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Lifestyle during pregnancy impacts the health of the mother and child. However, the extent to which physical activity affects maternal biomarkers and factors that might influence birth weight remains unclear. We analysed data from two lifestyle interventions in which the effects of an exercise programme (2x/week, 60–90 min) on the course of pregnancy with regard to adipokines and offspring were evaluated. A total of 70 women participated in this study (45, intervention group; 25, control group). Anthropometric data and maternal fasting serum leptin and resistin levels were measured at three time points (approximately 14th (T1), 24th (T2), and 36th (T3) weeks of gestation). Neonatal/child data were retrieved from screening examinations. Independent of the intervention, we found a positive correlation between the fat mass at T1 and both leptin and resistin levels at all time points. Leptin level was significantly higher in the control group at T3; however, no differences between the groups were found for resistin. The birth weight was influenced by the birth length, fat mass at T1/T3, and resistin level at T2. The BMI-SDS at one year of age was influenced by maternal fat-free mass at T3 and resistin at T1/T2. Even if these results can only be interpreted cautiously, lifestyle interventions during pregnancy are important in promoting maternal and child health. Further randomised controlled trials and translational studies are warranted to clarify the underlying mechanisms. [ABSTRACT FROM AUTHOR]

The alterations of circulating adipocytokines have been reported in thyroid diseases or type 2 diabetes mellitus (T2DM), but such data in T2DM coincident with clinical and subclinical thyroid-dysfunctions are limited, and remain to be investigated. We studied the changes in serum chemerin, resisitin and visfatin in T2DM patients with thyroid dysfunctions, and their association with inflammatory and insulin resistance-markers. A total of 272 female and male Iranian participants were selected and divided into six groups: the euthyroid group, T2DM, T2DM coincident with clinical and sub clinical hypothyroidism (SC-HO, and C-HO), and T2DM coincident with clinical and sub clinical hyperthyroidism (SC-HR, C-HR).Demographic characteristics, serum levels of adipocytokines, thyroid hormones, inflammatory factors (IL1-β, IL-6 and CRP) and insulin resistance-markers were determined in all participants. T2DM patients with clinical thyroid dysfunctions showed higher levels of circulating resistin, visfatin, chemerin and inflammatory factors, compared with the T2DM group and T2DM coexisted with subclinical thyroid diseases. No significant differences were observed in circulating adipocytokines and inflammatory markers between T2DM coexisting with subclinical thyroid diseases and those without thyroid dysfunctions. Our results revealed that clinical thyroid dysfunction in T2DM patients was associated with elevated levels of circulating resistin, chemerin, visfatin and inflammatory factors, while no such alteration was detected in T2DM coincident with subclinical thyroid dysfunction. [ABSTRACT FROM AUTHOR]

The formation and luteolysis of the corpus luteum (CL) is strictly controlled by many factors. Imbalance between proliferation and apoptosis processes leads to deficiency of the luteal phase and infertility. Our previous study showed resistin expression in porcine luteal cells and an inhibitory effect on progesterone synthesis. Thus, the aim of the present study was to examine the in vitro effect of resistin on the proliferation/viability, apoptosis and autophagy of porcine luteal cells as well as the involvement of mitogen-activated kinase (MAP3/1), protein kinase B (AKT) and signal transducer and activator of transcription 3 (STAT3) in these processes. Porcine luteal cells were incubated with resistin (0.1-10 ng/mL) for 24-72 h and viability was assessed using the alamarBlue or 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. Then, the time-dependent effect of resistin on mRNA and protein expression of proliferating cell nuclear antigen (PCNA), caspase 3, BCL2-like protein 4 (BAX), B-cell lymphoma 2 (BCL2), beclin1, microtubule-associated protein 1A/1B-light chain 3 (LC3) and lysosomal-associated membrane protein 1 (LAMP1) was measured by real-time polymerase chain reaction (PCR) and immunoblotting, respectively. We found that resistin enhanced luteal cell viability with no effect on caspase 3 mRNA and protein, increased the BAX/BCL2 mRNA and protein ratio and significantly stimulated the initiation of autophagy, which promotes the maintenance of CL function rather than its regression. Additionally, using pharmacological inhibitors of MAP3/1 (PD98059), AKT (LY294002) and STAT3 (AG490), we observed that the effect of resistin was reversed to the control level in viability and, by influence, MAP3/1 and STAT3 in autophagy. Taken together, our results suggest that resistin, in addition to its well-known effect on granulosa cell function has direct influence on CL luteolysis and the formation and maintenance of luteal cell function. [ABSTRACT FROM AUTHOR]

Psoriasis is a common chronic, inflammatory skin disease characterised by keratinocyte hyperproliferation, parakeratosis, and T-cell infiltration. Adipose tissue has an endocrine function, producing an abundance of cytokines and adipokines. It has also been described that the major adipokines, leptin, resistin, and adiponectin, may be involved in the pathogenesis of psoriasis. The aim of the study was to examine the plasma levels of adiponectin, leptin, and resistin in patients with psoriasis and their correlations with disease activity parameters: Psoriasis Activity Severity Index (PASI), Dermatology Life Quality Index (DLQI), and Body Surface Area (BSA) index, as well as selected clinical parameters. The study included 53 patients with the plaque type and 31 healthy controls. The plasma concentrations of adiponectin were significantly lower in patients with psoriasis (p < 0.001) than in the control group. The plasma concentrations of leptin were higher in patients with psoriasis, however, due to high intra-patient variability of leptin plasma concentrations these differences did not reach statistical significance (p = 0.2). The plasma concentrations of resistin were significantly increased in patients with psoriasis compared to healthy controls (p = 0.02). There were no statistically significant correlations between adiponectin and leptin plasma concentrations and values of PASI, DLQI, and BSA. The resistin plasma concentrations correlated significantly with DLQI values. Additionally, we examined the correlations between adiponectin, leptin, and resistin plasma concentrations, and selected clinical parameters. Plasma concentrations of adiponectin correlated significantly with CRP values and ALT values. Leptin plasma concentrations correlated significantly with creatinine values. The results of our study confirm the role of adiponectin, leptin, and resistin in the pathogenesis of psoriasis. [ABSTRACT FROM AUTHOR]

Obesity, through adipose tissue (AT) inflammation and dysregulation, represents a critical factor for COVID-19; here, we investigated whether serum levels of adiponectin, HMW oligomers, leptin, and resistin are modulated and/or correlated with clinical and biochemical parameters of severe COVID-19 patients. This study included 62 severe COVID-19 patients; 62 age and sex-matched healthy subjects were recruited as a control group. Anthropometric and biochemical parameters were obtained and compared. Adiponectin, HMW oligomers, leptin, and resistin were analyzed by ELISA. The adiponectin oligomerization state was visualized by Western blotting. When compared to healthy subjects, total adiponectin levels were statistically lower in severe COVID-19 while, in contrast, the levels of leptin and resistin were statistically higher. Interestingly, HMW adiponectin oligomers negatively correlated with leptin and were positively associated with LUS scores. Resistin showed a positive association with IL-6, IL-2R, and KL-6. Our data strongly support that adipose tissue might play a functional role in COVID-19. Although it needs to be confirmed in larger cohorts, adiponectin HMW oligomers might represent a laboratory resource to predict patient seriousness. Whether adipokines can be integrated as a potential additional tool in the evolving landscape of biomarkers for the COVID-19 disease is still a matter of debate. Other studies are needed to understand the molecular mechanisms behind adipokine's involvement in COVID-19. [ABSTRACT FROM AUTHOR]

The Single Point Insulin Sensitivity Estimator (SPISE) is a novel surrogate marker for insulin sensitivity and was found comparable to the gold standard clamp test as well as for predicting the Metabolic Syndrome (MetS) in several populations. The present study aimed to assess for the first time, the validity of SPISE in predicting MetS among Arab adolescents. In this cross-sectional study, 951 Saudi adolescents aged 10–17 years were randomly recruited from different schools across Riyadh, Saudi Arabia. Anthropometrics were measured and fasting blood samples were collected for the assessment of glucose, lipid profile, adipokines, C-reactive protein and 25 hydroxyvitamin (OH) D. MetS was defined using the National Cholesterol Education Program's (NCEP) criteria with age-specific thresholds for adolescents. The SPISE as well as insulin resistance (HOMA-IR) indices were calculated. The over-all prevalence of MetS was 8.6% (82 out of 951). SPISE index was significantly lower in MetS than non-MetS participants in both sexes (5.5 ± 2.5 vs. 9.4 ± 3.2, p < 0.001 in boys and 4.4 ± 1.4 vs. 8.6 ± 3.2, p < 0.001 in girls). The SPISE index showed a significant inverse correlation with resistin, leptin, and C-reactive protein, and a significant positive correlation with adiponectin and 25(OH) D. Areas under the curve (AUC) revealed fair and good accuracy for predicting MetS 84.1% and 90.3% in boys and girls, respectively. The sex-specific cut-off proposed was SPISE index ≤6.1 (sensitivity 72.2% and specificity 83.9%) for boys and ≤6.46 (sensitivity 96.3% and specificity 73.4%), for girls. This study suggests that the SPISE index is a simple and promising diagnostic marker of insulin sensitivity and MetS in Arab adolescents. [ABSTRACT FROM AUTHOR]

