%, 83.2%, 47.2% and 99.3%; and LDL, 81.0%, 100%, 100% and 68.3%, respectively. Conclusions: The CardioChek® PA analyser showed acceptable diagnostic accuracy for screening high-risk individuals more often in places where laboratories are inaccessible. It could also be used in clinical settings where patients would benefit from swift treatment decisions. [ABSTRACT FROM AUTHOR]

It had been observed that homozygous albumin knockout mice (Alb−/−) exhibit low plasma free fatty acid (FFA) concentration and improved blood glucose regulation. However, it was not yet known to what extent heterozygous albumin knockout (Alb+/−) mice would display a similar phenotype. Alb−/−, Alb+/−, and wild-type (WT) female mice were studied on a low-fat diet (LFD) or high-fat diet (HFD). On both diets, decreased plasma FFA concentration, and improved glucose tolerance test were observed in Alb−/−, but not in Alb+/−, compared to WT. Plasma adiponectin concentration showed greater elevation in Alb−/− than Alb+/−. Consistent with that, adiponectin gene expression was significantly higher in Alb−/− mice than in Alb+/− and WT mice. A dose-dependent response was observed for hepatic Acadl gene expression showing higher Acadl gene expression in Alb−/− mice than in Alb+/− and WT mice. In conclusion, although female Alb+/− mice exhibited some slight differences from WT mice (e.g., increased plasma adiponectin and hepatic Acadl gene expression), Alb+/− mice did not exhibit improved glucoregulation in comparison to WT mice, indicating that a minor suppression of albumin expression is not sufficient to improve glucoregulation. Furthermore, it is now clear that although the response of female mice to HFD might be unique from how males generally respond, still the complete albumin deficiency in Alb−/− mice and the associated FFA reduction is capable of improving glucoregulation in females on this diet. The present results have implications for the role of albumin and FFA in the regulation of metabolism. [ABSTRACT FROM AUTHOR]

Background: Presently, the majority of investigations primarily evaluate the association between lipid profiles and asthma. However, few investigations explore the connection between lipids and mortality related to the disease. This study aims to explore the association of serum lipids with all-cause mortality within asthmatic adults. Methods: The investigation included 3233 eligible patients with asthma from the NHANES (2011–2018). The potential associations were explored using three Cox proportional hazards models, restricted cubic splines (RCS), threshold effect models, and CoxBoost models. In addition, subgroup analyses were conducted to investigate these associations within distinct populations. Results: After controlling all covariables, the Cox proportional hazards model proved a 17% decrease in the probability of death for each increased unit of low-density lipoprotein-cholesterol (LDL-C) (mmol/L). Yet, there was no association seen between blood high-density lipoprotein cholesterol (HDL-C), total cholesterol, or triglyceride and all-cause mortality in asthmatics. The application of RCS and threshold effect models verified an inverse and linear association of LDL-C with all-cause mortality. According to the results from the CoxBoost model, LDL-C exhibited the most substantial impact on the follow-up status of asthmatics among the serum lipids. Conclusion: Our investigation concluded that in American asthmatic populations, LDL-C levels were inversely and linearly correlated with mortality. However, no independent relationship was found between triglycerides, total cholesterol, or HDL-C and mortality. [ABSTRACT FROM AUTHOR]

Background: The triglyceride-glucose (TyG) index is a risk marker for arterial stiffness; however, the extent to which the TyG index is associated with arterial stiffness via lipids and inflammation remains unknown. The first aim was to probe the relationship between the TyG index and arterial stiffness in two surveys. The second aim was to clarify whether lipids and inflammation mediate this relationship. Methods: The sample size of 13,726 U.S. individuals from the National Examination Survey (NHANES) and 3,964 Chinese individuals from the China Health and Retirement Longitudinal Study (CHARLS 2015) were enrolled. Weighted multivariate logistic and linear regression models, as well as restricted cubic spline (RCS) and mediation analyses, were utilized to estimate complex relationships between the TyG index, arterial stiffness, lipids (non-high-density lipoprotein cholesterol [non-HDL-C]) and inflammation (C-reactive protein [CRP]) biomarkers. Results: A total of 3,420 U.S. patients and 992 Chinese patients were diagnosed with increased arterial stiffness. Regression analyses demonstrated that higher quartiles of the TyG index were associated with a greater incidence of increased arterial stiffness (NHANES: OR = 2.610, 95% CI = 2.043–3.334, P < 0.001; CHARLS: OR = 1.579, 95% CI = 1.057–2.360, P < 0.001). Participants with a higher TyG index/higher CRP level or with a higher TyG index/higher non-HDL-C level had the highest incidence of increased arterial stiffness in the two surveys. The results were still consistent when the sensitivity analysis was implemented with stricter clinical cut-off values of non-HDL-C. Mediation analysis verified that lipids (mediated effect: β = 0.012, P < 0.001 in NHANES; β = 0.020, P < 0.001 in CHARLS) and inflammation (mediated effect: β = 0.003, P < 0.001 in NHANES; β = 0.006, P < 0.001 in CHARLS) partially mediated this relationship. Conclusions: These results indicated a positive linear correlation between the TyG index, non-HDL-C level, CRP level and increased arterial stiffness in two surveys. Furthermore, lipids and inflammation could partly mediate the correlation of the TyG index with arterial stiffness in both surveys. [ABSTRACT FROM AUTHOR]

Background: Studies have found that high density lipoprotein cholesterol (HDL-C) levels are linked to a variety of diseases. However, evidence for the relationship between stress urinary incontinence (SUI) and HDL-C remain limited. Methods: 590 eligible women were enrolled. Basic characteristic, gynecological examinations and blood sampling were collected. The examination of the possible link between HDL-C and SUI was done using univariate and multivariate logistic regression. Feature importance ranking and Receiver operating characteristic (ROC) curves were performed to further evaluate the association between HDL-C and SUI in women. Results: A significant association was found between HDL-C and SUI in women, revealing higher HDL-C levels were related to a lower risk of SUI (OR 0.238; 95%CI: 0.091–0.623; P < 0.01) after adjustment for potential key confounders. The AUC for the SUI predicted by the combined HDL-C was 0.845 (95%CI: 0.798–0.891, P < 0.001). The feature importance ranking revealed that vaginal delivery, HDL-C were the top two important factors. Conclusions: HDL-C levels were correlated with the development of SUI. In addition to physical and surgical treatments, HDL-C may offer the possibility of potential targeted treatment and prevention of SUI afterwards. [ABSTRACT FROM AUTHOR]

Cancer prognosis remains a critical clinical challenge. Lipidomic analysis via mass spectrometry (MS) offers the potential for objective prognostic prediction, leveraging the distinct lipid profiles of cancer patient-derived specimens. This review aims to systematically summarize the application of MS-based lipidomic analysis in prognostic prediction for cancer patients. Our systematic review summarized 38 studies from the past decade that attempted prognostic prediction of cancer patients through lipidomics. Commonly analyzed cancers included colorectal, prostate, and breast cancers. Liquid (serum and urine) and tissue samples were equally used, with liquid chromatography–tandem MS being the most common analytical platform. The most frequently evaluated prognostic outcomes were overall survival, stage, and recurrence. Thirty-eight lipid markers (including phosphatidylcholine, ceramide, triglyceride, lysophosphatidylcholine, sphingomyelin, phosphatidylethanolamine, diacylglycerol, phosphatidic acid, phosphatidylserine, lysophosphatidylethanolamine, lysophosphatidic acid, dihydroceramide, prostaglandin, sphingosine-1-phosphate, phosphatidylinosito, fatty acid, glucosylceramide and lactosylceramide) were identified as prognostic factors, demonstrating potential for clinical application. In conclusion, the potential for developing lipidomics in cancer prognostic prediction was demonstrated. However, the field is still nascent, necessitating future studies for validating and establishing lipid markers as reliable prognostic tools in clinical practice. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the leading cause of mortality globally. Low-density lipoprotein (LDL) plays an important role in CVD pathophysiology. Research has shown the safety and efficacy of keeping LDL at very low levels for CVD prevention. Therefore, experts recommend intense LDL-lowering approaches starting at young ages, promoting the mantras "the lower, the better" and "the earlier, the better." This commentary discusses the challenges regarding applying aggressive LDL-lowering approaches in the general population, including pharmacological efficacy and side effects, the cost-effectiveness of interventions, and patient adherence to treatment regimens. [ABSTRACT FROM AUTHOR]

Background: The objective was to investigate the efficacy of different doses of levothyroxine therapy among pregnant women exhibiting high-normal thyroid stimulating hormone levels and positive thyroid peroxidase antibodies throughout the first half of pregnancy. Methods: Pregnant women exhibiting high-normal thyroid stimulating hormone levels and thyroid peroxidase antibodies positivity throughout the initial half of pregnancy were selected from January 2021 to September 2023. Based on the different doses of levothyroxine, the pregnant women were categorized into the nonintervention group (G0, 122 women), 25 µg levothyroxine intervention group (G25, 69 women), and 50 µg levothyroxine intervention group (G50, 58 women). Serum parameters, gastrointestinal symptoms, small intestinal bacterial overgrowth (SIBO), maternal and neonatal outcomes were compared after the intervention among the three groups. Results: After the intervention, in the G25 and G50 groups, the thyroid stimulating hormone, triglyceride and low-density lipoprotein levels were notably less in contrast to those in the G0 group (P < 0.05). The rates of abdominal distension and SIBO in the G25 and G50 groups were notably lower in contrast to the G0 group (P = 0.043 and 0.040, respectively). The G50 group had a lower rate of spontaneous abortion and premature membrane rupture than the G0 group (P = 0.01 and 0.015, respectively). Before 11+ 2 weeks of gestation and at thyroid peroxidase antibodies levels ≥ 117 IU/mL, in contrast to the G0 group, the G50 group experienced a decreased rate of spontaneous abortion (P = 0.008). The G50 group had significantly higher newborn weight than the G0 group (P = 0.014), as well as a notably longer newborn length than the G0 and G25 groups (P = 0.005). Conclusions: For pregnant women with high-normal thyroid stimulating hormone levels and thyroid peroxidase antibodies positive during the first half of pregnancy, supplementation with 50 µg levothyroxine was more effective in improving their blood lipid status and gastrointestinal symptoms, reducing the incidence of SIBO and premature rupture of membranes, and before 11+2 weeks, TPOAb ≥ 117 IU/mL proved more beneficial in mitigating the risk of spontaneous abortion. [ABSTRACT FROM AUTHOR]

