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Liqun Yang,1– 3 Zhimei Zhang,3 Yunfeng Zhen,3 Jing Feng,3 Jinhu Chen,3 Guangyao Song1– 3 1Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei Province, People’s Republic of China; 2Hebei Key Laboratory of Metabolic Disease, Shijiazhuang, Hebei Province, People’s Republic of China; 3Department of Endocrinology, Hebei General Hospital, Shijiazhuang, Hebei Province, People’s Republic of ChinaCorrespondence: Guangyao Song, Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei Province, People’s Republic of China, Tel +86-0311-8598-8556, Email sguangyao2@163.comPurpose: Energy metabolism is regulated by SIRT3, no research has been done on the connection between lipid metabolism in the oral fat test and SIRT3 polymorphism. Thus, we conducted a case-control study to investigate the connection between postprandial lipid and SIRT3 polymorphism.Patients and Methods: 402 non-obese Chinese subjects were enrolled and their postprandial lipid response to oral fat tolerance test (OFTT) was observed to understand the relationship between rs11246020 gene and postprandial triglyceride metabolism.Results: In a binary logic regression model, a protective effect of the T allele of the rs11246020 SIRT3 for postprandial hypertriglyceridemia was shown (OR=0.417, 95% CI = 0.219– 0.794, p=0.008). Compared to the CC genotype, individuals with the TT+CT variant of the rs11246020 SIRT3 gene demonstrated significantly lower levels of homeostasis model assessment of insulin resistance (HOMA-IR) (p=0.04), postprandial plasma glucose (PPG) (p=0.037), fasting plasma glucose (FPG) (p=0.02), and 4-hour triglyceridemia (Tg) (p=0.032).Conclusion: The C allele of rs11246020 SIRT3 gene may be a risk factor to increased possibility of postprandial triglyceridemia after an oral fat test, which involved in the mechanism of glucose and insulin metabolism.Keywords: sirtuin, postprandial hypertriglyceridemia, insulin resistance, genetics

Aim: TCF7L2 gene is believed to increase the risk of T2DM by its effects on insulin secretion. However, the exact mechanism of this enhanced risk is not clearly known. While TCF7L2 gene has been shown to affect lipid metabolism, these effects have remained largely unexplored in the context of diabetes risk. Methods: Postprandial lipid responses to a standardized fat challenge test were performed in 620 Asian Indian subjects (310 with NGT and 310 with T2DM/prediabetes) and compared between the risk and wild genotypes of the rs7903146 TCF7L2 gene. In 30 subjects scheduled to undergo abdominal surgery (10 each with NGT, Prediabetes and T2DM), adipocyte TCF7L2 gene expression was also performed by real time qPCR and confirmed by protein expression in western blot. Results: T allele of rs7903146 TCF7L2 gene was confirmed as the risk allele for T2DM (OR=1.8(1.2-2.74), p=0.005). TT+CT genotypes of rs7903146 TCF7L2 gene showed significantly higher 4hrTg (p<0.01), TgAUC (p<0.01), peakTg (p<0.01) as well as higher postprandial plasma glucose (p=.006) levels and HOMA-IR (p=0.03) and significantly lower adiponectin levels (p=0.02) as compared to CC genotype. The expression of TCF7L2 gene in VAT was 11-fold higher in prediabetes group as compared to NGT (P<0.01) and 5.7-fold higher in T2DM group as compared to NGT group(P=0.003) and was significantly associated with PPTg and glucose levels. Conclusion: There is significant PPTg dysmetabolism associated with the risk allele of rs7903146 polymorphism as well as adipocyte expression of TCF7L2 gene. Significant upregulation of TCF7L2 gene expression in VAT that correlates with PPTg and glycaemia is also seen in Asian Indians with glucose intolerance. Modulation of PPTg metabolism by TCF7L2 gene and the resultant PPHTg may be a novel mechanism that contributes to its diabetes risk in them. [ABSTRACT FROM AUTHOR]