Background: The incidence rate of hepatocellular carcinoma (HCC) has risen in the last ten years, increasing the disease's burden in Egypt. Insulin resistance is a pathophysiological condition characterised by decreased insulin action in peripheral target tissues such as skeletal muscle, liver, and adipose tissue. Insulin resistance is thought to play a key role in the development of fibrosis as well as an increase in the risk of HCC. Objective: To assess the possible relation between serum levels of resistin and HCC in patients suffering of liver cirrhosis. Methods: PubMed, Egyptian Knowledge Bank, Google Scholar, were used to search for information on Hepatocellular carcinoma, Insulin resistance and Resistin. The authors also analysed references from relevant literature, but only the most recent or thorough study from May 2005 to October 2021 was included. Documents in languages other than English were excluded because there were insufficient translation-related sources. Dissertations, oral presentations, unpublished manuscripts, conference abstracts, and other works not related to major scientific research were removed. Conclusion: In conclusion, serum resistin level may serve as a new diagnostic marker for HCC patients, however, its accuracy in detection of early focal lesions and prognosis of these patients should be assessed in further larger studies. [ABSTRACT FROM AUTHOR]

Background: The development of coronary artery disease (CAD) is related to the impaired quantity and composition of inflammatory proteins found in plasma and tissue, such as interleukin 6 (IL-6), adipokines, and resistin. Therefore, the level of plasma resistin in patients with advanced CAD could be indicative of the condition of epicardial adipose tissue and thus have an impact on the frequency and severity of postoperative complications in the form of paroxysmal atrial fibrillation. Methods: The study included 108 patients who qualified for elective coronary artery bypass grafting (CABG) surgery from 2017 to 2020 and were categorized into two groups. The first group consisted of patients who developed atrial fibrillation in the postoperative period – the AF group, and the second group included patients who did not have arrhythmia – the non-AF group. The analysis incorporates the history, course of treatment, anthropometric characteristics of the test subjects, biochemical laboratory tests, and echocardiography. Perivascular adipose tissue (PVAT) sections were surgically harvested from the area of the left coronary trunk. Results: The resistin levels in the PVAT were significantly higher in the AF group than in the non-AF group (P = 0.000015). Similarly, plasma resistin levels increased significantly in the AF group compared to the non-AF group (P = 0.044). The values of other analyzed variables were not significantly different (analysis performed using the Mann–Whitney U test). Spearman's rank-order correlation technique found a correlation between resistin in PVAT and plasma (r = 0.5933; P < 0.0001) in the whole study group, as well as in the AF group (r = 0.4782; P = 0.021) and the non-AF group (r = 0.4938; P < 0.0001). A correlation arose between the level of resistin in PVAT and the level of hsCRP (r = 0.3463; P = 0.005) in the whole study group and the non-AF group (r = 0.4448; P = 0.0011); however, no such correlation appeared in the AF group (r = 0.3076; P = 0.306). Conclusions: Elevated levels of plasma resistin, which reflect PVAT resistin levels in patients qualified for myocardial revascularisation, may be associated with postoperative atrial fibrillation complications. [ABSTRACT FROM AUTHOR]

Rhinacanthin C (RC) is a naphthoquinone ester with an anti-inflammatory activity extracted from Rhinacanthus nasutus (L.) Kurz (Rn). It has been proven to improve hyperglycemia and hyperlipidemia, but the prevention and mechanism of RC in nonalcoholic fatty liver disease (NAFLD) are not clear. In the current study, we first extracted RC from Rn using ethyl acetate and identified it by HPLC, MS, and NMR. At the same time, molecular docking analysis of RC with AMPK and SREBP-1c was performed using AutoDock software. In addition, the mouse model of NAFLD was induced by a high-fat diet in vivo, and low, medium, and high concentrations of RC were used for intervention. The results showed that RC significantly reduced the body mass and liver body coefficient of NAFLD mice, inhibited liver inflammation and fat accumulation, and improved insulin resistance. Further studies showed that RC significantly reduced the levels of serum leptin and resistin, upregulated the expression levels of adiponectin and adiponectin receptor in the liver, and inhibited the expression levels of MCP-1, TNF-α, and IL-6. In terms of mechanism, RC upregulates the expression of p-AMPK and SIRT1 and downregulates the expression of p-p65, SREBP-1c, Fas, Acc-α, PPAR-γ, and SCD1. These studies suggest that RC improves insulin resistance and lipid accumulation in NAFLD by activating the AMPK/SIRT1 and SREBP-1c/Fas/ACC pathways, respectively. [ABSTRACT FROM AUTHOR]

Background: As a product of adipose tissue, resistin exceeds other adipokines in its role in regulating appetite, energy expenditure, insulin sensitivity, inflammation, and immunity, similar to thyroid hormones. This study aimed to evaluate the association between resistin levels and thyroid dysfunction and to explore variations in circulating resistin levels before and after treatment for thyroid dysfunction. Methods: This study was conducted according to the Preferred Reporting Items for Systematic Review and Meta-Analysis statement. A comprehensive search of PubMed, Embase, and Cochrane databases was conducted until June 15, 2022, with no start date restriction, according to the preregistered protocol (PROSPERO-CRD42022336617). RevMan version 5.4 and R software package version 4.2.0 were used for statistical analyses. Results: Fourteen studies with 1716 participants were included in this study. The findings of themeta-analysis confirmed that the resistin levels of patientswith thyroid dysfunction were significantly higher than those of the euthyroid function control group (mean difference [MD] = 2.11, 95% confidence interval [CI] = 1.11-3.11, P < 0.00001). Furthermore, the resistin levels of patientswith hyperthyroidism (MD = 3.23, 95% CI = 0.68-5.79, P = 0.01) and subclinical hypoidism(MD = 1.37, 95% CI = 0.31-2.42, P = 0.01) were significantly higher than those of euthyroid controls. The resistin levels of patients with thyroid dysfunction after treatment were significantly lower than those before treatment (MD = 1.00, 95% CI = 0.34-1.65, P = 0.003), especially in patientswithhyperthyroidism(MD=2.16,95%CI=1.00-3.32, P=0.0003). Correlation analysis confirmed a positive correlation between resistin levels and free triiodothyronine(FT3) levels inpatientswiththyroiddysfunction(r=0.27578,P=0.001). Conclusions: Our meta-analysis demonstrates that resistin levels are significantly higher in patients with thyroid dysfunction, and the resistin levels after treatment in patients with thyroid dysfunction are significantly lower than those before treatment. Correlation analysis shows a positive correlation between resistin levels and FT3 levels in patients with thyroid dysfunction. [ABSTRACT FROM AUTHOR]

The purpose of this study was to see how chrysin and/or bone marrow-derived mesenchymal stem cells (BM-MSCs) affected streptozotocin (STZ)/nicotinamide (NA)-induced diabetic rats as an animal model of type 2 diabetes mellitus (T2DM). Male Wistar rats were given a single intraperitoneal (i.p.) injection of 60 mg STZ/kg bodyweight (bw) 15 min after an i.p. injection of NA (120 mg/kg bw) to induce T2DM. The diabetic rats were given chrysin orally at a dose of 100 mg/kg bw every other day, BM-MSCs intravenously at a dose of 1 × 106 cells/rat/week, and their combination for 30 days after diabetes induction. The rats in the diabetic group displayed impaired oral glucose tolerance and a decrease in liver glycogen content and in serum insulin, C-peptide, and IL-13 levels. They also had significantly upregulated activities in terms of liver glucose-6-phosphatase and glycogen phosphorylase and elevated levels of serum free fatty acids, IL-1β, and TNF-α. In addition, the diabetic rats exhibited a significant elevation in the adipose tissue resistin protein expression level and a significant decrease in the expression of adiponectin, insulin receptor-beta subunit, insulin receptor substrate-1, and insulin receptor substrate-2, which were associated with a decrease in the size of the pancreatic islets and in the number of β-cells and insulin granules in the islets. The treatment of diabetic rats with chrysin and/or BM-MSCs significantly improved the previously deteriorated alterations, with chrysin combined with BM-MSCs being the most effective. Based on these findings, it can be concluded that combining chrysin with BM-MSCs produced greater additive therapeutic value than using them separately in NA/STZ-induced T2DM rats. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to evaluate the effect of supplementation with ground flaxseed (GF) on the concentrations of adiponectin, resistin, and visfatin in patients with ulcerative colitis (UC). Background: Inflammatory bowel disease (IBD) is one of the most common gastrointestinal diseases affecting people of all ages. Adipokines secreted from adipose tissue have been shown to play an essential role in the pathogenesis of UC. Methods: This trial is an open-labeled randomized controlled trial conducted on 70 patients with UC. The patients were randomly divided into two groups: flaxseed and control. The patients in the intervention received 30 g/day flaxseed powder for 12 weeks. Patients' anthropometric, nutritional, and biochemical factors were evaluated at the beginning and end of the intervention period. Results: Totally, 64 patients (36 men and 28 women) with a mean age of 31.12±9.67 were included in the final analysis. There was no significant difference between the two groups regarding baseline weight and height (P>0.05). After the 12-week intervention, flaxseed supplementation led to a significant reduction in the resistin (-4.85±1.89 vs. -1.10±2.25, P<0.001) and visfatin concentration (-1.33±1.14 vs. -0.53±1.63, P=0.018). Further, we found a significant increase in the adiponectin levels after the GF supplementation (3.49±1.29 vs. -0.35±0.96, P<0.001). Conclusion: Flaxseed supplementation could exert beneficial effects on adipokine levels in patients with UC. [ABSTRACT FROM AUTHOR]