Background: Direct-acting Antiviral Agents (DAAs) influence serum lipids of patients with Hepatitis C virus (HCV). This paper presents an analysis of the relevant literature to investigate the effects of DAAs in treating hepatitis C to achieve a sustained viral response (SVR) on lipid parameters. Methods: PubMed,Web of science, Embase and Central databases were searched, with a deadline of September 2023. Studies on the effects of sustained viral response on lipid parameters after DAAs treatment for hepatitis C were selected. The required information was extracted from the included studies, and then the Stata 12.0 was used to analyze the data quantitatively. Results: Of 32 studies, the results showed that total cholesterol (TC) levels increased from the end of treatment (WMD = 20.144, 95%CI = 3.404, 36.884,P = 0.018) to one year after treatment (WMD = 24.900, 95%CI = 13.669, 36.131, P < 0.001). From the end of treatment (WMD = 17.728, 95%CI = 4.375, 31.082, P = 0.009) to one year after treatment (WMD = 18.528, 95%CI = 7.622, 29.433, P < 0.001), the levels of low-density lipoprotein (LDL) were also increased. High-density lipoprotein (HDL) levels were elevated from 4 weeks after treatment (WMD = 6.665, 95%CI = 3.906, 9.424, P < 0.001) to 24 weeks after treatment (WMD = 3.159,95% CI = 0.176, 6.142, P = 0.038). Triglyceride (TG) levels showed no significant change after the treatment. Conclusions: Hepatitis C patients who achieved SVR on DAAs showed the increase of lipid levels and the improvement of hepatic inflammation indicators AST and ALT. This may provide evidence-based medical evidence for the follow-up and monitoring of blood lipids and hyperlipidemia treatment. Registration: PROSPERO CRD42020180793. [ABSTRACT FROM AUTHOR]

Background: Statins are routinely prescribed to lower cholesterol and have been demonstrated to have significant benefits in atherosclerotic cardiovascular disease. However, whether statin therapy has effects on cancer risk remains controversial. In this study, we investigated the influence of statin therapy on cancer incidence and mortality by conducting a comprehensive meta-analysis of randomized controlled trials. Methods: Systematic searches by Cochrane, Embase, Medline, and PubMed were performed to locate data from eligible randomized controlled trials related to statin therapy and oncology. Our main endpoints were cancer incidence and mortality. Fixed-effects models were used in this study. Results: This meta-analysis comprised thirty-five randomized controlled studies. Twenty-eight included studies reported cancer incidence, and eighteen reported cancer mortality. The pooled results indicated no reduction in cancer incidence with statins compared to placebo [OR = 0.99, 95% CI (0.95, 1.03)]. In addition, statins did not decrease cancer mortality [OR = 0.99, 95% CI (0.91, 1.07)]. This study also performed a number of subgroup analyses, which showed no effect of statins on cancer subtypes such as genitourinary and breast cancer. Neither the type of statin nor long-term treatment with statins had an effect on cancer incidence and mortality. Conclusion: Through comprehensive analysis, we found that statin therapy does not reduce cancer incidence or mortality while protecting the cardiovascular system. Trial registration: Prospero CRD42022377871. [ABSTRACT FROM AUTHOR]

Background: Chronic nonspecific low back pain (cNLBP) is a common health problem worldwide, affecting 65–80% of the population and greatly affecting people's quality of life and productivity. It also causes huge economic losses. Manual therapy (MT) and therapeutic exercise (TE) are effective treatment options for cNLBP physiotherapy-based treatment. However, the underlying mechanisms that promote cNLBP amelioration by MT or TE are incompletely understood. Methods: Seventeen recruited subjects were randomly divided into an MT group and a TE group. Subjects in the MT group performed muscular relaxation, myofascial release, and mobilization for 20 min during each treatment session. The treatment lasted for a total of six sessions, once every two days. Subjects in the TE group completed motor control and core stability exercises for 30 min during each treatment session. The motor control exercise included stretching of the trunk and extremity muscles through trunk and hip rotation and flexion training. Stabilization exercises consisted of the (1) bridge exercise, (2) single-leg-lift bridge exercise, (3) side bridge exercise, (4) two-point bird-dog position with an elevated contralateral leg and arm, (5) bear crawl exercise, and (6) dead bug exercise. The treatment lasted for a total of six sessions, with one session every two days. Serum samples were collected from subjects before and after physiotherapy-based treatment for lipidomic and metabolomic measurements. Results: Through lipidomic analysis, we found that the phosphatidylcholine/phosphatidylethanolamine (PC/PE) ratio decreased and the sphingomyelin/ceramide (SM/Cer) ratio increased in cNLBP patients after MT or TE treatment. In addition, eight metabolites enriched in pyrimidine and purine differed significantly in cNLBP patients who received MT treatment. A total of nine metabolites enriched in pyrimidine, tyrosine, and galactose pathways differed significantly in cNLBP patients after TE treatment during metabolomics analysis. Conclusion: Our study was the first to elucidate the alterations in the lipidomics and metabolomics of cNLBP physiotherapy-based treatment and can expand our knowledge of cNLBP physiotherapy-based treatment. [ABSTRACT FROM AUTHOR]

The tumor microenvironment (TME) is characterized by discrete changes in metabolic features of cancer and immune cells, with various implications. Cancer cells take up most of the available glucose to support their growth, thereby leaving immune cells with insufficient nutrients to expand. In the relative absence of glucose, T cells switch the metabolic program to lipid-based sources, which is pivotal to T-cell differentiation and activation in nutrient-stressed TME. Although consumption of lipids should provide an alternative energy source to starving T cells, a literature survey has revealed that it may not necessarily lead to antitumor responses. Different subtypes of T cells behave differently in various lipid overload states, which widely depends upon the kind of free fatty acids (FFA) engulfed. Key lipid metabolic genes provide cytotoxic T cells with necessary nutrients for proliferation in the absence of glucose, thereby favoring antitumor immunity, but the same genes cause immune evasion in Tmem and Treg. This review aims to detail the complexity of differential lipid metabolism in distinct subtypes of T cells that drive the antitumor or pro-tumor immunity in specific TME states. We have identified key drug targets related to lipid metabolic rewiring in TME. [ABSTRACT FROM AUTHOR]

Background: To investigate the characteristics and clinical significance of serum lipids in patients with gastrointestinal stromal tumors (GISTs). Methods: The clinical and pathological data of 694 GIST patients in Liyuan hospital and Union hospital from 2012 to 2016 were retrospectively analyzed. Blood lipid levels in patients with varying degrees of risk were compared. Results: The findings showed that LDL-C, HDL-C, and CHOL increased significantly in women, and CD34 positive. In patients with tumors size less than 5 cm in diameter, TG, HDL-C, and CHOL were significantly higher. TG levels were significantly higher in DOG-1 (a marker and has a high specificity and sensitivity in the diagnosis of GIST) positive patients than in DOG-1 negative patients (P < 0.05). S-100 positive patients had lower HDL-C levels than S-100 negative patients (P < 0.05). Lipids indexes were found to be correlated with GIST risk stratification and tumor site (P < 0.05). TG/HDL-C was were significantly different among patients with GIST in different locations (P < 0.05). Conclusion: The clinical and pathological characteristics of the patients with GIST are closely related to the level of blood lipids. To a certain extent, information about level of blood lipids can be helpful for distinguishing benign and malignant GIST. [ABSTRACT FROM AUTHOR]

Background: The studies, investigating the association of low-density lipoprotein cholesterol (LDL-C) with metabolic syndrome (MetS) are limited with controversial conclusions. Therefore, this study aimed at revealing the specific relationship between the serum LDL-C levels and MetS prevalence in a large working population. Methods: Secondary data analysis of a cross-sectional study, conducted between 2012 and 2016 in Spain on participants aged within the range of 20–70 years, involved 60,799 workers. Logistic regression analysis was applied to evaluate the association between the levels of serum LDL-C and MetS prevalence. Results: Among the 60,799 workers, the prevalence of MetS was 9.0%. The odds ratios (95% confidence intervals) of MetS prevalence were 1.27 (1.16–1.39) and 1.53 (1.41–1.65) for the individuals with the LDL-C levels in lower (< 103.8 mg/dL) and upper (> 135.8 mg/dL) tertiles as compared to those with the LDL-C levels in middle tertile (103.8–135.8 mg/dL) in the studied population. Similarly, a U-shaped relationship was also observed in male cohort. The serum LDL-C levels associated with the lowest risk of current MetS were 113.6 mg/dL and 117.6 mg/dL in the overall studied population and male cohort, respectively. The female workers with the levels of LDL-C higher than 135.0 mg/dL had an increased prevalence of MetS (P < 0.05). Conclusions: The low and high levels of serum LDL-C were associated with an increased prevalence of MetS in the working population and in male workers. Only the high (> 135.0 mg/dL) levels of LDL-C increased MetS prevalence in female workers. [ABSTRACT FROM AUTHOR]