AimTCF7L2 gene is believed to increase the risk of T2DM by its effects on insulin secretion. However, the exact mechanism of this enhanced risk is not clearly known. While TCF7L2 gene has been shown to affect lipid metabolism, these effects have remained largely unexplored in the context of diabetes risk.MethodsPostprandial lipid responses to a standardized fat challenge test were performed in 620 Asian Indian subjects (310 with NGT and 310 with T2DM/prediabetes) and compared between the risk and wild genotypes of the rs7903146 TCF7L2 gene. In 30 subjects scheduled to undergo abdominal surgery (10 each with NGT, Prediabetes and T2DM), adipocyte TCF7L2 gene expression was also performed by real time qPCR and confirmed by protein expression in western blot.ResultsT allele of rs7903146 TCF7L2 gene was confirmed as the risk allele for T2DM (OR=1.8(1.2-2.74), p=0.005). TT+CT genotypes of rs7903146 TCF7L2 gene showed significantly higher 4hrTg (p

Aim: Postprandial hypertriglyceridemia (PHTG) is an independent risk factor for coronary heart diseases. PHTG exhibits accumulation of apoB-48 containing chylomicron remnants (CM-Rs) and apoB-100 containing VLDL remnants (VLDL-Rs), which are both known to be atherogenic. However, unlike VLDL-Rs, structural and functional characterization of CM-Rs remains to be elucidated due to challenges in separating CM-Rs from VLDL-Rs. Recently, we successfully isolated CM-Rs and VLDL-Rs utilizing anti-apoB-48 or apoB-100 specific antibodies. This study aimed to characterize the proteome of CM-Rs along with that of VLDL-Rs., Methods: Eight healthy subjects were enrolled. Venous blood was drawn 3 hours after high-fat-containing meals. We isolated CM-Rs and VLDL-Rs from sera through combination of ultracentrifugation and immunoprecipitation using apoB-48 or apoB-100 specific antibodies, followed by shotgun proteomic analysis., Results: We identified 42 CM-Rs or VLDL-Rs-associated proteins, including 11 potential newly identified proteins such as platelet basic protein (PPBP) and platelet factor 4, which are chemokines secreted from platelets. ApoA-I, apoA-IV, and clusterin, which are also known as HDL-associated proteins, were significantly more abundant in CM-Rs. Interestingly, apoC-I, which reduces the activity of lipoprotein lipase and eventually inhibits catabolism of remnant proteins, was also more abundant in CM-Rs. Moreover, we identified proteins involved in complement regulation such as complement C3 and vitronectin, and those involved in acute-phase response such as PPBP, serum amyloid A protein 2, and protein S100-A8, in both CM-Rs and VLDL-Rs., Conclusions: We have firstly characterized the proteome of CM-Rs. These findings may provide an explanation for the atherogenic properties of CM-Rs.

Introduction: Leptin resistance is believed to cause insulin resistance though the exact mechanism is not fully understood. The present study aims to investigate the temporal profile of postprandial triglyceride (PPTG) and leptin levels, and their association with each other as well as with markers of metabolic syndrome. Materials and Methods: Serum leptin and PPTG levels were measured longitudinally till 26 weeks in Wistar rats fed on controlled diet (group 1) and high sucrose diet (HSD) (group 2). Two additional groups fed on HSD were taken and treated with pioglitazone (group 3) and atorvastatin (group 4). Body weight, homeostasis model assessment of insulin resistance (HOMA-IR), and glucose intolerance were also measured during this period. Comparison of the groups were done and Pearson's correlation coefficient was used to ascertain the association. Results: Leptin levels were significantly higher in all three groups receiving HSD compared to controlled diet group from week 2 to week 26 (P < 0.01). The postprandial triglyceride area under the curve (PPTG AUCs) were significantly higher in group 2 than controls during this period (P < 0.001). Body weight, HOMA-IR and glucose AUC were found to be significantly higher in group 2 rats than controls only from week 6, 8, and 12 respectively. In HSD-fed rats, but not in control, mean serum leptin levels from 2-26 weeks as well as peak (10th week) and 26th week were strongly associated with corresponding as well as preceding PPTG levels. Leptin levels significantly predicted HOMA-IR and prediabetes in group 2. Conclusion: This study found significant hyperleptinemia associated with postprandial hypertriglyceridemia that predicted insulin resistance and prediabetes in high sucrose diet–fed rats. [ABSTRACT FROM AUTHOR]