Background and objectives: Coronary artery bypass graft (CABG) is a surgical procedure used to treat coronary heart disease. The present study aimed to investigate effects of 8 weeks of combined rehabilitation training on plasma levels of leptin, adiponectin, and resistin in middle-aged men who have undergone CABG. Methods: The present research was a quasi-experimental study with a pretest-posttest design. The statistical population included all patients who have undergone CABG in Mashhad, Iran. Overall, 26 middle-aged men who have undergone CABG were enrolled in the study. The subjects were divided into a training group (n=14) and a control group (n=12). Data were analyzed in SPSS software (version 21) using analysis of covariance and paired t-test at significance level of 0.05. Results: Plasma levels of leptin did not change significantly (p=0.709), adiponectin increased significantly (p=0.001), and resistin decreased significantly (p=0.005) after the training intervention. Conclusion: As a non-pharmacological intervention, the rehabilitation training has cardioprotective effects on patients who undergone CABG. [ABSTRACT FROM AUTHOR]

Introduction: The enzyme methylene tetrahydrofolate reductase (MTHFR) is the major regulator of homocysteine (HCY) levels in humans. Three missense mutations have a significant impact on the activity of this enzyme. Aim: The present study aimed to evaluate the association between HCY and MTHFR mutations in ovarian cancer. Materials and Methods: A cohort of 64 females suffering from ovarian cancer was investigated for resistin, malondialdehyde (MDA), glutathione (GSH), vitamin C (Vit. C) and HCY. MTHFR mutations were included in the study. Results: A significant increase in resistin and MDA while a significant decrease in GSH, Vit. C and HCY were detected in ovarian cancer patients. Also, a significant association between homocysteine and MTHFR was also observed in these patients. Interestingly, the results showed a correlation between ovarian cancer risk and MTHFR. Conclusion: MTHFR mutations were found to be associated with an increased risk of ovarian cancer in Mosul, Iraq. [ABSTRACT FROM AUTHOR]

Background: Achieving an acceptable neurological outcome in cardiac arrest survivors remains challenging. Ischemia‐reperfusion injury induces inflammation, which may cause secondary neurological damage. We studied the association of ICU admission levels of inflammatory biomarkers with disturbed 48‐hour continuous electroencephalogram (cEEG), and the association of the daily levels of these markers up to 72 h with poor 6‐month neurological outcome. Methods: This is an observational, post hoc sub‐study of the COMACARE trial. We measured serum concentrations of procalcitonin (PCT), high‐sensitivity C‐reactive protein (hsCRP), osteopontin (OPN), myeloperoxidase (MPO), resistin, and proprotein convertase subtilisin/kexin type 9 (PCSK9) in 112 unconscious, mechanically ventilated ICU‐treated adult OHCA survivors with initial shockable rhythm. We used grading of 48‐hour cEEG monitoring as a measure for the severity of the early neurological disturbance. We defined 6‐month cerebral performance category (CPC) 1–2 as good and CPC 3–5 as poor long‐term neurological outcome. We compared the prognostic value of biomarkers for 6‐month neurological outcome to neurofilament light (NFL) measured at 48 h. Results: Higher OPN (p =.03), MPO (p <.01), and resistin (p =.01) concentrations at ICU admission were associated with poor grade 48‐hour cEEG. Higher levels of ICU admission OPN (OR 3.18; 95% CI 1.25–8.11 per ln[ng/ml]) and MPO (OR 2.34; 95% CI 1.30–4.21) were independently associated with poor 48‐hour cEEG in a multivariable logistic regression model. Poor 6‐month neurological outcome was more common in the poor cEEG group (63% vs. 19% p <.001, respectively). We found a significant fixed effect of poor 6‐month neurological outcome on concentrations of PCT (F = 7.7, p <.01), hsCRP (F = 4.0, p <.05), and OPN (F = 5.6, p <.05) measured daily from ICU admission to 72 h. However, the biomarkers did not have independent predictive value for poor 6‐month outcome in a multivariable logistic regression model with 48‐hour NFL. Conclusion: Elevated ICU admission levels of OPN and MPO predicted disturbances in cEEG during the subsequent 48 h after cardiac arrest. Thus, they may provide early information about the risk of secondary neurological damage. However, the studied inflammatory markers had little value for long‐term prognostication compared to 48‐hour NFL. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to compare adiponectin, resistin, visfatin, and irisin levels between pregnant women diagnosed gestational diabetes mellitus (GDM) and healthy pregnant women and to evaluate the role of these parameters in GDM pathophysiology and early diagnosis. Methods: Fifty GDM and 50 healthy pregnant women were included in the study. Anthropometric measurements of pregnant women were performed. Fasting blood glucose, hemoglobin A1c, 75 gr OGTT, low density lipoprotein, triglyceride, and complete blood count results were recorded. Adiponectin, irisin, visfatin, resistin, and C-reactive protein (CRP) levels were evaluated. Results: Serum adiponectin levels were significantly lower (p<0.001) and serum resistin and CRP levels were significantly higher (p=0.000 and p=0.027, respectively) in pregnant women with GDM compared to healthy pregnants. There was no significant difference between groups according to serum irisin and visfatin levels (p=0.942 and p=0.332, respectively). There was a negative correlation between adiponectin level and FPG, visfatin, and resistin, while a positive correlation was found between irisin level. While there was a positive correlation between resistin and CRP levels, there was a negative correlation between adiponectin level. While there was a positive correlation between irisin and adiponectin levels, there was a negative correlation between weight and body mass index. Conclusion: In this study, we think that elevated serum resistin and CRP levels and decreased adiponectin levels in GDM patients may play a role in glucose metabolism changes. Further studies are needed on this subject. [ABSTRACT FROM AUTHOR]

Aims People with diabetes mellitus (DM] represent a population group that is at high risk of developing a poor prognosis for Covid-19. Having diabetes increases the risk of serious illness, ICU stay, and death from Covid-19. The present study aimed to determine RETN gene polymorphisms as a risk factor in diabetic patients with Covid-19 infection. Instruments & Methods The current study included 150 participants with diabetes, 100 patients of whom had Covid-19 (46 male, 54 female], and 50 had diabetes only (28 male, 22 female]. Five ml of venous blood was collected from participants, then used for examining the blood sugar and HbAlc levels and molecular study. Finding: There was a significant increase in random blood sugar and HbAlC concentrations in diabetic patients infected with Covid-19 compared to diabetic patients only. Regarding the molecular study of the gene encoding the protein resistin, diabetic patients with Covid-19 had a high frequency of single nucleotide polymorphisms compared to diabetic patients only. Polymorphisms of X494T.C, X663A.C, X494T.C, and X663A.C recorded significant differences, while the polymorphisms of rs3219177, X542A.C, and rs3745367 did not show a significant difference. Conclusion Diabetic parameters increase in diabetic patients with covid-19 compared to diabetic patients without Covid-19. In addition, diabetic patients with Covid-19 have a high frequency of single nucleotide polymorphisms of the RETN gene. [ABSTRACT FROM AUTHOR]

Background: Gestational diabetes mellitus (GDM) is the most common association with hyperglycemia and glucose intolerance during pregnancy. The adipokines play an important to control insulin secretion and glucose. This study aimed to investigate the association between maternal circulating adipokine levels and ADIPOQ gene polymorphism among pregnant women subjects with GDM and normal glucose tolerance (NGT). Methods: Participants including 229 normal pregnant women and 197 GDM pregnant women were enrolled from 2015 to 2018 at Siriraj hospital. Serum adipokine levels including adiponectin, adipsin/factor D, NGAL/Lipocalin-2, total PAI-1, and resistin were measured by immunoassay. ADIPOQ variations were investigated including − 11377C/G (rs266729), +45T/G (rs2241766), and +276G/T (rs1501299). Results: Serum adiponectin concentration was also significantly decreased among the GDM who had aged less than 35 years old whereas adipsin levels were significantly lower among the GDM who had aged more than 35 years old. Also, adiponectin and total PAI-1 levels were significantly lower among the GDM who had a BMI of less than 30 kg/m2. The G allele frequency of ADIPOQ +45T/G was significantly different between GDM and controls (p = 0.03). ADIPOQ +45T/G was associated with an increased risk of GDM (odds ratio [OR]: 1.554; 95% confidence interval [CI]: 1.010– 2.390; p=0.045). The − 11377C/G was affected by the level of adiponectin (p = 0.04). The C allele of − 11377C/G SNP declined serum adiponectin levels and may be a risk factor for GDM. Conclusion: This study revealed that genetics play important roles in circulating adipokines among pregnant women. ADIPOQ polymorphisms had significant associations with adiponectin levels in GDM patients. [ABSTRACT FROM AUTHOR]