Background: Dyslipidemia is a predisposing factor for coronary heart disease (CHD). High-intensity statin therapy is recommended as secondary prevention. ABCB1 and SLCO1B1 genes influence the efficacy and safety of statins. Xinjiang is a multi-ethnic area; however, little is known about the prevalence of dyslipidemia and gene polymorphisms of ABCB1 and SLCO1B1 in minority groups with CHD. Objective: To measure levels of lipid and apolipoprotein and the prevalence of dyslipidemia and gene polymorphisms of ABCB1, SLCO1B1 in Han, Uygur, Kazak, Hui, Tatar, Kirgiz, and Sibe populations with CHD in Xinjiang. Methods: This descriptive retrospective study compares lipid levels in ethnic groups using Kruskal-Wallis test or analysis of variance. The study compared gene polymorphisms and the prevalence of dyslipidemia among different ethnic groups using the chi-square test. The lipid profiles in plasma were measured before lipid-lowering therapy using commercially available kits. Genotyping of SLCO1B1 and ABCB1 variants was performed using sequencing by hybridization. Results: A total of 2218 patients were successfully screened, including 1044 Han, 828 Uygur, 113 Kazak, 138 Hui, 39 Tatar, 36 Kirgiz, and 20 Sibe patients. The overall mean age was 61.8 ± 10.8 years, and 72.5% of participants were male. Dyslipidemia prevalence in these ethnic groups was 42.1, 49.8, 52.2, 40.6, 48.7, 41.7, and 45.0%, respectively. The prevalence of dyslipidemia, high total cholesterol (TC), high triglycerides (TG), and high low density lipoprotein cholesterol (LDL-C) differed significantly among the groups (P = 0.024; P < 0.001; P < 0.001; P < 0.001, respectively). For the Han group, high LDL-C, high TC, and high TG prevalence differed significantly by gender (P = 0.001, P = 0.022, P = 0.037, respectively). The prevalence of high TC, high TG, and low high density lipoprotein cholesterol (HDL-C) differed significantly by gender in the Uygur group (P = 0.006, P = 0.004, P < 0.001, respectively). The prevalence of high TC in Hui patients significantly differed by gender (P = 0.043). These findings suggest that polymorphisms in ABCB1 and C3435T differ significantly across ethnicities (P < 0.001). Conclusions: The prevalences of dyslipidemia, high TC, high TG, and high LDL-C in Han, Uygur, Kazak, Hui, Tatar, Kirgiz, and Sibe CHD patients in Xinjiang differed concerning ethnicity. Ethnic, gender, and lifestyle were the key factors that affected the lipid levels of the population. The prevalence of polymorphisms of ABCB1 and C3435T significantly differed across ethnicities. These findings will aid the selection of precision lipid-lowering medications and prevention and treatment of CHD according to ethnicity in Xinjiang. [ABSTRACT FROM AUTHOR]

Background: About 20–40 % of autistic people experience a phenomenon of regression. Retinol binding protein 4 (RBP4) plays an important role as an inflammatory neurotrophic adipokine and is a promising mediator of the fat-brain axis. Abnormal fatty acid metabolism and lipid mediators have been reported to be related to the etiological mechanism in autism, and amelioration of impaired lipid metabolism can be recognized as a treatment strategy for autism. The purpose of this study is to explore the relationship between RBP4, lipids, and the autistic regression phenomenon, and to discuss their potentials as biomarkers for the autistic regression phenomenon. Methods: A total of 60 autistic individuals (18 with regression phenomenon, 42 without regression phenomenon) (ASD group) and 36 healthy controls were enrolled in this case-control study. The levels of RBP4, total cholesterol (TC), high-density lipoprotein (HDLC), low–density lipoprotein (LDLC), and triglyceride (TG) were measured. Childhood Autism Rating Scale (CARS) is used to assess the severity of autism. Ethical measures were performed in compliance with the current Declaration of Helsinki and written informed consent was obtained from the parents before enrollment of the children and adolescents. Results: Compared with control subjects, autistic individuals had lower levels of TC (P = 0.007), RBP4 (P = 0.001), and HDLC (P = 0.027). The levels of RBP4 in ASD group were positively correlated with TG (r = 0.355, P = 0.005), HDLC (r = 0.257, P = 0.047), TG/TC (r = 0.376, P = 0.003) and TG/LDLC (r = 0.363, P = 0.004), and were negatively correlated with CARS (r=-0.296, P = 0.003). Further logistic regression demonstrated that decreased RBP4 concentration was associated with the presentation of the autistic regression phenomenon even after the adjustment of the potential confounding factors. Conclusions: Serum RBP4 is associated with the autistic regression phenomenon and the severity of ASD. Further studies are needed to expound whether decreased RBP4 participates in the development of the autistic regression phenomenon. [ABSTRACT FROM AUTHOR]

Background: Polycystic ovary syndrome (PCOS) is associated with obesity, diabetes, and insulin resistance. The circulating C1Q/TNF-related proteins (CTRP-2, CTRP-9) and growth differentiation factors (GDF-8, GDF-15) contribute to glucose and lipid homeostasis. The effects of intralipids and insulin infusion on CTRP-2, CTRP-9, GDF-8 and GDF-15 in PCOS and control subjects before and after chronic exercise training were examined. Methods: Ten PCOS and nine healthy subjects were studied at baseline status and after moderate-intensity chronic exercise training (1 h exercise, 3 times per week, 8 weeks). All participants were infused with 1.5 mL/min of saline or intralipids (20%) for 5 h, and during the last 2 h of saline or intralipids infusion hyperinsulinemic-euglycemic clamp (HIEC) was performed. CTRP-2, CTRP-9, GDF-8 and GDF-15 levels were measured at 0, 3 and 5 h. Results: Intralipids dramatically increased CTRP-2 levels in PCOS (P = 0.02) and control (P = 0.004) subjects, which was not affected by insulin infusion or by exercise. Intralipids alone had no effects on CTRP-9, GDF-8, or GDF-15. Insulin increased the levels of GDF-15 in control subjects (P = 0.05) during the saline study and in PCOS subjects (P = 0.04) during the intralipid infusion. Insulin suppressed CTRP9 levels during the intralipid study in both PCOS (P = 0.04) and control (P = 0.01) subjects. Exercise significantly reduced fasting GDF-8 levels in PCOS (P = 0.03) and control (P = 0.04) subjects; however, intralipids infusion after chronic exercise training increased GDF-8 levels in both PCOS (P = 0.003) and control (P = 0.05) subjects and insulin infusion during intralipid infusion reduced the rise of GDF-8 levels. Conclusion: This study showed that exogenous lipids modulate CTRP-2, which might have a physiological role in lipid metabolism. Since chronic exercise training reduced fasting GDF-8 levels; GDF-8 might have a role in humoral adaptation to exercise. GDF-15 and CTRP-9 levels are responsive to insulin, and thus they may play a role in insulin responses. [ABSTRACT FROM AUTHOR]

Background: The present study aims to estimate whether high-density lipoprotein cholesterol (HDL-C) is correlated with cardiovascular events (CVEs) and cardiovascular mortality (CVM) in a large sample of the general population in rural areas of China. Methods: Adult participants (n = 10,266, age = 53.79 ± 10.49 years; 46.5% men) were enrolled from the Northeast China Rural Cardiovascular Health Study (NCRCHS). Laboratory testing, blood pressure, weight, height, and questionnaires about socioeconomic status were collected. Results: In all, 585 nonfatal or fatal CVEs and 212 cardiovascular deaths were documented during a 4.66-year follow-up. Compared to the reference groups (HDL-C between 1.5 and 1.99 mmol/L), either lower or higher levels of HDL-C were correlated with an increased incidence of CVEs but not CVM [hazard ratio (HR) the lowest = 1.369, 95% confidence interval, 1.007–1.861; HR the highest = 1.044, 0.509–2.231]. Elevated CVM was seen in the lowest HDL-C category (1.840; 1.121–3.021). Conclusions: Lower or higher HDL-C was associated with a higher incidence of CVEs but not CVM in the general population of rural China. Perhaps if an appropriate level of HDL-C is maintained, CVEs can be effectively prevented. [ABSTRACT FROM AUTHOR]

Objective: The mechanism between smoking and coronary artery disease (CAD) remains unclear. It is likely that lipid (including triglycerides (TG), total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C)) have been functioning as one of the mediators between smoking and the CAD occurrence. The study aimed to investigate the mediating effect of lipid on the relationship between smoking and CAD risk. Methods: The case-control study included 2048 subjects. General linear regression analysis was used to corroborate the association between smoking and lipid levels. Univariate and multivariate logistic regression analysis were performed to reveal the relationship between smoking, lipid and the risk of CAD. Mediation analysis was used to investigate whether the association between smoking and CAD risk was mediated by lipid. Results: Smoking was found to be associated with the risk of CAD (odds ratio (OR) = 1.34, 95% confidence interval (CI): 1.05–1.71, P = 0.019). Regression analysis showed that TG, TC and HDL-C were associated with CAD (OR = 2.69, 95%CI: 2.12–3.40, P < 0.001; OR = 0.34, 95%CI: 0.29–0.43, P < 0.001; OR = 0.37, 95%CI: 0.30–0.47, P < 0.001). Moreover, the ratio of TG to HDL-C (TG/HDL-C) was also related to CAD (OR = 4.45, 95%CI: 3.52–5.64, P < 0.001). Mediation analysis showed that among the effects of smoking on CAD, 17.52% was mediated by lipid, in which HDL-C accounted for 11.16% and TG accounted for 6.36%. Further analysis showed that the effect was also partially mediated by TG/HDL-C, which was accounted for 28%. Conclusions: Lipid plays a partial mediation on the association between smoking and CAD risk. The study provides a clue on the mediation effect of lipids on the relationship between smoking and CAD risks, which is a novel insight to the progression of CAD. [ABSTRACT FROM AUTHOR]

Background: Nonalcoholic steatohepatitis (NASH) progresses from simple nonalcoholic fatty liver (NAFL) and has a poor prognosis. Abnormal lipid metabolism is closely related to the occurrence and development of nonalcoholic fatty liver disease (NAFLD). This study aimed to study the relationships between serum lipid metabolites and NASH, and to improve the early diagnosis of NASH. Methods: This study included 86 NAFLD patients (23 NASH and 63 NAFL), and 81 unaffected individuals as controls from West China Hospital between October 2018 and May 2019. With lipid metabolites as the focus of the study, the differences in lipid metabolites were compared between the control group, NAFL patients, and NASH patients. Logistic regression analysis was used to examine the risk factors of NASH. Finally, receiver operating characteristic curve (ROC curve) was used to analyze the efficacy of the metabolites in NASH prediction. Results: The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lipoprotein A (LPA) increased with the severity of NAFLD. In NAFLD patients, LPA (OR:1.61; 95%CI: 1.03–2.52) was a potential risk factor for NASH, and ROC analysis showed that the combination of LPA, ALT, and AST had a greater predictive efficiency for NASH. Conclusions: Abnormal apolipoprotein/lipoprotein is closely related to lipid metabolism disorder in patients with NAFLD. In NAFL, the combination of LPA, ALT, and AST contributes to predicting the occurrence of NASH. LPA may be a potential biomarker and therapeutic target for diagnosing and treating NASH. [ABSTRACT FROM AUTHOR]