Abstract Aims/Introduction Preprandial metformin administration significantly reduces postprandial plasma triglyceride levels in animal studies by reducing intestinal absorption through delayed gastric emptying. However, this effect has not been shown in a clinical study. Therefore, we planned to investigate the efficacy of preprandial metformin administration on postprandial hypertriglyceridemia and the related gastrointestinal effects in patients with type 2 diabetes mellitus. Materials and Methods A total of 11 patients taking single‐dose metformin at 500–1,000 mg, with non‐fasting plasma triglyceride levels of 150–1,000 mg/dL, were recruited at a single university hospital. The difference between preprandial and postprandial metformin administration on postprandial hypertriglyceridemia was examined by a meal test. The gastrointestinal effects of metformin, including stomach heaviness, heartburn and satiety, were also assessed using a visual analog scale. Results The mean bodyweight of patients was 80.6 kg (body mass index 27.9 kg/m2), and the mean non‐fasting plasma triglyceride level was 275.9 ± 57.0 mg/dL. The area under the curve of triglyceride during the meal test was significantly lower in the preprandial protocol than in the postprandial protocol (P

Abstract Background Exercise has proved effective in attenuating the unfavourable response normally associated with postprandial hypertriglyceridemia (PHTG) and accompanying oxidative stress. Yet, the acute effects of prior exercise and PHTG on DNA damage remains unknown. The purpose of this study was to examine if walking alters PHTG-induced oxidative damage and the interrelated inflammatory mechanisms. Methods Twelve apparently healthy, recreationally active, male participants (22.4 ± 4.1 years; 179.2 ± 6 cm; 84.2 ± 14.7 kg; 51.3 ± 8.6 ml·kg− 1·min− 1) completed a randomised, crossover study consisting of two trials: (1) a high-fat meal alone (resting control) or (2) a high-fat meal immediately following 1 h of moderate exercise (65% maximal heart rate). Venous blood samples were collected at baseline, immediately post-exercise or rest, as well as at 2, 4 and 6 h post-meal. Biomarkers of oxidative damage (DNA single-strand breaks, lipid peroxidation and free radical metabolism) and inflammation were determined using conventional biochemistry techniques. Results DNA damage, lipid peroxidation, free radical metabolism and triglycerides increased postprandially (main effect for time, p

BackgroundTo investigate possible mechanisms of postprandial hypertriglyceridemia (PPT), we analyzed serum lipid and apolipoprotein (Apo) AI, B, CII and CIII levels before and after a high-fat meal.MethodsThe study has been registered with the China Clinical Trial Registry (registration number:ChiCTR1800019514; URL: http://www.chictr.org.cn/index.aspx). We recruited 143 volunteers with normal fasting triglyceride (TG) levels. All subjects consumed a high-fat test meal. Venous blood samples were obtained during fasting and at 2, 4, and 6 hours after the high-fat meal. PPT was defined as TG ≥2.5 mmol/L any time after the meal. Subjects were divided into two groups according to the high-fat meal test results: postprandial normal triglyceride (PNT) and PPT. We compared the fasting and postprandial lipid and ApoAI, ApoB, ApoCII and ApoCIII levels between the two groups.ResultsSignificant differences were found between the groups in fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR), TG, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), TG-rich lipoprotein remnants (TRLRs), ApoB, ApoCIII, ApoAI/ApoB and ApoCII/ApoCIII. The insulin, HOMA-IR, TG, TC, LDL-C, non-HDL-C, TRLRs, ApoB, ApoCIII and ApoCII/ApoCIII values were higher in the PPT group, while the ApoAI/ApoB ratio was higher in the PNT group. The postprandial TG level peaked in the PNT group 2 hours after the meal but was significantly higher in the PPT group and peaked at 4 hours. TRLRs gradually increased within 6 hours after the high-fat meal in both groups. The area under the curve (AUC) of TG and TRLRs and the AUC increment were higher in the PPT group (P < 0.001). ApoCIII peaked in the PNT group 2 hours after the meal and gradually decreased. ApoCIII gradually increased in the PPT group within 6 hours after the meal, exhibiting a greater AUC increment (P < 0.001). Fasting ApoCIII was positively correlated with age, systolic and diastolic blood pressure, body mass index (BMI), waist circumference, TC, TG, LDL-C, non-HDL-C, TRLRs, and ApoB (P