Background: Osteopontin, an extracellular matrix protein involved in bone remodeling, tissue repair and inflammation, has previously been associated with increased inflammation and neurodegeneration in multiple sclerosis (MS), promoting a worse disease course. Osteopontin is also likely involved in acute MS relapses. Methods: In 47 patients with relapsing-remitting MS, we explored the correlation between the time elapsed between the last clinical relapse and lumbar puncture, and the cerebrospinal fluid (CSF) levels of osteopontin and a group of inflammatory cytokines and adipokines such as resistin, plasminogen activator inhibitor-1, osteoprotegerin, interleukin (IL)-1β, IL-2, IL-6 and IL-1 receptor antagonist (IL-1ra). We also analyzed the correlations between CSF levels of osteopontin and the other CSF molecules considered. Results: Osteopontin CSF concentrations were higher in patients with a shorter time interval between the last clinical relapse and CSF withdrawal. In addition, CSF levels of osteopontin were positively correlated with the proinflammatory cytokines IL-2 and IL-6 and negatively correlated with the anti-inflammatory molecule IL-1ra. Conclusions: Our results further suggest the role of osteopontin in acute MS relapses showing that, in proximity to relapses, osteopontin expression in CSF may be increased along with other proinflammatory mediators and correlated with decreased concentrations of anti-inflammatory molecules. [ABSTRACT FROM AUTHOR]

Obesity has a significant role in the emergence of severe health disorders, associated comorbidities, and morbidity. According to epidemiological and clinical evidence, obesity has been linked to a number of heart related diseases, such as heart failure, coronary heart disease, hypertension, atrial fibrillation, stroke and cardiac arrest. The obesity is characterized by changes in adipose tissue's cell size, which interferes with the tissue's normal function. Furthermore, a variety of bioactive substances are produced and secreted by adipose tissue. Both local and systemic effects of obesity's abnormal expansion of adipose tissue, such as hypoxia, inflammation, dysregular secretion of adipokine, hypertension, improper function of mitochondria, insulin resistance, abnormal lipid/glucose metabolism, pro-inflammatory/pro-thrombotic state, as well as endothelial dysfunction results in variety of heart diseases. In this review, we will discuss various biomolecules such as hormones, genes, enzymes, receptors, cytokines, etc., involved in the mechanisms linking obesity to cardiovascular diseases, and how their regulation can be helpful in the treatment of these diseases.

Resistin has been shown to play a key role in inducing vascular smooth muscle cells (VSMCs) malfunction in the atherosclerosis progression. Ginsenoside Rb1 is the main component of ginseng, which has been used for thousands of years and has been reported to have a powerful vascular protective effect. The aim of this study was to explore the protective effect of Rb1 on VSMCs dysfunction induced by resistin. In the presence or absence of Rb1, human coronary artery smooth muscle cells (HCASMC) were treated at different time points with or without 40 ng/ml resistin and acetylated low-density lipoprotein (acetylated LDL). Cell migration and proliferation were analyzed using wound healing test and CellTiter Aqueous Cell Proliferation Assay (MTS) test, respectively. Intracellular reactive oxygen species (ROS) (H2DCFDA as a dye probe) and superoxide dismutase (SOD) activities were measured by a microplate reader and the differences between groups were compared. Rb1 significantly reduced resistin-induced HCASMC proliferation. Resistin increased HCASMC migration time-dependently. At 20 µM, Rb1 could significantly reduce HCASMC migration. Resistin and Act-LDL increased ROS production to a similar level in HCASMCs, while Rb1 pretreated group reversed the effects of resistin and acetyl-LDL. Besides, the mitochondrial SOD activity was significantly reduced by resistin but was restored when pretreated with Rb1. We confirmed the protection of Rb1 on HCASMC and suggested that the mechanisms involved might be related to the reduction of ROS generation and increased activity of SOD. Our study clarified the potential clinical applications of Rb1 in the control of resistin-related vascular injury and in the treatment of cardiovascular disease.

Resistin is an adipokine with metabolic and inflammatory functions. Epidemiological and translational studies report that an increase in plasma levels and tissue expression of resistin increases the aggressiveness of prostate tumor cells. Extracellular vesicles (EVs) are secreted constitutively and induced by cytokines, growth factors, and calcium and are found in multiple biological fluids such as saliva, serum, semen, and urine. In particular, EVs have been shown to promote tumor progression through the induction of proliferation, growth, angiogenesis, resistance to chemotherapy, and metastasis. However, the role of resistin in the migration, invasion, and secretion of EVs in invasive prostate tumor cells remains to be studied. In the present study, we demonstrate that resistin induces increased migration and invasion in PC3 cells. In addition, these phenomena are accompanied by increased p-FAK levels and increased secretion of MMP-2 and MMP-9 in resistin-treated PC3 cells. Interestingly, EVs isolated from supernatants of PC3 cells treated with resistin induce an increase in migration and invasion accompanied by high MMP-2 and MMP-9 secretion in an autocrine stimulation model. In summary, our data for the first time demonstrate that resistin induces migration and invasion, partly through the secretion of EVs with pro-invasive characteristics in PC3 cells.

The rising incidence of obesity has coincided with rising levels of poor reproductive outcomes. The molecular basis for the association of infertility in obese males is now being explained through various mechanisms. Insulin resistance, hyperglycemia, and changes in serum and gonadal concentrations of adipokines, like leptin, adiponectin, resistin, and ghrelin have been implicated as causes of male infertility in obese males. The effects of obesity and hypogonadism form a vicious cycle whereby dysregulation of the hypothalamic–pituitary–testicular axis—due to the effect of the release of multiple mediators, thus decreasing GnRH release from the hypothalamus—causes decreases in LH and FSH levels. This leads to lower levels of testosterone, which further increases adiposity because of increased lipogenesis. Cytokines such as TNF-α and interleukins, sirtuins, and other inflammatory mediators like reactive oxygen species are known to affect fertility in obese male adults. There is evidence that parental obesity can be transferred through subsequent generations to offspring through epigenetic marks. Thus, negative expressions like obesity and infertility have been linked to epigenetic marks being altered in previous generations. The interesting aspect is that these epigenetic expressions can be reverted by removing the triggering factors. These positive modifications are also transmitted to subsequent generations.

The high morbidity and mortality rates associated with sepsis highlight the challenges of finding specific remedies for this condition in the intensive care unit (ICU). This study aimed to explore the differentially expressed genes (DEGs) specific to cell types in sepsis and investigate the role of resistin in the survival of sepsis patients through Mendelian randomization (MR) analyses. We used single-cell and bulk transcriptome data to identify cell type-specific DEGs between sepsis and healthy controls. MR analyses were then conducted to investigate the causal relationships between resistin (one of the identified DEGs) levels and the survival of sepsis patients. Additionally, we utilized meQTL (methylation quantitative trait loci) to identify cytosine-phosphate-guanine (CpG) sites that may directly affect sepsis. We identified 560 cell type-specific DEGs between sepsis and healthy controls. Notably, we observed the upregulation of resistin levels in macrophages during sepsis. In bulk transcriptome, RETN is also upregulated in sepsis samples compared with healthy controls. MR analyses revealed a negative association existed between the expression of resistin, at both gene and protein levels, and the mortality or severity of sepsis patients in ICU. Moreover, there were no associations observed between resistin levels and death or organ failure due to other causes. We also identified three methylation CpG sites, located in RETN or its promoter region—cg06633066, cg22322184, and cg02346997—that directly affected both resistin protein levels and sepsis death in the ICU. Our findings suggest that resistin may provide feasible protection for sepsis patients, particularly those with severe cases, without serious side effects. Therefore, resistin could be a potential drug candidate for sepsis treatment. Additionally, we identified two CpG sites, cg06633066 and cg22322184, that were associated with RETN protein levels and sepsis death, providing novel insights into the underlying mechanisms of sepsis.