Background: Previous studies on the effects of lipotoxicity and oxidative stress on islet beta cell function mainly focused on patients with diabetes, whereas studies on normal glucose tolerance (NGT) are few. The aim of this study was to explore the relationships among triglyceride (TG), high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), oxidative stress indicators, insulin resistance, and beta cell function in populations with different glucose and lipid metabolism states. Methods: A total of 517 individuals were recruited from a rural community in Beijing, China. Glucose metabolism status was defined according to the results of a 75-g oral glucose tolerance test (OGTT). Dyslipidemia was defined as abnormal TG, HDL-c, or LDL-c levels. The population was divided into four groups: individuals with normal glucose and lipid levels (group A, n = 62); those with dyslipidemia alone (group B, n = 82); those with dysglycemia alone (group C, n = 121); and those with dysglycemia and dyslipidemia (group D, n = 247). Oxidative stress indicators, including superoxide dismutase (SOD), glutathione reductase (GR) and 8-hydroxydeoxyguanosine (8-OHdG), were measured. Homeostasis model assessment of insulin resistance (HOMA-IR) and glucose disposition index (DI30, DI120) were calculated to assess insulin resistance and islet beta cell function, respectively. Stratified multiple linear regression analysis was used to explore relationships between TG, HDL-c, LDL-c, oxidative stress indicators, and insulin resistance (natural log transformation of HOMA-IR, LnHOMA-IR) and beta cell function (natural log transformation of DI30, Ln DI30). Results: Compared with the control group, populations with dyslipidemia and/or dysglycemia showed significantly increased insulin resistance. Dyslipidemia aggravated insulin resistance and beta cell dysfunction in individuals with dysglycemia. Stratified regression analysis showed that TG positively correlated with LnHOMA-IR in individuals with normal glucose levels (beta = 0.321, 0.327, P = 0.011, 0.003 in groups A and B, respectively) and negatively correlated with LnDI30 in participants with dyslipidemia (beta = − 0.225, − 0.122, P = 0.035, 0.048 in groups B and D, respectively). Reduced serum SOD levels in individuals with dysglycemia plus dyslipidemia were observed, and a negative association between TG and SOD levels was found (r = − 0.461, P < 0.001). Conclusion: TG correlated with both insulin resistance and beta cell function in individuals with dyslipidemia alone. SOD negatively correlated with TG, indicating a close relationship between oxidative stress and glucose-lipid metabolism. Due to the adverse effect of hypertriglyceridemia on insulin sensitivity and islet beta cell function, more attention should be paid to the detection and management of hypertriglyceridemia. [ABSTRACT FROM AUTHOR]

Background: Cigarette smoke (CS) exposure impairs serum lipid profiles and the function of vascular endothelial cells, which accelerates the atherosclerosis. However, the precise mechanism and effect on the expression of low-density lipoprotein receptor (LDLR) in the liver by CS exposure is still unclear. Methods: In this study, adult male C57BL/6 J mice were divided into three groups, with one group being exposed to CS for 6 weeks. HepG2 cells were treated with CS extract at concentrations of 1, 2.5, 5, and 10%. Results: The serum levels of total cholesterol (TC), triglycerides (TGs), and low-density lipoprotein cholesterol (LDL-C) for the CS-exposure group were significantly higher than those in the control group (P < 0.05). Moreover, CS exposure decreased the LDLR expression in the hepatocytes and promoted inflammation in the blood vessel walls. Melatonin was intraperitoneally injected at 10 mg/kg/d for 6 weeks alongside CS exposure, and this significantly decreased the levels of TC, TGs, and LDL-C and decreased the expression of intercellular adhesion molecule-1 and the infiltration of cluster determinant 68-cells. In vitro, CS extract prepared by bubbling CS through phosphate-buffered saline decreased the LDLR expression in HepG2 cells in a time- and concentration-dependent manner, and this effect was prevented by pretreatment with 100 μM melatonin. Conclusions: In conclusion, CS exposure impaired lipid metabolism and decreased LDLR expression in hepatocytes, and these effects could be prevented by melatonin supplementation. These findings implied that melatonin has the potential therapeutic applicability in the prevention of lipid metabolic disorder in smokers. [ABSTRACT FROM AUTHOR]

Background: Dyslipidemia is a key driver of coronary artery disease (CAD) development. This study aimed to determine whether the atherogenic index of plasma (AIP), a novel comprehensive lipid index, is an independent and reliable predictor of CAD risk in postmenopausal women. Methods: A cohort of consecutive 4644 postmenopausal women (aged 50 or above) undergoing coronary angiography (CAG) in Anzhen Hospital (Beijing, China) from January–December 2014 was included in the analysis. Of them, 3039 women were CAD patients, and 1605 were non-CAD subjects. Results: Relative to control subjects, TG levels in CAD patients were higher and HDL-C levels were lower. In CAD patients, non-traditional lipid profile values (TC/HDL-C, AI, and AIP) were significantly elevated relative to controls. AIP was positively correlated with TC (r = 0.157), TG (r = 0.835), LDL-C (r = 0.058), non-HDL-C (r = 0.337), TC/HDL-C (r = 0.683), LDL-C/HDL-C (r = 0.437), LCI (r = 0.662), and AI (r = 0.684), and negatively correlated with HDL-C (r = − 0.682) (all P < 0.001), but was independent of age (r = − 0.022; P = 0.130) and BMI (r = 0.020, P = 0.168). Aunivariate logistic regression analysis revealed AIP to be the measured lipid parameter most closely related to CAD, and its unadjusted odds ratio was 1.824 (95% CI: 1.467–2.267, P < 0.001). After adjusting for several CAD risk factors (age, BMI, smoking, drinking, EH, DM, hyperlipidemia, and family history of CVD, AIP was still found to represent a significant CAD risk factor (OR 1.553, 95% CI: 1.234–1.955, P < 0. 001). Conclusion: AIP may be a powerful independent predictor of CAD risk in Chinese Han postmenopausal women, and may be superior to the traditional lipid indices. [ABSTRACT FROM AUTHOR]

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9), which plays a crucial role in lipoprotein metabolism, has been also regarded as an important marker for atherosclerosis. Available evidence indicated that 2-h postchallenge plasma glucose (2-hPG) could be another biomarker for atherosclerosis. However, currently the association between circulating PCSK9 and 2-hPG remains unclear. Here, we explored this potential link in a Chinese Han population. Methods: Totally, 600 Chinese Han subjects from Nanjing district, China, were enrolled for the 75-g oral glucose tolerance test (OGTT), and they included normal glucose tolerance (NGT, n = 200), impaired glucose regulation (IGR, n = 200), and type 2 diabetes (T2DM, n = 200). Anthropometric and biochemical determinations such as serum lipid measurements were made. A sandwich ELISA assay was performed to measure serum PCSK9 levels in all subjects. Results: Serum PCSK9 concentrations were higher in IGR group (77.63 ± 28.14 ng/ml) and T2DM group (90.62 ± 39.96 ng/ml) than in NGT group (65.33 ± 32.68 ng/ml), and it was significantly higher in T2DM group than in IGR group (p < 0.01). Serum PCSK9 levels positively correlated with 2-hPG and LDL-C in all subgroups, but presented a positive correlation with fasting blood glucose (FBG) only in T2DM group. Using multiple regression model analysis, we also found that PCSK9 levels closely correlated with 2-hPG in all tested groups. According to multinomial logistic regression analysis, PCSK9 levels positively correlated with T2DM (OR = 1.017[1.010-1. 025], p < 0.001) even after adjustment for lipid levels. Moreover, in subjects with normal FBG level, 2-hPG gradually and significantly increased across PCSK9 tertiles (6.68 ± 2.01, 7.48 ± 2.10 and 8.27 ± 2.41 mmol/L, respectively, p < 0.01); however, in subjects with normal 2-hPG levels, no such difference was observed. Conclusions: PCSK9 levels increase as glucose metabolism deteriorated. Serum PCSK9 levels positively correlated with 2-hPG in patients with metabolic diseases. [ABSTRACT FROM AUTHOR]

Background: The associations of the apolipoprotein B gene ( APOB) rs693 and rs17240441 polymorphisms with plasma levels of APOB and lipids have been widely explored, but the results were inconclusive. This meta-analysis aimed to clarify the associations of the rs693 and rs17240441 polymorphisms with fasting APOB and lipid levels. Methods: Sixty-one studies (50,018 subjects) and 23 studies (8425 subjects) were respectively identified for the rs693 and rs17240441 polymorphisms by searching in PubMed, Google Scholar, Web of Science, Cochrane Library, Wanfang, VIP and CNKI databases. The following information was collected for each study: first author, age, gender, ethnicity, health condition, sample size, genotyping, lipid assay method, mean and standard deviation or standard error of APOB and lipid variables by genotypes. A dominant model was used for this meta-analysis. Results: The carriers of the rs693 variant allele (T) had higher levels of APOB [standardized mean difference (SMD) = 0.26, 95% confidence interval (CI) = 0.16-0.36, P < 0.01], triglycerides (TG) (SMD = 0.12, 95% CI = 0.05-0.20, P < 0.01), total cholesterol (TC) (SMD = 0.24, 95% CI = 0.17-0.30, P < 0.01) and low-density lipoprotein cholesterol (LDL-C) (SMD = 0.22, 95% CI = 0.14-0.30, P < 0.01), and lower levels of high-density lipoprotein cholesterol (HDL-C) (SMD = −0.06, 95% CI = −0.11-0.01, P = 0.01) than the non-carriers. The carriers of the rs17240441 deletion allele had higher levels of APOB (SMD = 0.13, 95% CI = 0.06-0.20, P < 0.01), TC (SMD = 0.17, 95% CI = 0.07-0.26, P < 0.01) and LDL-C (SMD = 0.15, 95% CI = 0.07-0.23, P < 0.01) than the non-carriers. Conclusions: The rs693 polymorphism is significantly associated with higher levels of APOB, TG, TC and LDL-C, and lower levels of HDL-C. The rs17240441 polymorphism is significantly associated with higher levels of APOB, TC and LDL-C. Further studies are needed to elucidate the underlying mechanisms. [ABSTRACT FROM AUTHOR]