Background: To investigate possible mechanisms of postprandial hypertriglyceridemia (PPT), we analyzed serum lipid and apolipoprotein (Apo) AI, B, CII and CIII levels before and after a high-fat meal. Methods: The study has been registered with the China Clinical Trial Registry (registration number:ChiCTR1800019514; URL: http://www.chictr.org.cn/index.aspx). We recruited 143 volunteers with normal fasting triglyceride (TG) levels. All subjects consumed a high-fat test meal. Venous blood samples were obtained during fasting and at 2, 4, and 6 hours after the high-fat meal. PPT was defined as TG ≥2.5 mmol/L any time after the meal. Subjects were divided into two groups according to the high-fat meal test results: postprandial normal triglyceride (PNT) and PPT. We compared the fasting and postprandial lipid and ApoAI, ApoB, ApoCII and ApoCIII levels between the two groups. Results: Significant differences were found between the groups in fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR), TG, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), TG-rich lipoprotein remnants (TRLRs), ApoB, ApoCIII, ApoAI/ApoB and ApoCII/ApoCIII. The insulin, HOMA-IR, TG, TC, LDL-C, non-HDL-C, TRLRs, ApoB, ApoCIII and ApoCII/ApoCIII values were higher in the PPT group, while the ApoAI/ApoB ratio was higher in the PNT group. The postprandial TG level peaked in the PNT group 2 hours after the meal but was significantly higher in the PPT group and peaked at 4 hours. TRLRs gradually increased within 6 hours after the high-fat meal in both groups. The area under the curve (AUC) of TG and TRLRs and the AUC increment were higher in the PPT group (P < 0.001). ApoCIII peaked in the PNT group 2 hours after the meal and gradually decreased. ApoCIII gradually increased in the PPT group within 6 hours after the meal, exhibiting a greater AUC increment (P < 0.001). Fasting ApoCIII was positively correlated with age, systolic and diastolic blood pressure, body mass index (BMI), waist circumference, TC, TG, LDL-C, non-HDL-C, TRLRs, and ApoB (P <0.05). ApoCIII was an independent risk factor of PPT after adjustment for BMI, waist circumference, TC, LDL-C, and ApoB (P < 0.001, OR=1.188). Conclusions: Elevated ApoCIII levels may cause PPT. [ABSTRACT FROM AUTHOR]

Background and Aims: the effect of subclinical hypothyroidism on the dynamics of lipid spectrum during lipid-tolerance test was studied. Subclinical hypothyroidism (SH) is the earliest thyroid dysfunction and is the most common. However, data on the presence of dyslipidemia in subclinical hypothyroidism are controversial. The aim of this study was the early detection of lipid metabolism disorders in patients with subclinical hypothyroidism on the basis of lipid-tolerance testing. Materials and Methods: the study involved 96 people. The main group included 37 patients with subclinical hypothyroidism, but seven of them had fasting hypercholesterolemia, dyslipidemia, and they were excluded from further study. Thus, 30 patients with SH formed the main group 1. Two comparison groups were presented by 59 comparisons by main characteristics (age, sex, exclusion criteria) of individuals without thyroid pathology (group 2) - 30 people, and with overt hypothyroidism (group 3) - 29 people. An oral fat tolerance test was used to evaluate postprandial lipemia. Results and Conclusions: As a result of the study, data were obtained according to which fat load stimulated the development of different levels of postprandial hyperlipidemia, depending on the thyroid status of patients. Patients with subclinical hypothyroidism had postprandial hypertriglyceridemia, which was combined with an increase in low-density lipoprotein levels and a decrease in high-density lipoprotein levels. The proposed method allows the detection of early disorders of lipid metabolism in patients with subclinical hypothyroidism. [ABSTRACT FROM AUTHOR]