ObjectiveResistin is a hormone that has been associated with metabolic syndrome and cardiovascular disease. The role of resistin in patients with peripheral artery disease (PAD) has not been fully explored. This study seeks to understand the relationship between serum resistin, vascular function, and cardiovascular outcomes in patients with PAD.MethodsThere were 106 patients with PAD who were recruited between 2011 and 2016. Patients attended a baseline visit during which a comprehensive vascular physiology assessment including medical and surgical history, radial artery tonometry, and flow mediated-vasodilation (FMD) was completed. A blood sample was drawn, and serum resistin was assayed using enzyme-linked immunosorbent assay kits. Using the time of study enrollment as the time of origin, incident major adverse cardiac events (MACEs) were identified by subsequent chart review and defined as a composite end point of myocardial infarction, coronary revascularization, transient ischemic attack, stroke, or death from a cardiac cause.ResultsPatients had a mean age of 68 ± 8 years, were largely white (75%), and had comorbidities commonly associated with PAD including hypertension (92%), hyperlipidemia (87%), coronary artery disease (37%), and diabetes mellitus (38%). After stratification by resistin quartile, higher resistin quartiles were significantly associated with an older age, a greater number of pack-years smoked, and a lower estimated glomerular filtration rate. Despite similar comorbidities and medication use, endothelial function, as measured by FMD, was significantly lower with increasing resistin quartile (I, 9.1% ± 3.3%; II, 7.1% ± 3.5%; III, 5.8% ± 4.0%; IV, 5.6% ± 3.5%; P = .002). In multivariable linear regression, higher resistin quartiles (III and IV) were associated with lower FMD relative to quartile I after adjusting for several patient characteristics, medications, and comorbidities (III, -2.26 [95% confidence interval (CI), -4.51 to -0.01; P = .05]; IV, -2.53 [95% CI, -4.87 to -0.20; P = .03]). During a median follow-up period of 36 months (interquartile range, 29-45 months), 21 patients experienced the primary end point. In a Cox proportional hazards model adjusted for smoking status, coronary artery disease, and age, each 1 ng/mL increase in resistin was associated with a 10% increased risk of MACEs (hazard ratio, 1.10; 95% CI, 1.00-1.20; P = .04).ConclusionsIn patients with PAD, higher levels of resistin were associated with impaired endothelial function and an increased rate of MACEs. These results suggest that resistin may be a marker or effector of impaired vascular physiology and adverse cardiac outcomes in patients with PAD. Further research is needed to determine the potential mechanisms by which resistin may impair endothelial function and increase MACEs in this population.

Objectives: Insulin resistance (IR) is major cause of type 2 diabetes (T2D), and adipokines (e.g., adiponectin, leptin, and resistin) play an important role in insulin sensitivity. Medicinal plants are frequently used for T2D treatment. This study investigates the effect of Artemisia annua L. (AA) extracts on adipokines in mice with high-fat-diet (HFD)/streptozotocin (STZ)-induced T2D.Methods : : We divided 60 mice into 12 groups (n = 5 per group): control, untreated T2D, treated T2D, and 9 other groups. T2D was induced in all groups, except controls, by 8 weeks of HFD and STZ injection. The treated T2D group was administered 250 mg/kg of metformin (MTF), while the nine other groups were treated with 100, 200, and 400 mg/kg of hot-water extract (HWE), cold-water extract (CWE), and alcoholic extract (ALE) of AA (daily oral gavage) along with 250 mg/kg of MTF for 4 weeks. The intraperitoneal glucose tolerance test (IPGTT) was performed, and the homeostasis model assessment of adiponectin (HOMA-AD) index and blood glucose and serum insulin, leptin, adiponectin, and resistin levels were measured.Results : : Similar to MTF, all three types of AA extracts (HWEs, CWEs, and ALEs) significantly (p < 0.0001) decreased the area under the curve (AUC) of glucose during the IPGTT, the HOMA-AD index, blood glucose levels, and serum insulin, leptin, and resistin levels and increased serum adiponectin levels in the MTF group compared to the T2D group (p < 0.0001). The HWEs affected adipokine release, while the CWEs and ALEs decreased leptin and resistin production.Conclusion : : Water and alcoholic AA extracts have an antihyperglycemic and antihyperinsulinemic effect on HFD/STZ diabetic mice. In addition, they decrease IR by reducing leptin and resistin production and increasing adiponectin secretion from adipocytes.

Abstract Objective The present study aimed to investigate the effects of nano-curcumin supplementation on adipokines levels and clinical signs in obese and overweight patients with migraine. Results Forty-four patients with episodic migraine participated in this clinical trial and were divided into two groups nano-curcumin (80 mg/day) and the control group over 2-month period. At the baseline and the end of the research, the serum levels of MCP-1, Resistin, and Visfatin were measured using the ELISA method. In addition, the headache attack frequencies, severity, and duration of pain were recorded. The results of the present study showed that nano-curcumin can significantly reduce MCP-1 serum levels in the nano-curcumin supplemented group (P = 0.015, size effect = 13.4%). In the case of resistin and visfatin, nano-curcumin supplementation exerted no statistically significant changes in serum levels (P > 0.05). Nano-curcumin also significantly reduced the attack frequencies, severity, and duration of headaches (P

ObjectiveThis study examined the associations between abdominal IMAT area and density with inflammatory markers associated with cardiometabolic disease.Methods1897 participants enrolled in the Multi-Ethnic Study of Atherosclerosis underwent computed tomography to quantify body composition and measurements of adiponectin, leptin, interleukin-6 (IL-6), C-reactive protein (CRP), and resistin.ResultsThe mean age and body mass index of participants was 65years and 28kg/m2, respectively, and 50% were female. After adjustment for age, sex, and race/ethnicity, as IMAT area increased and density decreased from the first to fourth quartile, markers of inflammation increased linearly (p0.05).ConclusionsAbdominal IMAT area and density are associated with inflammatory markers, with these associations attenuated by central adiposity.

The Resistin-Like Molecules (RELM) α, β, and γ and their namesake, resistin, share structural and sequence homology but exhibit significant diversity in expression and function within their mammalian host. RELM proteins are expressed in a wide range of diseases, such as: microbial infections (eg. bacterial and helminth), inflammatory diseases (eg. asthma, fibrosis) and metabolic disorders (eg. diabetes). While the expression pattern and molecular regulation of RELM proteins are well characterized, much controversy remains over their proposed functions, with evidence of host-protective and pathogenic roles. Moreover, the receptors for RELM proteins are unclear, although three receptors for resistin, decorin, adenylyl cyclase-associated protein 1 (CAP1), and Toll-like Receptor 4 (TLR4) have recently been proposed. In this review, we will first summarize the molecular regulation of the RELM gene family, including transcription regulation and tissue expression in humans and mouse disease models. Second, we will outline the function and receptor-mediated signaling associated with RELM proteins. Finally, we will discuss recent studies suggesting that, despite early misconceptions that these proteins are pathogenic, RELM proteins have a more nuanced and potentially beneficial role for the host in certain disease settings.

Background: The published findings on the link between the resistin (RETN) gene polymorphism and type 2 diabetes mellitus (T2DM) risk are still contradictory. Here, through a meta-analysis, we summarized a more precise evaluation of their connection by synthesizing existing research. Methods: PubMed, Google Scholar, and Web of Science were electronically searched, and all cited sources were manually searched. The heterogeneity of effects was tested and all statistical analyses were performed in Stata 12.0. Results: A total of 23 studies with 10,651 cases and 14,366 controls on RETN -420C/G polymorphism were included. The overall results showed that the association of RETN -420C/G polymorphism and T2DM susceptibility was not significant [for the allelic model: odds ratio (OR) = 0.98, 95% confidence interval (CI) = 0.87-1.10, pheterogeneity <.001; I² = 84.6%; for the dominant model: OR = 0.96, 95% CI = 0.80-1.15, pheterogeneity <.001; I²=87.1%; andfor the recessivemodel: OR=0.96,95%CI = 0.82-1.12, pheterogeneity <.001; I² = 56.9%] but with high heterogeneity across studies (p <.0001). Meta-regression found that the median age of T2DM participants (using age 50 as the cutoff) could be a factor in the observed variation. The RETN -420C/G polymorphism seems to be linked to an increased risk of T2DM in younger individuals [for dominant: OR = 0.84 (95% CI, 0.72-0.98; pheterogeneity <.001; I² = 80.9%)] and decreased risk in older people [for dominant: OR = 3.14 (95% CI, 2.35-4.19; pheterogeneity = .98; I² = 0.0%)]. Conclusions: Current results found no evidence that the RETN -420C/G variant was linked to T2DM susceptibility, but the patient's age appears to be a potential factor that contributed to high heterogeneity across studies. Additional high-quality and well-designed investigations are required to confirm these results. [ABSTRACT FROM AUTHOR]