Background: Previous studies suggest that dipeptidyl peptidase-4 (DPP-4) inhibitors and sodium glucose cotransporter 2 (SGLT2) inhibitors have different effects on the lipid profile in patients with type 2 diabetes. We investigated the effects of DPP-4 inhibitors and SGLT2 inhibitors on the lipid profile in patients with type 2 diabetes. Methods: From January 2013 to December 2015, a total of 228 patients with type 2 diabetes who were receiving a DPP-4 inhibitor or SGLT2 inhibitor as add-on therapy to metformin and/or a sulfonylurea were consecutively enrolled. We compared the effects of DPP-4 inhibitors and SGLT2 inhibitors on the lipid profile at baseline and after 24 weeks of treatment. To compare lipid parameters between the two groups, we used the analysis of covariance (ANCOVA). Results: A total of 184 patients completed follow-up (mean age: 53.1 ± 6.9 years, mean duration of diabetes: 7.1 ± 5. 7 years). From baseline to 24 weeks, HDL-cholesterol (HDL-C) levels were increased by 0.5 (95% CI, -0.9 to 2.0) mg/dl with a DPP-4 inhibitor and by 5.1 (95% CI, 3.0 to 7.1) mg/dl with an SGLT2 inhibitor (p = 0.001). LDL-cholesterol (LDL-C) levels were reduced by 8.4 (95% CI, -14.0 to -2.8) mg/dl with a DPP-4 inhibitor, but increased by 1.3 (95% CI, -5.1 to 7.6) mg/dl with an SGLT2 inhibitor (p = 0.046). There was no significant difference in the mean hemoglobin A1c (8.3 ± 1.1 vs. 8.0 ± 0. 9%, p = 0.110) and in the change of total cholesterol (TC) (p = 0.836), triglyceride (TG) (p = 0.867), apolipoprotein A (p =0. 726), apolipoprotein B (p= 0.660), and lipoprotein (a) (p = 0.991) between the DPP-4 inhibitor and the SGLT2 inhibitor. Conclusions: The SGLT2 inhibitor was associated with a significant increase in HDL-C and LDL-C after 24 weeks of SGLT2 inhibitor treatment in patients with type 2 diabetes compared with those with DPP-4 inhibitor treatment in this study. [ABSTRACT FROM AUTHOR]

Background: Lipids, which are associated with atherogenesis, clotting, and the fibrinolytic pathway, may be important prognostic indicators of recurrent myocardial infarction. The aim of this study was to determine the predictive value of baseline lipid fractions for nonfatal recurrent myocardial infarction in patients with ST segment elevation myocardial infarction 2 years after primary percutaneous coronary intervention in China. Methods: Cox proportional-hazards models were used to evaluate the association between potential risk factors, including lipid fractions, and the occurrence of nonfatal recurrent myocardial infarction in 2402 consecutive patients who underwent primary percutaneous coronary intervention for ST segment elevation myocardial infarction. Results: The cumulative incidence of recurrent myocardial infarction was 2.7% at 1 year, 3.8% at 2 years, and 5.8% at 3 years after percutaneous coronary intervention. The effects of collinearity of lipids were investigated. In concerning the principal components analysis, composing factor 1 (scoring factors were 0.689 for non-HDL, 0.702 for LDL, 0.182 for HDL) which had eigenvalues of 1.86 and explained 62% of the variability among lipid cholesterols was significantly associated with recurrent MI in the final adjusted analysis of the lipid cholesterols principal components. Non-high-density lipoprotein cholesterol was the strongest independent predictor of nonfatal recurrent myocardial infarction. The adjusted hazards ratios for nonfatal recurrent myocardial infarction were 1.26 (95% confidence interval (CI): 1.05-1.51) for non-high-density lipoprotein cholesterol, 1.17 (95% CI: 0.99-1.39) for low-density lipoprotein and 1.15 (95% CI: 0.95-1.40) for HDL. After adjusting for gender and age, the odds ratio for patients in the highest non-high-density lipoprotein cholesterol quartile was 2.10 (95% CI: 1.19-3.72). Conclusions: Non-high-density lipoprotein cholesterol value is a stronger predictor of nonfatal recurrent myocardial infarction than other lipid risk factors in patients with ST segment elevation myocardial infarction. Moreover, the occurrence of reinfarction after percutaneous coronary intervention was highest for patients in the highest nonhigh- density lipoprotein cholesterol quartile. [ABSTRACT FROM AUTHOR]

Background: High-fat diets may contribute to metabolic disease via postprandial changes in serum endotoxin and inflammation. It is unclear how dietary fat composition may alter these parameters. We hypothesized that a meal rich in n-3 (ω3) fatty acids would reduce endotoxemia and associated inflammation but a saturated or n-6 (ω6) fatty acid-rich meal would increase postprandial serum endotoxin concentrations and systemic inflammation in healthy adults. Methods: Healthy adults (n = 20; mean age 25 ± 3.2 S.D. years) were enrolled in this single-blind, randomized, crossover study. Participants were randomized to treatment and reported to the laboratory, after an overnight fast, on four occasions separated by at least one week. Participants were blinded to treatment meal and consumed one of four isoenergetic meals that provided: 1) 20 % fat (control; olive oil) or 35 % fat provided from 2) n-3 (ω3) (DHA = 500 mg; fish oil); 3) n-6 (ω6) (7.4 g; grapeseed oil) or 4) saturated fat (16 g; coconut oil). Baseline and postprandial blood samples were collected. Primary outcome was defined as the effect of treatment meal on postprandial endotoxemia. Serum was analyzed for metabolites, inflammatory markers, and endotoxin. Data from all 20 participants were analyzed using repeated-measures ANCOVA. Results: Participant serum endotoxin concentration was increased during the postprandial period after the consumption of the saturated fat meal but decreased after the n-3 meal (p < 0.05). The n-6 meal did not effect a different outcome in participant postprandial serum endotoxin concentration from that of the control meal (p > 0. 05). There was no treatment meal effect on participant postprandial serum biomarkers of inflammation. Postprandial serum triacylglycerols were significantly elevated following the n-6 meal compared to the n-3 meal. Non-esterified fatty acids were significantly increased after consumption of the saturated fat meal compared to other treatment meals. Conclusions: Meal fatty acid composition modulates postprandial serum endotoxin concentration in healthy adults. However, postprandial endotoxin was not associated with systemic inflammation in vivo. [ABSTRACT FROM AUTHOR]

Background: Little is known regarding the interactions of methylenetetrahydrofolate reductase (MTHFR) C677T and methionine synthase reductase (MTRR) A66G polymorphisms with overweight/obesity on serum lipid profiles. The aim of the current study was to explore interactions between the two polymorphisms and overweight/obesity on four common lipid levels in a Chinese Han population and further to evaluate whether these interactions exhibit gender-specificity. Methods: A total of 2239 participants (750 females and 1489 males) were enrolled into this study. The genotypes of the MTHFR C677T and MTRR A66G were determined by a TaqMan assay. Overweight and obesity were defined as a body mass index between 24 and 27.99 and ≥ 28 kg/m2, respectively. The interactions were examined by factorial design covariance analysis, and further multiple comparisons were conducted by Bonferroni correction. Results: There was no significant difference in the genotypic and allelic frequencies between females and males (MTHFR 677 T allele: 54.47 % for females and 54.40 % for males; MTRR 66G allele: 24.73 % for females and 24.71 % for males). Interaction between the MTHFR C677T polymorphism and overweight/obesity on serum triglyceride levels, and interaction between the MTRR A66G polymorphism and overweight/obesity on serum high-density lipoprotein cholesterol levels were detected in women (P = 0.015 and P = 0.056, respectively). For female subjects with overweight/obesity, the serum triglyceride levels in MTHFR 677TT genotype [1.09 (0.78-1.50) mmol/L] were significantly higher as compared with MTHFR 677CC genotype [0.90 (0.60-1.15) mmol/L, P = 0.007], and the MTRR 66GG genotype carriers had higher serum high-density lipoprotein cholesterol levels than those with MTRR 66AG genotype (1.46 ± 0.50 vs. 1.19 ± 0.31 mmol/L, P = 0.058). Furthermore, in male subjects with overweight/obesity, the MTHFR 677CT genotype carriers had higher low-density lipoprotein cholesterol levels than those with MTHFR 677TT genotype (2.96 ± 1.07 vs. 2.74 ± 0.88 mmol/L, P = 0.015). Conclusions: Our results indicate that there exist interactive effects of the MTHFR C677T and MTRR A66G polymorphisms with overweight/obesity on some lipid traits in Chinese Han population, and the effects were gender-specific. [ABSTRACT FROM AUTHOR]

Background: The APOA5 rs662799 polymorphism has been widely reported regarding its associations with the plasma lipid levels and the occurrence of coronary heart disease (CHD), whereas its relationship with the severity of CHD has not yet been explored. Methods: Four hundred and seventy-eight angiografically defined subjects (325 CHD patients and 153 CHD-free controls) were enrolled in this study. The rs662799 polymorphism was genotyped, and the fasting lipid data were collected for all participants. The severity of CHD was evaluated for the CHD patients by using Gensini scores. Results: The variant C allele of the rs662799 polymorphism was associated with lower levels of HDL-C in CHD-free women, and higher levels of TG and TG/HDL-C in women with CHD (P < 0.05 for all). The C allele was associated with higher prevalence of dyslipidemia and higher levels of Gensini scores only in women (P < 0.05 for both), but not in men. Multivariate linear regression analysis showed that the rs662799 polymorphism was independently associated with the Gensini scores in women after adjustment for other potential CHD risk factors (Beta = 0.157, 95 % CI: 0.017-0.298, P = 0.028). Conclusion: Our data indicate that the rs662799 polymorphism is associated with dyslipidemia and the severity of CHD in Chinese women. [ABSTRACT FROM AUTHOR]