In addition to acquiring a better understanding of foods that may have intrinsic health benefits, increasing our knowledge of dietary components that may adversely impact health and wellness, and the levels of consumption at which these adverse effects may occur, should also be an important priority for the Foods for Health initiative. This review discusses the evidence that additional research is needed to determine the adverse effects of consuming added sugars containing fructose. Current guidelines recommend limiting sugar consumption in order to prevent weight gain and promote nutritional adequacy. However, recent data suggest that fructose consumption in human results in increased visceral adiposity, lipid dysregulation, and decreased insulin sensitivity, all of which have been associated with increased risk for cardiovascular disease and type 2 diabetes. A proposed model for the differential effects of fructose and glucose is presented. The only published study to directly compare the effects of fructose with those of commonly consumed dietary sweeteners, high fructose corn syrup and sucrose, indicates that high fructose corn syrup and sucrose increase postprandial triglycerides comparably to pure fructose. Dose-response studies investigating the metabolic effects of prolonged consumption of fructose by itself, and in combination with glucose, on lipid metabolism and insulin sensitivity in both normal weight and overweight/obese subjects are needed.

Postprandial hypertriglyceridemia is an independent risk factor for cardiovascular disease. The aim of this study was to assess the effects of a single fat-rich meal on barrier functions and inflammatory status on human umbilical vascular endothelial cells (HUVECs), furthermore we assess the effects of mixture of palmitic acid and 25-hydroxycholesterol (PA +25OHCH) on integrity of endothelial cells and their inflammatory properties. HUVECs were induced with serum of healthy volunteers taken before, and 3 h after, the consumption of a meal with a standardized daily required dose of fats. In addition, endothelial cells were induced with PA +25OHCH (800 μM/L+10 μg/mL). Total cholesterol, triglycerides (TGs), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, high sensitivity c-reactive protein, and glucose were measured at fasting and postprandially. HUVEC integrity was measured in the RTCA-DP xCELLigence system. mRNA expression of interleukin (IL)-33, IL-32, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), CX3C-chemokine, vascular endothelial growth factor (VEGF) occludin, and VE-cadherin was analyzed by real-time polymerase chain reaction. Viability and apoptosis were assessed in flow cytometry. The level of VEGF and IL-33 in fasting and postprandial serum was assessed by enzyme-linked immunosorbent assay (ELISA). Three hours after consumption of a fatty meal, all patients displayed increased levels of TGs and Toll-like receptors (110 ± 37 mg/dL versus 182 ± 64 mg/dL P < 0.05) (24 ± 11 mg/dL versus 42 ± 14 mg/dL P < 0.05). Postprandial serum and PA +25OHCH caused >20% decrease of HUVEC integrity than fasting serum (P < 0.001). HUVEC disintegration was accompanied by a decrease of occludin mRNA expression as compared with fasting serum (P < 0.05). The fatty meal affected neither VE-cadherin mRNA expression nor its apoptosis (P > 0.05). Mixture of PA +25OHCH caused decrease of VE-cadherin mRNA expression as compared with fasting serum (P < 0.01). PA +25OHCH did not affect HUVEC apoptosis (P > 0.05). Postprandial serum and PA +25OHCH caused increase of IL-33, MCP-1, ICAM-1, IL-32, VEGF, and CX3C-chemokine mRNA expression as compared with fasting serum (P < 0.05). Moreover, level of VEGF in fatty serum was significantly higher (P < 0.001). Postprandial lipemia after a single fatty meal may destabilize the endothelial barrier and initiate inflammatory processes. [ABSTRACT FROM AUTHOR]