It has been reported that adiponectin (ADPN) and resistin are co-secreted by white mouse adipocytes and exert similar inhibitory effects in the mouse gastric fundus, in which resistin was observed to increase neuronal nitric oxide synthase (nNOS) expression. On these grounds, the present work aimed to investigate whether the effects of the two adipokines on the neurally-induced relaxant responses potentiate each other and whether there is a possible correlation with changes in nNOS expression in preparations from the mouse gastric fundus. In carbachol (CCh)-precontracted strips, electrical field stimulation elicited nitrergic relaxant responses, whose amplitude was increased by ADPN or resistin, but no additional enhancements were observed in their concomitant presence. Western blot and immunofluorescence analyses revealed that ADPN, like resistin, was able to up-regulate nNOS expression and to increase the percentage of nNOS-positive neurons in the myenteric plexus: co-treatment with the two adipokines did not induce additional changes. The results indicate that the two adipokines modulate nitrergic neurotransmission, and both do so by up-regulating nNOS expression. Therefore, nNOS appears to be a shared target for the two adipokines' effects, which, rather than mutually reinforcing each other, may represent a dual physiological control mechanism to guarantee gastric fundus relaxation. [ABSTRACT FROM AUTHOR]

Background. Resistin is closely related to cardiovascular diseases, and this study is aimed at examining the role of resistin in doxorubicin- (DOX-) induced cardiac injury. Methods. First, 48 mice were divided into 2 groups and treated with saline or DOX, and the expression of resistin at different time points was examined (N = 24). A total of 40 mice were pretreated with the antiresistin neutralizing antibody (nAb) or isotype IgG for 1 hour and further administered DOX or saline for 5 days. The mice were divided into 4 groups: saline-IgG, saline-nAb, DOX-IgG, and DOX-nAb (N = 10). Cardiac injury, cardiomyocyte apoptosis, inflammatory factors, and the biomarkers of M1 and M2 macrophages in each group were analyzed. Result. DOX administration increased the expression of resistin. DOX treatment exacerbated the loss of body and heart weight and cardiac vacuolation in mice. The antiresistin nAb reversed these conditions, downregulated the expression of myocardial injury markers, and decreased apoptosis. In addition, the antiresistin nAb decreased p65 pathway activation, decreased M1 macrophage differentiation and the expression of related inflammatory factors, and increased M2 macrophage differentiation and the expression of related inflammatory factors. Conclusion. The antiresistin nAb protected against DOX-induced cardiac injury by reducing cardiac inflammation and may be a promising target to relieve DOX-related cardiac injury. [ABSTRACT FROM AUTHOR]

Plasminogen activator inhibitor 1 (PAI-1) and resistin are associated with dysfunctional adipose tissue (AT)-related metabolic complications. The role of dietary eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids in this relationship is unknown. To investigate the association of EPA and DHA with PAI-1 and resistin, as well as the role of this association on the glucose metabolism of apparently healthy subjects. Thirty-six healthy individuals were included. Validated food frequency questionnaires were used to analyse dietary habits. Inflammatory and glucose metabolism markers were quantified. Subcutaneous AT samples were obtained, and adipocyte number, area, and macrophage content were assessed. In 36 subjects aged 56 ± 8 years and with a body mass index of 26 ± 4 kg/m2, logEPA, and logDHA showed significant association with logresistin and a marginal association with PAI-1. Adipocyte number, area, and lognumber of macrophages per adipocyte significantly correlated with PAI-1 but not with logresistin. Although logEPA and logDHA were independently associated with loginsulin, loginsulin resistance, and C-Peptide, the addition of logresistin, but not of PAI-1, into the multivariable model, abolished the associations. EPA and DHA could modulate glucose metabolism across AT functional states. Our data indicate that this association is independent of other metabolic risk factors. [ABSTRACT FROM AUTHOR]

Simple Summary: Chronic inflammation is associated with the development of nasopharyngeal carcinoma (NPC). Mounting evidence has indicated that resistin is an inflammatory cytokine that is associated with the risk of tumorigenesis. However, the correlation between serum resistin levels and the risk of NPC remains unclear. Here, we found that high serum resistin levels in NPC patients were positively correlated with lymph node metastasis and that resistin promoted the metastasis of NPC cells both in vitro and in vivo. Furthermore, we elucidated the underlying molecular mechanisms through which resistin promotes metastasis in NPC cells by inducing the epithelial-mesenchymal transition (EMT). NPC is a type of malignant tumor with a high risk of local invasion and early distant metastasis. Resistin is an inflammatory cytokine that is predominantly produced from the immunocytes in humans. Accumulating evidence has suggested a clinical association of circulating resistin with the risk of tumorigenesis and a relationship between blood resistin levels and the risk of cancer metastasis. In this study, we explored the blood levels and the role of resistin in NPC. High resistin levels in NPC patients were positively associated with lymph node metastasis, and resistin promoted the migration and invasion of NPC cells in vitro. These findings were also replicated in a mouse model of NPC tumor metastasis. We identified TLR4 as a functional receptor in mediating the pro-migratory effects of resistin in NPC cells. Furthermore, p38 MAPK and NF-κB were intracellular effectors that mediated resistin-induced EMT. Taken together, our results suggest that resistin promotes NPC metastasis by activating the TLR4/p38 MAPK/NF-κB signaling pathways. [ABSTRACT FROM AUTHOR]

Some studies proposed the anti‐inflammatory effect of soy protein and soy isoflavones by changing the serum adiponectin and resistin levels. The purpose of this research was to determine the impact of soy isoflavones and soy protein on blood adiponectin and resistin levels in adults. Scopus, PubMed, Cochrane Library, ISI Web of Science, and ClinicalTrials.gov databases were searched until April 2022. The effect size was computed by the mean changes from the beginning for intervention and comparison groups and their standard deviation. In the case of significant heterogeneity, DerSimonian and Laird random‐effects model was used. Six and five clinical trials were selected for the systematic review and meta‐analysis, respectively. The overall estimate indicated that soy isoflavones in combination with soy protein did not significantly change serum adiponectin level (weighted mean differences (WMD) = 0.36 μg/ml; 95% confidence interval (CI): −0.26, 0.99; p =.25), but significantly increased serum resistin level (WMD = 0.64 ng/ml, 95% CI: 0.25, 1.04; p =.001). In combination with soy protein, soy isoflavones nonsignificantly increased serum adiponectin levels, but significantly increased resistin levels. New intervention studies with a high dose of soy isoflavones and soy protein in different parts of the world and an updated meta‐analysis are needed to confirm the results of our study. [ABSTRACT FROM AUTHOR]

Objectives: The aim of (this) study was to investigate concentrations of galanin and resistin in patients with endometrioid type endometrium cancer. Material and methods: A total of 85 patients (52 Endometrioid type Endometrium Cancer patients and 33 healthy controls) were included in the study. Serum galanin and resistin levels were measured by an enzyme-linked immunosorbent assay (ELISA). Results: It was found that the sensitivity and specificity of galanin at the cut off level of 0,37 ng/mL, was 82.96% and 68.78% respectively (AUC = 0.795, CI:0.691-0.898, p < 0.001). Sensitivity and specificity of resistin at the 0.27 ng/mL cut off level, was found to be 82.95% and 59.12% respectively (AUC = 0.705, CI:0.588-0.822, p < 0.001) for prediction of endometrioid type endometrium cancer diagnosis. Bivariate logistic regression analysis showed that, increased galanin concentration, greater than 0.37 ng/mL, increased the risk of having endometrioid type endometrium cancer 10.2 times (95% CI: 3.425-30.881, p < 0.001) and resistin concentration > 0.27 ng/mL, increased the risk of having endometrioid type endometrium cancer 5.6 fold (95% CI: 1.939-16.282, p = 0.001). On the other hand, according to adjusted Odds Ratio results of the multiple logistic regression analysis, effect of interaction between galanin and resistin on having endometrioid type endometrium cancer was statistically significant. Increased galanin concentration > 0.37 ng/mL with increased resistin concentration > 0.27 ng/mL had adjusted Odds Ratio = 27.182 times greater risk of having endometrioid type endometrium cancer (95% CI: 6.653 to 111.109, p < 0.001). Conclusions: Increased galanin and resistin levels, either separately or together with, seemed to increase the risk of endometrioid type endometrium cancer other than different risk factors. [ABSTRACT FROM AUTHOR]

Background: Resistin is a proinflammatory adipokine involved in metabolic disorders. Its interplay with hypertriglyceridemia remains to be elucidated. We aimed to evaluate the relationship between resistin (−420C/G) single nucleotide variant (SNV) and metabolic parameters and preference for fried food consumption in hypertriglyceridemia. Methods: The study enrolled 179 hypertriglyceridemic (HTG) and 182 normotriglyceridemic (NTG) patients. Anthropometric measurements, serum resistin, insulin and fasting glucose concentration, a homeostatic model assessment—insulin resistance (HOMA-IR), triglycerides (TG), cholesterol concentration, and fried food taste preference (FP) or other cooking methods preference (OP) were assessed in the study. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. Results: HTG and NTG groups did not differ significantly in serum resistin concentration; HTG individuals demonstrated significantly increased serum levels of TG, glucose, total cholesterol (TCH), and HOMA-IR and decreased HDL cholesterol. Resistin, insulin, glucose, HOMA-IR, and cholesterol fractions were similar among particular resistin genotypes in HTG, NTG, FP, or OP groups. TG and TCH concentrations differ significantly among CG and CC genotypes in the FP group. Considering the FP group, GG and CG genotypes appeared more frequently in hyperlipidemic (OR 2.6 95% CI; 1.16–5.82; p = 0.01; significant after Bonferroni correction) than in NTG patients. Multivariable logistic regression models showed that the G allele and CG genotype of SNV (−420C/G), adjusted for selected confounders such as fried food preference, increased the odds of hypertriglyceridemia about twofold. Conclusions: Allele G and CG genotype of resistin SNV (−420C/G) are linked with the preference for fried food taste in hypertriglyceridemic patients. [ABSTRACT FROM AUTHOR]