Background: High lipid levels may constitute a more important risk factor for cognitive health in previous studies. However, the association of plasma lipids with mild cognitive impairment (MCI) among elderly people had not been studied exactly. This study aims to explore the relationship between plasma lipids/lipoproteins and the risk of MCI in elderly Chinese individuals. Methods: CSI-MCI study was a preliminary case-control study of the association of plasma lipids/lipoproteins with MCI in 112 MCI cases and 115 cognitively normal controls. Plasma total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) levels were measured in fasting blood samples. Multivariable logistic regression was used to evaluate the potential association between MCI and these factors. Statistical models were adjusted for multiple demographic and biological covariates. Results: The subjects with MCI were significantly older, higher percentage of females and less educated than controls (P <0.05). As expected, subjects with MCI had lower MMSE score compared with controls (P <0.05). Multivariate logistic regression analysis showed that higher plasma TC level was associated with the risk of MCI in models adjusting for age, sex and education. However, This association was attenuated after adjusting for BMI, Type 2 diabetes mellitus, heart disease and hypertension. Plasma TG level was negatively associated with the risk of MCI. The adjusted odds ratio (OR) of MCI was significantly reduced for the highest quartile of plasma TG level (OR: 0.76, 95 % CI: 0.48-0.97), but not for the second or third quartile, compared with the lowest quartile (adjusted models). Plasma HDL level was significantly negatively associated with the risk of MCI. There was no association between plasma LDL level and the risk of MCI, adjustment for demographics, vascular disorders did not change this relation. Conclusions: Plasma TC was significantly higher in MCI subjects compared to cognitively normal controls, Elevated plasma HDL and triglyceride were associated with the occurrence of MCI. These findings need to be confirmed in further longitudinal studies. [ABSTRACT FROM AUTHOR]

Background: No previous meta-analysis was to report the association between the apolipoprotein B (APOB) XbaI and EcoRI polymorphisms and serum lipids in Chinese. We performed the study to investigate their potentially association. Methods and Results: Studies in English and Chinese were found via a systematic search of Pubmed, Embase, CNKI and Wanfang databases. The dominant genetic model and random-effects model were used to pool data from individual studies. As a result, a total of 30 articles with 5611 subjects for XbaI and 2653 subjects for EcoRI were included in the current study. For the XbaI polymorphism, overall, subjects carrying X+ allele were significantly associated with higher TC,TG and LDL compared with X-X- genotype (Pvalue =0.0006, OR (95 %) = -0.55 (-0.86,-0.23); Pvalue = 0.0004, OR (95 %) = -0.30 (-0.47,-0.14); (Pvalue = 0.05, OR (95 %) = -0.23(-0.46,-0.00), respectively). Similar results were observed in the subgroups of Han, healthy individuals (HT), coronary heart disease (CHD), cerebral infarction (CI), and cholelithiasis. For HDL, positive association between X+ allele with Lower lipid value was found in CHD and CI subgroups. For EcoRI polymorphism, overall, the E- allele carriers were found to be obviously linked with elevated LDL and lower HDL compared with E + E+ genotype (Pvalue = 0.02,OR (95 %) = -0.27 (-0.49,-0.05); Pvalue = 0.01, OR (95 %) = 0.17 (0.03, 0.30), respectively). TC was significantly high in subjects carrying E- allele in the subgroup of hyperlipidemia. No evidence of publication bias was observed. Conclusions: The two genetic variants of APOB may be associated with serum lipids in Chinese. [ABSTRACT FROM AUTHOR]

Background: Recent genome-wide association studies (GWAS) have identified the variants near TRIB1 gene affecting blood lipid levels. However, the association between the reported variants and risk of coronary heart disease (CHD) was not confirmed. Methods: We conducted two independent case-control studies. The first study consisted of 300 CHD patients and 300 controls and the second study had 1,332 CHD patients and 2,811 controls. The genotypes of two variants rs3201475 and rs17321515 in TRIB1 were determined by TaqMan assay. The dual-luciferase reporter assay was performed for evaluating the function of the SNP rs3201475. Results: The statistical analysis indicated that single nucleotide polymorphism (SNP) rs17321515 was replicated to be associated with triglyceride (TG) level, which was also significantly associated with CHD risk when using the stratified analysis after adjusting for conventional risk factors. Compared with GG genotype, AA carriers of SNP rs17321515 had higher risk in males (odds ratio (OR) = 1.28, 95 %CI = 1.01-1.61; P = 0.03) and smokers (OR = 1.41, 95%CI = 1.09-1.88; P = 0.01). We did not find significantly association between genotypes of rs3201475 and CHD risk. In addition, no significant difference was found in the luciferase activity assay of SNP rs3201475. Conclusions: Our findings indicated that SNP rs17321515 is significantly associated with plasma TG level and the increasing risk of CHD among males and smokers in Chinese, whereas there is no positive association between SNP rs3201475 and CHD risk. Smoking could modify the effects of TRIB1 on CHD risk. [ABSTRACT FROM AUTHOR]

Background: Serum lipid levels are associated with the risk of intracerebral hemorrhage (ICH). Genetic variants in the apolipoprotein C3 (APOC3) gene were associated with plasma triglyceride (TG) and very-low-density lipoprotein (VLDL) levels. The aim of this study was to evaluate the effect of two genetic variants (1100 C/T and 3238 C/G) of APOC3 on serum lipid levels and risk of ICH. Methods: A prospective hospital-based case-control design and logistic regression analysis were utilized. We enrolled 150 ICH patients and 150 age- and gender-matched controls. The APOC3 gene polymorphisms were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: ICH patients had a significantly higher frequency of APOC3 3238 GG genotype [odds ratio (OR) =2.97, 95 % confidence interval (CI) = 1.20, 7.38; P = 0.02] and APOC3 3238 G allele (OR =1.53, 95 % CI = 1.03, 2.27; P = 0.04) than controls. The APOC3 3238 G allele was significantly associated with increasing plasma TG levels and VLDL levels both in ICH cases (P = 0.01) and controls (P = 0.02). No association was found between APOC3 1100 C/T polymorphisms and ICH. Conclusion: To the best of our knowledge, this is the first report in the literature that the APOC3 3238 GG genotype and G allele might contribute to an increased risk of ICH as a result of its effect on serum lipid levels. [ABSTRACT FROM AUTHOR]

Background: Studies of the association between the apolipoprotein C3 gene (APOC3) rs5128 polymorphism and plasma levels of apolipoprotein C3 (APOC3) and lipids have reported apparently conflicting findings. This meta-analysis aimed to investigate the associations of the rs5128 polymorphism with fasting APOC3 and lipid levels. Methods: The following information was abstracted for each study: ethnicity, age, sex, health condition, sample size, genotyping and lipid assay methods, mean and standard deviation or standard error by genotypes for APOC3 and lipid variables. There were 42 eligible studies with 23846 subjects included in this meta-analysis. A dominant model was used for this meta-analysis. Results: The results showed that the carriers of the variant allele G had higher levels of APOC3 [standardized mean difference (SMD): 0.22, 95% confidence interval (CI): 0.12-0.31, P < 0.00001], triglycerides (TG) (SMD: 0.33, 95% CI: 0.23-0.44, P < 0.00001), total cholesterol (TC) (SMD: 0.15, 95% CI: 0.09-0.22, P < 0.00001), and low-density lipoprotein cholesterol (LDL-C) (SMD: 0.11, 95% CI: 0.04-0.17, P = 0.001) than the non-carriers. No significant association between the APOC3 rs5128 polymorphism and lower levels of high-density lipoprotein cholesterol (HDL-C) was detected under the dominant model (SMD: -0.03, 95% CI: -0.06-0.01, P = 0.156). Conclusions: The results from the present meta-analysis demonstrate a significant association between the APOC3 rs5128 polymorphism and higher levels of APOC3, TG, TC and LDL-C, but further studies are needed to elucidate the underlying mechanisms. [ABSTRACT FROM AUTHOR]

Background: The disorder of triglyceride (TG) metabolism leading to hypertriglyceridemia is an independent risk factor for coronary artery disease (CAD). Variants in the apolipoprotein C3 (APOC3) gene were found to be associated with elevated TG levels. The purpose of this study was to investigate the effect of two polymorphisms (1100 C/T and 3238 C/G) of APOC3 on plasma lipid and risk of CAD in a Chinese population. Methods: The study population consisted of 600 patients with CAD and 600 age- and gender-matched controls. The APOC3 gene polymorphism was analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: Patients with CAD had a significantly higher frequency of APOC3 3238 GG genotype [odds ratio (OR) =1.64, 95% confidence interval (CI) =1.10, 2.43; P = 0.01] and APOC3 3238 G allele (OR =1.27, 95% CI =1.04, 1.55; P = 0.02) than controls. The findings are still emphatic by the Bonferroni correction. When stratifying by hyperlipidemia, CAD patients with hyperlipidemia had a significantly higher frequency of APOC3 3238 GG genotype (OR =1.73, 95% CI =1.13, 2.64; P = 0.01) than without hyperlipidemia. The APOC3 3238 G allele was significantly associated with increasing plasma TG levels and very-low-density lipoprotein cholesterol (VLDL-C) levels both in cases and controls (P < 0.001). Conclusions: The APOC3 3238 G allele might contribute to an increased risk of CAD as a result of its effect on TG and VLDL-C metabolism. [ABSTRACT FROM AUTHOR]