Recent evidence suggests that postprandial hypertriglyceridemia (PPT) is associated with the incidence of CVD. Several non-modifiable factors (genetics, age, gender) and lifestyle factors (physical activity, smoking, regular alcohol) have shown their ability to modulate PPT. We evaluate the influence of regular alcohol intake, physical activity and smoking habit modulating PPT in the CORDIOPREV study (NCT00924937). 1002 patients were subject to an oral fat load test meal and serial blood samples were drawn at 0, 1, 2, 3 and 4 h during postprandial state. A PPT concentration above 2.5 mmol/L (220 mg/dL) at any time point has been established as a detrimental response. Alcohol consumption was defined as non-drinkers, moderate and severe intake; regular physical activity exceeding than or lower than 1000 MET/week; smoking habit was classified in current, never, recent ex-smokers and long-term ex-smokers. The prevalence of undesirable PPT response was 68% in current, 58% in recent ex-smokers, 49% in long-term ex-smokers and 48% in never smokers (p < 0.001). Current and recent ex-smokers displayed higher PPT response as well as a greater area under the curve (AUC) and higher incremental (iAUC) of triglycerides (TG) compared with long-term ex-smokers and never smokers (p < 0.05), without differences among these subgroups. No differences were observed in the magnitude of PPT according to regular physical activity or alcohol intake habits. Smoking is an independent risk factor modulating the magnitude of PPT. However, after tobacco cessation, ex-smokers show a progressive decrease on their PPT to reach levels similar to those of never smokers. Image 1 • We studied the influence of regular alcohol intake, physical activity and smoking habit modulating PPT in the CORDIOPREV study. • PPT and the prevalence of undesirable response was evaluate in each subgroups. We assessed the main determinants risk factors in the presence of undesirable response. • Smoking is an independent risk factor modulating the magnitude of PPT. • After tobacco cessation, in long-term ex-smokers, PPT progressively decreases to similar magnitude to never smokers. • No differences observed in the magnitude of PPT according to regular physical activity or alcohol intake habits. [ABSTRACT FROM AUTHOR]

Aims/Introduction: Preprandial metformin administration significantly reduces postprandial plasma triglyceride levels in animal studies by reducing intestinal absorption through delayed gastric emptying. However, this effect has not been shown in a clinical study. Therefore, we planned to investigate the efficacy of preprandial metformin administration on postprandial hypertriglyceridemia and the related gastrointestinal effects in patients with type 2 diabetes mellitus. Materials and Methods: A total of 11 patients taking single‐dose metformin at 500–1,000 mg, with non‐fasting plasma triglyceride levels of 150–1,000 mg/dL, were recruited at a single university hospital. The difference between preprandial and postprandial metformin administration on postprandial hypertriglyceridemia was examined by a meal test. The gastrointestinal effects of metformin, including stomach heaviness, heartburn and satiety, were also assessed using a visual analog scale. Results: The mean bodyweight of patients was 80.6 kg (body mass index 27.9 kg/m2), and the mean non‐fasting plasma triglyceride level was 275.9 ± 57.0 mg/dL. The area under the curve of triglyceride during the meal test was significantly lower in the preprandial protocol than in the postprandial protocol (P < 0.05). Compared with postprandial administration, preprandial administration of metformin increased satiety (P = 0.036) without stomach heaviness or heartburn. Conclusions: Preprandial metformin administration significantly reduced plasma triglyceride level during meal testing without marked exacerbation of gastrointestinal adverse effects. The present results suggest that a simple change in the timing of metformin administration represents a novel approach for enhancing triglyceride‐lowering strategies in patients with type 2 diabetes mellitus and postprandial hypertriglyceridemia. [ABSTRACT FROM AUTHOR]

Postprandial glucose level is an independent risk factor for cardiovascular disease that exerts effects greater than glucose levels at fasting state, whereas increase in serum triglyceride level, under both fasting and postprandial conditions, contributes to the development of arteriosclerosis. Insulin resistance is a prevailing cause of abnormalities in postabsorptive excursion of blood glucose and postprandial lipid profile. Excess fat deposition renders a vicious cycle of hyperglycemia and hypertriglyceridemia in the postprandial state, and both of which are contributors to atherosclerotic change of vessels especially in patients with type 2 diabetes mellitus. Several therapeutic approaches for ameliorating each of these abnormalities have been attempted, including various antidiabetic agents or new compounds targeting lipid metabolism. [ABSTRACT FROM AUTHOR]