Resistin is upregulated in obese humans and mice, and elevated serum resistin induces insulin resistance and hepatic steatosis. Previous studies have revealed that mulberry 1-deoxynojirimycin (DNJ) is important for a variety of physiological processes, especially carbohydrate and lipid metabolism. However, it remains unclear whether DNJ has a positive effect on insulin resistance and hepatic steatosis, and what the exact mechanism is. Male C57BL/6J mice were treated with resistin with or without DNJ. DNJ reversed the homeostasis model assessment of insulin resistance (HOMA-IR)-induced by resistin and significantly decreased triglyceride levels both in the serum and liver. A histological analysis demonstrated that lipid accumulation significantly decreased in the DNJ group compared to the resistin group. A mechanistic analysis showed that DNJ significantly inhibited the resistin-induced decline in enzyme activities of hormone-sensitive lipase (HSL) and hepatic lipase (HL) in serum and lipoprotein lipase (LPL) in liver. FAS and Acox1α were significantly altered by resistin but restored by DNJ. Furthermore, DNJ partially but significantly restored insulin-stimulated glucose uptake compared with the resistin group, suggesting that DNJ reversed the insulin sensitivity impaired by hyperresistinemia. Treatment of AML12 cells with DNJ significantly restored the expression level and phosphorylation of Akt. The transcriptional levels of InsR and IRS1, as well as the protein levels of InsR and Glut4 and phosphorylation of PI3K and GSK3β, were also normalized in the DNJ-treated group. In conclusion: mulberry DNJ significantly alleviated liver steatosis and insulin resistance in hyperresistinemia. [ABSTRACT FROM AUTHOR]

Aim: Metabolic syndrome (MS) refers to a group of co-morbidities which include central obesity, hypertension, hyperglycemia and dyslipidemia. Previously, we reported that childhood lymphatic filariasis (LF) confers significant protection against type-1 and type-2 forms of diabetes, by means of immunomodulation. In the present study, we studied the effect of LF on endocrine dysfunction in MS and Non-MS patients in baseline and after 10 years of follow-up. Methods: We quantified the serum levels of pancreatic hormones (insulin and glucagon), incretins (Ghrelin, GIP and GLP-1) and adipokines (leptin, adiponectin, adipsin, visfatin, PAI-1 and resistin) by multiplex bead array system. Results: MS (both LF- and LF+) subjects had increased insulin levels compared to NMS (both LF- and LF+) subjects. MS-LF+ subjects had significantly increased levels of glucagon, ghrelin, GIP and GLP-1 and decreased levels of adipsin, compared to MS-LF- subjects. Interestingly this effect was short-lived and was not seen in the follow-up samples. Conclusion: Overall, LF infection might confer limited short-term beneficial effects against MS, by means of modulating the incretin levels,either directly or indirectly. [ABSTRACT FROM AUTHOR]

Serum resistin is a pro-inflammatory cytokine that has been described as a risk factor associated with mortality in several clinical sets including type 2 diabetes. Mortality studies in the general population are needed to find out the risk of death associated to this cytokine. In a follow-up study of a cohort of adult population (n = 6636) in Spain over a period of fifteen years (447 deaths/102,255 person-years), serum resistin measurements and death records were obtained. The risks of all-cause deaths, and deaths from cardiovascular and oncological diseases were estimated. Hazard ratios (HR) and its confidence intervals (CI) were calculated using multivariable Cox models, adjusting the effect of 11 traditional risk factors. The risk of all-cause mortality among participants exposed to the highest quintile of resistin was always higher than among those in the lowest quintile (HR varied between 1.55 when smoking was the adjusted factor [95% CI 1.17–2.05], and 1.68 when the adjusted factor was physical activity [95% CI 1.27–2.21]). The maximally adjusted model, accounting for the effect of all traditional factors, corroborated this higher risk of all-cause mortality among people in the highest resistin quintile (HR = 1.52; 95% CI 1.13–2.05). The effect of resistin was even higher for cardiovascular deaths (HR = 2.14; 95% CI 1.13–4.06), being exceeded only by suffering diabetes (HR = 3.04; 95% CI 1.98–4.69) or previous acute coronary syndrome (HR = 3.67; 95% CI 2.18–6.18). This findings corroborate the role of resistin as a risk factor for all-cause (and cardiovascular) death in the general population. [ABSTRACT FROM AUTHOR]

Simple Summary: Resistin has been proposed to link to cancer development via inflammatory processes. Prior case-control studies suggest higher post-diagnosis resistin concentrations in CRC cases compared to controls. Here, we found no association between pre-diagnostic circulating resistin concentrations and the risk of CRC; however, we observed a marginally significant association among cases (and their matched controls) diagnosed with CRC within the first two years of follow-up, whereas no such association was observed among cases (and their matched controls) diagnosed with CRC after two years of follow-up. We speculate that resistin is more likely a marker of existing tumors than a risk factor of CRC. Resistin is a polypeptide implicated in inflammatory processes, and as such could be linked to colorectal carcinogenesis. In case-control studies, higher resistin levels have been found in colorectal cancer (CRC) patients compared to healthy individuals. However, evidence for the association between pre-diagnostic resistin and CRC risk is scarce. We investigated pre-diagnostic resistin concentrations and CRC risk within the European Prospective Investigation into Cancer and Nutrition using a nested case-control study among 1293 incident CRC-diagnosed cases and 1293 incidence density-matched controls. Conditional logistic regression models controlled for matching factors (age, sex, study center, fasting status, and women-related factors in women) and potential confounders (education, dietary and lifestyle factors, body mass index (BMI), BMI-adjusted waist circumference residuals) were used to estimate relative risks (RRs) and 95% confidence intervals (CIs) for CRC. Higher circulating resistin concentrations were not associated with CRC (RR per doubling resistin, 1.11; 95% CI 0.94–1.30; p = 0.22). There were also no associations with CRC subgroups defined by tumor subsite or sex. However, resistin was marginally associated with a higher CRC risk among participants followed-up maximally two years, but not among those followed-up after more than two years. We observed no substantial correlation between baseline circulating resistin concentrations and adiposity measures (BMI, waist circumference), adipokines (adiponectin, leptin), or metabolic and inflammatory biomarkers (C-reactive protein, C-peptide, high-density lipoprotein cholesterol, reactive oxygen metabolites) among controls. In this large-scale prospective cohort, there was little evidence of an association between baseline circulating resistin concentrations and CRC risk in European men and women. [ABSTRACT FROM AUTHOR]

Adipokine human Resistin (hResistin), is known to be associated with insulin resistance and secrete low-grade pro-inflammatory cytokines in obesity. Although studies on low-grade inflammation of adipokine hResistin are known, studies on the effects and mechanisms of intervertebral disc degeneration (IVDD) are still lacking. Thus, we investigated the adipokine hResistin with or without pro-inflammatory cytokine IL-1β in intervertebral disc (IVD) cells such as human annulus fibrosus (hAF) and nucleus pulposus (hNP). The protein expression changes in IL-1β, IL-6, IL-8, MMP-1, MMP-3, and MMP-13, induced by the combined-hResistin and IL-1β stimulation on hAF cells, was significantly greater than that of the same induced by mono-IL-1β stimulation. Similarly, in the case of the protein expression change of inflammatory mediators induced by the combined-hResistin and IL-1β stimulation on hNP cells was also significantly greater than that of the same induced by mono-IL-1β stimulation. These results improve understanding of hResistin on inflammatory IVDD but also with other obesity-related inflammatory diseases. [ABSTRACT FROM AUTHOR]