Background: The effects of fish oil supplements on lipid profile in dialysis patients are controversial. With increasing interest in the potential health benefits of fish oil, it is important to explore its real effects. Objective: We aimed to identify and quantify the effects of fish oil on triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in dialysis patients. Methods: PubMed, EMBASE and the Cochrane Central Register of Controlled Trials were searched for relevant trials of fish oil and lipid profile in dialysis patients. We identified 209 potential studies and included 13 randomized controlled trials. Eligible studies, determined by consensus using predefined criteria, were reviewed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and a meta-analysis was performed. Results: Compared with the control group, serum TG and TC levels in the fish oil group were reduced by 0.23 mmol/L (95% CI, −0.31, −0.14, P <0.01) and 0.12 mmol/L (95% CI, −0.23, −0.01, P =0.03), respectively. HDL-C levels were increased by 0.20 mmol/L (95% CI, 0.01, 0.40, P <0.01) attributable to fish oil. In contrast, fish oil did not influence serum LDL-C levels. Subgroup analysis showed the effects of fish oil were stronger in subjects with higher baseline TG levels, and the long-term intervention (>12w) demonstrated a tendency towards greater improvement of serum HDL-C and LDL-C levels compared with short-term intervention (≤12 w). However, both of the changes were not statistically significant in meta-regression analysis. There were no obvious difference in effects of different doses and components of fish oil on lipid levels. Conclusion: Fish oil supplements reduced serum TG and TC levels, and increased HDL-C levels, without affecting LDL-C levels among dialysis patients. It should benefit patients at risk of cardiovascular diseases. Based on randomized controlled trials, we suggested a daily supplement dose of fish oil for dialysis patients of >1 g, but a high dose might not be necessary. [ABSTRACT FROM AUTHOR]

Background Some experimental animal studies reported that vanadium had beneficial effects on blood total cholesterol (TC) and triglyceride (TG). However, the relationship between vanadium exposure and lipid, lipoprotein profiles in human subjects remains uncertain. This study aimed to compare the serum lipid and lipoprotein profiles of occupational vanadium exposed and non-exposed workers, and to provide human evidence on serum lipid, lipoprotein profiles and atherogenic indexes changes in relation to vanadium exposure. Methods This cross-sectional study recruited 533 vanadium exposed workers and 241 non-exposed workers from a Steel and Iron Group in Sichuan, China. Demographic characteristics and occupational information were collected through questionnaires. Serum lipid and lipoprotein levels were measured for all participants. The ratios of total cholesterol to high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) to HDL-C and apoB to apoA-I were used as atherogenic indexes. A general linear model was applied to compare outcomes of the two groups while controlling possible confounders and multivariate logistic regression was performed to evaluate the relationship between low HDL-C level, abnormal atherogenic index and vanadium exposure. Results Higher levels of HDL-C and apoA-I could be observed in the vanadium exposed group compared with the control group (P < 0.05). Furthermore, atherogenic indexes (TC/HDL-C, LDL-C/HDL-C, and apoB/apoA-I ratios) were found statistically lower in the vanadium exposed workers (P < 0.05). Changes in HDL-C, TC/HDL-C, and LDL-C/HDL-C were more pronounced in male workers than that in female workers. In male workers, after adjusting for potential confounding variables as age, habits of smoking and drinking, occupational vanadium exposure was still associated with lower HDL-C (OR 0.41; 95% CI, 0.27-0.62) and abnormal atherogenic index (OR 0.38; 95% CI, 0.20-0.70). Conclusion Occupational vanadium exposure appears to be associated with increased HDL-C and apoA-I levels and decreased atherogenic indexes. Among male workers, a significantly negative association existed between low HDL-C level, abnormal atherogenic index and occupational vanadium exposure. This suggests vanadium has beneficial effects on blood levels of HDL-C and apoA-I. [ABSTRACT FROM AUTHOR]

Background: Women often lag behind men in their risk of cardiovascular events. However, with age and the onset of menopause, women's cardiovascular risk eventually becomes similar to that of men. This change in risk may, in part, be attributable to a shift to a more atherogenic lipid profile. Our objective was to evaluate standard- and sub-lipid parameters and the apo A1 remnant ratio: (apo A1/[VLDL3-C+IDL-C]) for their associations with death/ myocardial infarction among peri- and post-menopausal women. Methods: Women (N=711) >50 years of age undergoing coronary angiography were evaluated. Baseline clinical and angiographic characteristics, lipids, and sub-lipid levels (Vertical Auto Profile method) were collected. Cox regression analysis, adjusted by standard cardiovascular risk factors, was utilized to determine associations of lipid and sub-lipid tertiles(T) with death/myocardial infarction at 1 and 3 years. Results: Patients averaged 67.7±9.4 years and 53.6% had underlying severe (⩾70% stenosis) coronary artery disease. The apo A1 remnant ratio was found to have stronger associations for 1 year (T1 vs. T3: HR=2.13, p=0.03, T2 vs. T3: HR=1.57, p=0.21) and 3 year (T1 vs. T3: HR=2.32, p=0.002, T2 vs. T3: HR=1.97, p=0.01) death/myocardial infarction than any individual lipid (LDL-C, HDL-C, triglycerides, non-HDL-C) or sub-lipid (apo A1, apo B, VLDL3-C+IDL-C) measure, or any other well-known ratio (triglyercies/HDL-C, apo B/A1, TChol/HDL-C, HDL-C/[VLDL3-C+IDL-C]). Conclusions: The apo A1 remnant ratio was a significant predictor of short and intermediate-term death/ myocardial infarction risk among women >50 years of age. Furthermore, this ratio was found to have greater predictive ability than traditional lipid and sub-lipid parameters and represents a potential new risk marker. [ABSTRACT FROM AUTHOR]

Background: The study was designed to investigate lipid profile and SYNTAX score in patients with non-ST segment elevation myocardial infarction (NSTEMI). Methods: 311 patients with NSTEMI were enrolled. The demographic, clinical data, blood samples and SYNTAX score were documented. The Pearson linear correlation was used to detect confounding factors linearly correlated with SYNTAX score. The significantly correlated confounding factors were put into the multiple linear regressions. Results: The Pearson linear correlation showed that high-density lipoprotein- cholesterol (HDL-C) and apolipoprotein A1 (ApoA1) were significantly correlated with Syntax Score (r = − 0.119, P = 0.044 and r = − 0.182, P = 0.002, respectively). The multiple linear regressions for Syntax Score were built using HDL-C and ApoA1, respectively. After the adjustment of other significantly correlated confounding factors such as white blood cell count (WBC), myohemoglobin (MB), glutamic-oxalacetic transaminase (AST) and creatinine, the ApoA1 still showed significant association with Syntax Score (β = − 0.151, P = 0.028). The area under curve was (AUC) 0.624 and the optimal cutoff value is 1.07 g/L when using ApoA1 to predict moderate and severe coronary artery lesions. The patients with ApoA1 ≥ 1.07 g/L and < 1.07 g/L have the Syntax Scores of 12.21 ± 11.58 and 16.33 ± 11.53, respectively (P = 0.001). Conclusions: The ApoA1 is the only lipid factor significantly associated with complexity of coronary artery lesion in patients with NSTEMI, the patients with ApoA1 < 1.07 g/L may have more complex coronary artery lesions. [ABSTRACT FROM AUTHOR]

Background: Combination of statins and clopidogrel is frequently administered in patients with coronary artery disease (CAD). They are mainly activated and eliminated in the liver by cytochrome P450 isoenzyme 3A4 (CYP3A4). The aim was to clarify whether the coadministration of clopidogrel and statins attenuate respective efficacy. Methods: PubMed, Embase, the Cochrane Library, Web of Science and Clinical Trials. gov were searched for until August 2018. Randomized controlled trials (RCTs) and cohort studies were taken into quality evaluation. Data were pooled using random effect models to estimate standard mean difference (SMD) or risk ratio (RR) with 95% confidence interval (CI). Results: In total, 28 studies representing 25,267 participants were included. Statins reduce the mortality of patients administered clopidogrel (RR 0.54; 95% CI 0.40,0.74; p = 0.000), no differences were found in platelet aggregation (PA) (SMD 0.02; 95% CI -0.38,0.42; p = 0.920) and the expressions of P-selectin (SMD -0.04; 95% CI -0.14,0.05; p = 0.346), CD40L (SMD 0.09; 95% CI -0.29,0.48; p = 0.633), CD63 (SMD 0.09; 95% CI -0.01,0.19; p = 0.079) and PAC-1 (SMD 0.03; 95% CI -0.08,0.13; p = 0.633). Furthermore, CYP3A4 metabolized or non-CYP3A4 metabolized statins have no discrepancies in PA (SMD 0.13; 95% CI -0.31,0.58; p = 0.556), P-selectin (SMD 0.17; 95% CI -0.16,0.51; p = 0310), death (RR 0.89; 95% CI 0.38,2.07; p = 0.791), except for triglyceride (TG) (SMD -0.19; 95% CI –0.33,-0.06; p = 0.005). Conclusions: This meta-analysis confirmed that statins reduce mortality in patients undergoing clopidogrel treatment without affecting platelet activation and aggregation. [ABSTRACT FROM AUTHOR]

Objective: The value of atherogenic index of plasma (AIP) as a predictive biomarker for coronary artery disease (CAD) remains controversial. In addition, whether AIP is associated with the risk of acute coronary syndrome (ACS) in very young adults has not been well established. Methods: We consecutively collected very young adults (≤35 years of age) undergoing coronary angiography (CAG) at Anzhen Hospital, between January 2008 and December 2017. Total of 1, 478 very young participants, including 1, 059 ACS patients and 419 non-CAD subjects, were enrolled in the present study. Results: Very young patients with ACS had higher AIP level compared with non-CAD participants (0.35 ± 0.30 vs 0.21 ± 0.33, P < 0.001). According to Gensini Score (GS) and number of lesion vessel, patients were divided into four groups, respectively. With the elevated GS score and number of lesion vessels, the AIP level increased gradually (Pfor trend all< 0.05). Multivariate logistic regression analyses suggested that AIP remained to be independently associated with the presence of ACS and was superior to traditional lipid profiles (for AIP, OR = 2.930, 95% CI = 1.855–4.627, P < 0.001; for total cholesterol, OR = 1.152, 95% CI = 1.048–1.266, P = 0.003; for triglyceride, OR = 1.078, 95% CI = 0.991–1.172, P = 0.079; for low-density lipoprotein cholesterol, OR = 1.046, 95% CI = 1.015–1.078, P < 0.001), after adjustment for other traditional confounders. Moreover, the prevalence of ACS, acute myocardial infarction, unstable angina pectoris and the value of GS were also elevated as AIP quartiles increased (Pfor trend < 0.001). Subgroup analysis based on gender revealed that AIP was only independently associated with the ACS risk in male. Conclusions: AIP was independently associated with the presence and severity of ACS in very young patients in a gender-dependent manner, which might be superior to traditional lipid profiles. [ABSTRACT FROM AUTHOR]