Many recent studies have acknowledged postprandial hypetriglyceridemia as a distinct risk factor for cardiovascular disease. This dysmetabolic state is the result of the hepatic overproduction of very low-density lipoproteins (VLDLs) and intestinal secretion of chylomicrons (CMs), which leads to highly atherogenic particles and endothelial inflammation. Postprandial lipid metabolism does not only depend on consumed fat but also on the other classes of nutrients that a meal contains. Various mechanisms through which carbohydrates exacerbate lipidemia have been identified, especially for fructose, which stimulates de novo lipogenesis. Glycemic index and glycemic load, despite their intrinsic limitations, have been used as markers of the postprandial glucose and insulin response, and their association with metabolic health and cardiovascular events has been extensively studied with contradictory results. This review aims to discuss the importance and pathogenesis of postprandial hypertriglyceridemia and its association with cardiovascular disease. Then, we describe the mechanisms through which carbohydrates influence lipidemia and, through a brief presentation of the available clinical studies on glycemic index/glycemic load, we discuss the association of these indices with atherogenic dyslipidemia and address possible concerns and implications for everyday practice.

Green-plant membrane is a phytonutrient present in green leafy vegetables at high concentration. Postprandial increases in blood triglyceride levels result in insulin resistance and type 2 diabetes. Additionally, dietary life and eating order also affect postprandial hypertriglyceridemia. In this study, the effects of once-daily intake of green-plant membrane with dietary oil on postprandial hypertriglyceridemia were investigatedin vitroandin vivo. In vitro,green-plant membrane bound hydrophobic bile acids but did not inhibit pancreatic lipase activity. Following the administration, green-plant membrane with dietary oil in rats, oral fat tolerance tests, increases in serum triglycerides levels were significantly reduced. Moreover, fecal total lipid and bile acid volumes were significantly increased in rats that administered 200 mg/mL green-plant membrane. These results suggest that green-plant membrane with dietary oil inhibits dietary fat absorption via promotion of bile acid excretion in feces and the effectiveness of eating green-plant membrane, such as green leafy vegetables, with meals. Green-plant membrane with meal inhibits dietary fat absorption via excretion of bile acid in feces and the effectiveness of taking such as green leafy vegetables. [ABSTRACT FROM PUBLISHER]

Introduction: Coronary heart disease is the leading cause of death in Western countries and it is now an increasing problem in developing countries too, due to changes in life style and dietary habits. Heart Disease is responsible for more deaths and disability among Western Population, both male and female, than any other killer disease, and it is quickly establishing itself as the leading cause of death and disability among Indians as well. Aim of the Study: To study relation between risk factors for atherosclerosis and fasting and postprandial triglyceride levels in patients of Coronary artery disease. To establish that post-prandial triglycerides level is a better indicator as a 'risk factor' for atherosclerosis. Materials and methods: A complete physical and cardiovascular system examination performed. Blood pressure measurements were performed with mercury sphygmomanometer in a standardized fashion. Waist circumference was measured at umbilical level. Hip circumference was measured at maximum girth at hip. Recording of ECG was done with 12 leads recording in standard fashion with B.P.L machine. Fasting samples of blood glucose, Fasting Lipid profile was measured. Results: In our study, out of 56 male 34 (62.5%) were suffering from diabetes mellitus while 30 female out of 44 were (68.18%) diabetic. So out of 100 patients 64 patients were suffering from diabetes. In our study, 57 patients were hypertensive. 32 male patients out of 56 male patients were hypertensive (57.14%) and 25 female patients out of 44 patients (56.81%) were hypertensive. In the present study, postprandial hypertriglyceridemia was found in 16 patients out of 23 patients (69.5%) in the age group 35-45, 31 patients out of 46 patients (67.39%) in the age group 46-55, 9 out of 21 patients (42.8%) in the age group 56,-65, and 8 patients out of 10 (80%) in the age > 66 years. Conclusion: In our study with reference to patient of ischemic heart disease, postprandial Hypertriglyceridemia was found in 64% patients, having normal fasting triglyceride level. There is statistically a significant correlation between postprandial triglyceride and ischemic heart disease, even in patients having normal fasting triglyceride level. It means that patients having high postprandial triglyceride levels have higher risk of Ischemic heart disease. The relative risk is 1.44. [ABSTRACT FROM AUTHOR]