Background: In patients with systemic lupus erythematosus (SLE), a higher frequency of atherosclerotic lesions is associated with poor prognosis. Hydroxychloroquine (HCQ) has been reported to improve the lifespan and the prognosis of dyslipidaemia in patients with SLE, but the mechanism is unclear. We investigated the effect of supplemental HCQ treatment on the levels of serum cytokines associated with atherosclerosis in patients with stable SLE. Methods: Patients with SLE who received supplemental HCQ and maintained low disease activity between January 2016 and September 2020 were included in this study. Disease activity was assessed using Safety of Estrogens in Lupus National Assessment-SLE Disease Activity Index, Cutaneous Lupus Erythematous Disease Area and Severity Index, and Lupus Low Disease Activity State. Serum complement titres, anti-dsDNA antibodies, and serum cytokines (adiponectin, resistin, and leptin) were analyzed before and after HCQ treatment. Results: Forty-one patients (4 males and 37 females, mean age 41.3 ± 13.2 years) were included. Serum adiponectin levels were significantly increased after 3 months of HCQ treatment compared to baseline, and serum resistin levels were significantly reduced. The change in serum resistin level after HCQ administration was correlated with a significant reduction in serum TNF-α, interleukin (IL)-6, IL-8, and IL-1RA levels. Conclusions: Supplemental HCQ treatment in patients with SLE improved adipokine levels. HCQ may improve prognosis by controlling disease activity in SLE and reducing risk factors for atherosclerosis. Key Points • Hydroxychloroquine has been reported to improve the prognosis of dyslipidaemia in patients with SLE, but the underlying mechanism is unclear. • In this study, hydroxychloroquine improved adipokine levels in patients with SLE, implicating adipokines as a potential mechanism underlying the benefit of hydroxychloroquine on dyslipidaemia. • Supplemental hydroxychloroquine should be considered in patients with SLE harboring lipid abnormalities and risk factors for atherosclerosis. [ABSTRACT FROM AUTHOR]

Maternal metabolic status influences pregnancy and, consequently, the perinatal outcome. Resistin is a pro-inflammatory adipokine predominantly expressed and secreted by mononuclear cells, adipose tissue, and placental trophoblastic cells during pregnancy. Recently, we reported an inverse association between maternal resistin levels and fetal low-density lipoprotein cholesterol (LDL-C). Then, in this work, we used a human placental explant model and the trophoblast cell line JEG-3 to evaluate whether resistin affects placental LDL-C uptake. Resistin exposure induced the transcription factor SREBP-2, LDLR, and PCSK9 mRNA expression, and changes at the protein level were confirmed by immunohistochemistry and Western blot. However, for LDLR, the changes were not consistent between mRNA and protein levels. Using a labeled LDL-cholesterol (BODIPY FL LDL), uptake assay demonstrated that the LDL-C was significantly decreased in placental explants exposed to a high dose of resistin and a lesser extent in JEG-3 cells. In summary, resistin induces PCSK9 expression in placental explants and JEG-3 cells, which could be related to negative regulation of the LDLR by lysosomal degradation. These findings suggest that resistin may significantly regulate the LDL-C uptake and transport from the maternal circulation to the fetus, affecting its growth and lipid profile. [ABSTRACT FROM AUTHOR]

Background: In current intensive care treatment, some patients with severe burns cannot be saved due to progressive organ failure. Further investigation of the pathogenesis of severe burns is needed to improve the mortality rate. In burns, inflammatory cytokines form a network that leads to an inflammatory response. Adipocytes secrete physiologically active substances (adipokines). The roles of adipokines have not been completely clarified in burn patients. This study aimed to determine the relation between serial changes of adipokines and clinical course in severely burned patients.Methods: This was a single-center, retrospective, observational study. Patients' blood samples were collected on the day of injury and around 1 week later. Adipokines (adiponectin, angiotensinogen, chemerin, CXCL-12/SDF-1, leptin, resistin, vaspin, visfatin), various inflammatory cytokines, syndecan-1 and C1 esterase inhibitor were measured.Results: Thirty-eight patients were included. Resistin levels were significantly higher in the non-survivors versus survivors on Day 1 after burn injury. Hierarchical clustering analysis showed common clusters on Day 1 and at 1 Week after burn injury (resistin, IL-6, IL-8, IL10 and MCP-1). The correlation coefficient of resistin to SOFA score at 1 Week was significant. Logistic regression analysis showed a significant relation of resistin levels on Day 1 with prognosis; the area under the ROC curve for resistin was 0.801.Conclusions: In the acute phase of burns, resistin was associated with other pro-inflammatory cytokines and was related to the severity and prognosis of major burns. [ABSTRACT FROM AUTHOR]

Background: Periodontitis is a major inflammatory disease of the oral mucosa that is not limited to the oral cavity but also has systemic consequences. Although the importance of chronic periodontitis has been emphasized, the systemic immune response induced by periodontitis and its therapeutic effects remain elusive. Here, we report the transcriptomes of peripheral blood mononuclear cells (PBMCs) from patients with periodontitis.Methods: Using single-cell RNA sequencing, we profiled PBMCs from healthy controls and paired pre- and post-treatment patients with periodontitis. We extracted differentially expressed genes and biological pathways for each cell type and calculated activity scores reflecting cellular characteristics. Intercellular crosstalk was classified into therapy-responsive and -nonresponsive pathways.Results: We analyzed pan-cellular differentially expressed genes caused by periodontitis and found that most cell types showed a significant increase in CRIP1, which was further supported by the increased levels of plasma CRIP1 observed in patients with periodontitis. In addition, activated cell type-specific ligand-receptor interactions, including the BTLA, IFN-γ, and RESISTIN pathways, were prominent in patients with periodontitis. Both the BTLA and IFN-γ pathways returned to similar levels in healthy controls after periodontal therapy, whereas the RESISTIN pathway was still activated even after therapy.Conclusion: These data collectively provide insights into the transcriptome changes and molecular interactions that are responsive to periodontal treatment. We identified periodontitis-specific systemic inflammatory indicators and suggest unresolved signals of non-surgical therapy as future therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: This study aimed to investigate the effects of 8-week aerobic training (AT) and saffron supplementation on inflammation and metabolism in middle-aged obese women with type 2 diabetes mellitus (T2DM). Methods: Thirty-two obese women with T2DM were randomly divided into four groups (n = 8 in all groups): saffron + training (ST), placebo + training (PT), saffron supplementation (SS), and placebo (P). The ST and PT groups performed eight weeks of aerobic training (AT) (three sessions/week at 60–75% HRmax). A daily dose of 400 mg saffron powder was consumed by the ST and SS groups for 8 weeks. Blood samples were taken after 12 h of fasting, 48 h before the first AT session, 48 h and two weeks after the last AT session. Results: AT, saffron supplementation, and their combination affected body mass index (BMI), homeostatic model assessment for insulin resistance (HOMA-IR), and serum levels of insulin, adiponectin, interleukin-6 (IL-6), high-density lipoprotein cholesterol (HDL-C), cholesterol, and triglyceride (TG) (p < 0.05). However, body weight, body fat percentage, and serum levels of glucose, resistin, tumor necrosis factor-alpha (TNF-α), irisin, and low-density lipoprotein cholesterol (LDL-C) showed significant changes in the ST group only (p < 0.05). In addition, a significant difference was seen between all factors in post-training and follow-up in the ST group (p < 0.05). Conclusions: Saffron supplementation at a dose of 400 mg/day, when combined with AT, could improve inflammation, metabolism, glycemic status, and lipid profile in T2DM patients, and these changes are sustainable at up to 2 weeks of detraining. [ABSTRACT FROM AUTHOR]

Adolescent idiopathic scoliosis (AIS) is a three-dimensional malformation of the spine of unknown cause that develops between 10 and 18 years old and affects 2–3% of adolescents, mostly girls. It has been reported that girls with AIS have a taller stature, lower body mass index (BMI), and bone mineral density (BMD) than their peers, but the causes remain unexplained. Energy metabolism discrepancies, including alterations in adipokine and incretin circulatory levels, could influence these parameters and contribute to disease pathophysiology. This pilot study aims to compare the anthropometry, BMD, and metabolic profile of 19 AIS girls to 19 age-matched healthy controls. Collected data include participants' fasting metabolic profile, anthropometry (measurements and DXA scan), nutritional intake, and physical activity level. AIS girls (14.8 ± 1.7 years, Cobb angle 27 ± 10°), compared to controls (14.8 ± 2.1 years), were leaner (BMI-for-age z-score ± SD: −0.59 ± 0.81 vs. 0.09 ± 1.11, p = 0.016; fat percentage: 24.4 ± 5.9 vs. 29.2 ± 7.2%, p = 0.036), had lower BMD (total body without head z-score ± SD: −0.6 ± 0.83 vs. 0.23 ± 0.98, p = 0.038; femoral neck z-score: −0.54 ± 1.20 vs. 0.59 ± 1.59, p = 0.043), but their height was similar. AIS girls had higher adiponectin levels [56 (9–287) vs. 32 (7–74) μg/mL, p = 0.005] and lower leptin/adiponectin ratio [0.042 (0.005–0.320) vs. 0.258 (0.024–1.053), p = 0.005]. AIS participants with a Cobb angle superior to 25° had higher resistin levels compared to controls [98.2 (12.8–287.2) vs. 32.1 (6.6–73.8), p = 0.0013]. This pilot study suggests that adipokines are implicated in AIS development and/or progression, but more work is needed to confirm their role in the disease. [ABSTRACT FROM AUTHOR]