Background: The majority of pregnant women present an increase in lipids. To investigate the influence of the non-fasting state in the lipid and lipoprotein profile in pregnancy, we have aimed to assess the dynamic change of serum lipid and lipoprotein profile with serum glucose in pregnancy to contrast the differences between fasting and non-fasting state. Methods: Forty-five pregnant women and 41 controls were included in our study. All serum samples were assayed for TC, TG, HDL-C, LDL-C, ApoB, ApoA-1, Lp(a), sdLDL, and Glu concentrations. The comparison between pregnant women and controls (fasting and 2 h after breakfast), differences of these measurement results at three point-in-time, the associations between the concentrations of serum lipid and some maternal and fetus characteristics was conducted with statistical analysis. Results: Except Glu (p < 0.001), there were no significant differences of all lipids between three point-in-time in pregnant women (p > 0.1). The statistically higher levels were found in fasting TC (p = 0.003), TG (p = 0.019), LDL-C (p = 0.002), ApoB (p = 0.001), ApoA1 (p = 0.013) and sdLDL (p < 0.001) of pregnant women compared with controls. Besides, the statistically significances were also found in 2-h TC (p = 0.001), LDL-C (p = 0.001), ApoB (p < 0.001), Glu (p = 0.013), ApoA-1 (p = 0.009) and sdLDL (p < 0.001) of pregnant women compared with controls. Otherwise, in non-fasting status (2 h after breakfast), pregnancy complication was relevant to TC (p = 0.041), HDL-C (p = 0.014), Glu (p = 0.004). Delivery mode was relevant to TC (p = 0.012), HDL-C (p = 0.013), LDL-C (p = 0.026), ApoA-1 (p = 0.012), and sdLDL (p = 0.044). BMI was relevant to TG (p = 0.027). Conclusion: We have suggested the non-fasting lipids detection can be used for estimate lipid metabolism in pregnant women. [ABSTRACT FROM AUTHOR]

Background: Few studies looked at the prevalence of dyslipidemia in pediatric Middle-Eastern countries. In addition, worldwide longitudinal changes of lipid profile is not well documented. The purpose of this study is to look at the longitudinal changes of lipid parameters in Lebanese school-age children. Materials and methods: A total of 97 subjects (41 girls and 56 boys) aged between 11 and 21 years were included in this study. The subjects were selected among 339 school-age children with a previous abnormal lipid profile who were recruited from 10 schools of varying socio-economic levels (SEL). A fasting lipid profile [total cholesterol (TC), triglycerides (TG) and HDL-cholesterol (HDL-C)] was performed. Non-HDL-cholesterol (Non-HDL-C) was calculated. Weight and height were measured under the same conditions, and BMI percentiles were calculated. A multivariate covariance analysis model (MANCOVA) was used with TG, HDL-C and non-HDL-C as dependent variables with additional post-MANCOVA F tests. Results: The age of the current cohort is 16.5 ± 2.9 years with no significant difference according to gender. The current lipid profile was obtained 3.1 ± 0.7 years following the initial one, with 53.6% of the subjects having it normalized. TC, TG, and non-HDL-C decreased significantly over time in girls, while only TG decreased significantly in boys. No significant changes were observed for HDL-C. Using MANCOVA, a significant time by age interaction was observed (p < 0.0001), while gender, BMI and SEL were found not to be significant. Post-hoc F tests showed that the time by age interaction was driven by TG (p = 0.03) and non-HDL-C (p < 0.001), the larger effect being observed in younger children. Conclusion: A high proportion of school-age children normalize their abnormal lipid profile with time. Screening for lipid disorders could be postponed until post puberty age. [ABSTRACT FROM AUTHOR]

Background: Several meta-analyses have demonstrated that the rs662 polymorphism in Paraoxonase 1 gene (PON1) gene is associated with coronary heart disease (CHD). However, it is still uncertain whether this polymorphism is associated with the plasma levels of oxidized low-density lipoprotein (Ox-LDL) and lipids. This meta-analysis is aimed to clarify the relationships between the rs662 polymorphism and plasma levels of Ox-LDL and lipids. Methods: By searching in PubMed, Google Scholar, Web of Science, Cochrane Library, Wanfang, VIP and CNKI databases, 5 studies (1369 subjects) and 85 studies (46,740 subjects) were respectively identified for Ox-LDL association analysis and lipid association analysis. Standardized mean difference (SMD) was used to estimate the effects of the rs662 polymorphism on plasma Ox-LDL and lipid levels. Results: The carriers of the variant R allele had higher levels of Ox-LDL (SMD = 0.23, 95% CI = 0.10–0.36, P < 0.01), triglyceride (TG) (SMD = 0.06, 95% CI = 0.01–0.11, P = 0.02), total cholesterol (TC) (SMD = 0.04, 95% CI = 0.00–0.07, P = 0.05) and low-density lipoprotein cholesterol (LDL-C) (SMD = 0.04, 95% CI = 0.00–0.08, P = 0.04) than the non-carriers. Conclusions: This meta-analysis suggests that the association between the PON1 rs662 polymorphism and CHD may partly be mediated by abnormal Ox-LDL and lipid levels caused by the R allele. [ABSTRACT FROM AUTHOR]

Background: Abnormal lipid levels have been suggested as a mechanism leading to atherosclerosis of the lumbar vessels, resulting in low back pain (LBP). This study examined whether abnormal lipid levels were associated with LBP among middle-aged adults in Japan. Methods: The present study included adults between 40 and 64 years old who underwent an annual health checkup. A total of 258,367 eligible participants were analyzed to investigate associations of LBP with low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and LDL-C/HDL-C ratio. Participants were categorized into two groups according to each of LDL-C, HDL-C, and LDL-C/HDL-C ratio (LDL-C: ≥ 140 vs. < 140 mg/dL; HDL-C: ≥ 40 vs. < 40 mg/dL; LDL-C/HDL-C ratio: ≥ 2.5 vs. < 2.5). Information on LBP was obtained using a self-administered questionnaire. Logistic regression modeling was used to calculate the odds ratio (OR) and 95% confidence interval (CI) for LBP. Results: The prevalence of LBP was 2.2% in men and 2.1% in women. Multivariable analysis adjusting for age, body mass index, and lifestyle factors found significant associations for HDL-C < 40 mg/dL (OR, 1.34; 95%CI, 1.20–1.48 in men; OR, 1.32; 95%CI, 1.02–1.72 in women) and LDL-C/HDL-C ratio ≥ 2.5 (OR, 1.17; 95%CI, 1.09–1.26 in men; OR, 1.15; 95%CI, 1.03–1.29 in women) with LBP. Conclusions: Low HDL-C and high LDL-C/HDL-C ratio were significantly associated with LBP in a middle-aged Japanese population. These findings might support the atherosclerosis-LBP hypothesis. [ABSTRACT FROM AUTHOR]

Background: Lipid dysregulation is a classical risk factor for cardiovascular disease (CVD), yet scanty evidence existed regarding cardiac lipid metabolism that is directly related to heart damage. Recently, the relationship between dyslipidemia and pro-inflammatory insults has led to further understanding on the CVD-predisposing effects of dyslipidemia. The aims of the present study were to investigate whether high-fat high-cholesterol (HFHC) diet-induced hyperlipidemia would cause heart damage and to study the potential role of local cardiac lipid dysregulation in the occurrence of cellular injury. Methods: Male Sprague–Dawley rats were divided into normal chow or HFHC diet groups, and sacrificed after 2 or 4 weeks, respectively. Lipid peroxidation marker level was measured. Lipid parameters in the rat hearts were detected. Cardiac damage was evaluated. Results: HFHC diet increased serum levels of cholesterol and free fatty acids (FFAs) and led to systemic oxidative stress and pro-inflammatory status. Cardiac lipid dysregulation, which was characterized by elevated levels of cholesterol and adipocyte (A)- and heart (H)-fatty acid binding proteins (FABPs), occurred after HFHC diet for 4 weeks. Cardiac damage was further evident with elevated circulating H-FABP levels, increased cardiac interstitial fibrosis and the loss of troponin I. Conclusion: Our data demonstrated that HFHC diet led to systemic and cardiac lipid dysregulation, accompanied by systemic oxidative and pro-inflammatory stresses, and these may finally cooperate to cause a series of pathological changes of the heart tissue. Our findings suggest that maintenance of lipid regulation may be essential in the prevention of heart damage. [ABSTRACT FROM AUTHOR]

Background: The liver plays an important role in the metabolism of lipid and lipoprotein. Dyslipidemia has been demonstrated to be related with several cancers, but the association between serum lipid and hepatocellular carcinoma (HCC) in the absence of cirrhosis remains unclear. Methods: A total of 2528 patients with HCC at the Beijing Ditan Hospital between February 2008 and December 2017 were retrospectively included in the study. We identified 200 patients with HCC without cirrhosis by histopathology, imaging, endoscopic findings, and laboratory tests. Multivariate regression analysis was performed to determine the independent characteristics associated with HCC without cirrhosis and its prognosis. Results: In the logistics regression analysis, compared to patients with HCC with cirrhosis, patients with HCC without cirrhosis were more likely to have elevated triglyceride (TG) levels (OR = 2.66; 95% CI, 1.18–6.01; P = 0.019). The Kaplan-Meier analysis revealed that a lower TG level was a risk factor regardless of the presence of cirrhosis. The results of the Cox proportional hazard regression analysis showed that a decreased TG level was significantly related to a worse overall survival (HR = 0.51; 95% CI, 0.29–0.89; P = 0.017). Conclusion: Serum TG level may be an independent factor to predict the prognosis of patients with HCC in the absence of cirrhosis. [ABSTRACT FROM AUTHOR]