Postprandial hypertriglyceridemia is a potential target for cardiovascular disease prevention in patients with diabetic dyslipidemia. Metformin has been reported to reduce plasma triglyceride concentrations in the postprandial states. However, little is known about the mechanisms underlying the triglyceride-lowering effect of metformin. Here, we examined the effects of metformin on lipid metabolism after olive oil-loading in 129S mice fed a high fat diet for three weeks. Metformin administration (250 mg/kg) for one week decreased postprandial plasma triglycerides. Pre-administration (250 mg/kg) of metformin resulted in a stronger triglyceride-lowering effect (approximately 45% lower area under the curve) than post-administration. A single administration (250 mg/kg) of metformin lowered plasma postprandial triglycerides comparably to administration for one week, suggesting an acute effect of metformin on postprandial hypertriglyceridemia. To explore whole body lipid metabolism after fat-loading, stomach size, fat absorption in the intestine, and fat oxidation (13C/12C ratio in expired CO2 after administration of glyceryl-1-13C tripalmitate) were measured with and without metformin (250 mg/kg) pre-treatment. In metformin-treated mice, larger stomach size, lower fat oxidation, and no change in lipid absorption were observed. In conclusion, metformin administration before fat loading reduced postprandial hypertriglyceridemia, most likely by delaying gastric emptying. [ABSTRACT FROM AUTHOR]

Excessive lipid intake, associated with a qualitative imbalance, favors the development of obesity and associated diseases. From organs involved in the lipid homeostasis, the small intestine remains the most poorly known although it is responsible for the lipid bioavailability and largely contributes to the regulation of postprandial hypertriglyceridemia. The mechanism of long chain fatty acid (LCFA) intestinal absorption is not totally elucidated. Over the two last decades, cloning of lipid binding proteins (LBP), proteins involved in trafficking and metabolic fate of LCFA in gut have provided new insights on cellular and molecular mechanisms involved in fat absorption. The synthesis of recent literature indicates that intestine is able to adapt its absorption capacity to the fat content of the diet. This adaptation takes place through a fat-coordinated induction of LBP and apolipoproteins. CD36 could operate as a lipid sensor responsible for a transducing signal related to the lipid content of the diet at the origin of this intestinal adaptation. This lipid-mediated metabolic response may lead to the formation of large chylomicrons rapidly degraded in the blood. All together, these new data indicate that this intestinal lipid sensing mechanism may be a therapeutic target for reducing the postprandial hypertriglyceridemia and associated cardiovascular risks.

Postprandial hyperlipidemia is an important risk factor for cardiovascular diseases in the context of obesity. Inulin is a non-digestible carbohydrate, known for its beneficial properties in metabolic disorders. We investigated the impact of inulin on postprandial hypertriglyceridemia and on lipid metabolism in a mouse model of diet-induced obesity. Mice received a control or a western diet for 4 weeks and were further supplemented or not with inulin for 2 weeks (0.2 g/day per mouse). We performed a lipid tolerance test, measured mRNA expression of genes involved in postprandial lipid metabolism, assessed post-heparin plasma and muscle lipoprotein lipase activity and measured lipid accumulation in the enterocytes and fecal lipid excretion. Inulin supplementation in western diet-fed mice decreases postprandial serum triglycerides concentration, decreases the mRNA expression levels of Cd36 (fatty acid receptor involved in lipid uptake and sensing) and apolipoprotein C3 (Apoc3, inhibitor of lipoprotein lipase) in the jejunum and increases fecal lipid excretion. In conclusion, inulin improves postprandial hypertriglyceridemia by targeting intestinal lipid metabolism. This work confirms the interest of using inulin supplementation in the management of dyslipidemia linked to obesity and cardiometabolic risk.

Postprandial hypertriglyceridemia and low plasma HDL levels, which are principal features of the metabolic syndrome, are displayed by transgenic mice expressing human apolipoprotein A-II (hapoA-II). In these mice, hypertriglyceridemia results from the inhibition of lipoprotein lipase and hepatic lipase activities by hapoA-II carried on VLDL. This study aimed to determine whether the association of hapoA-II with triglyceride-rich lipoproteins (TRLs) is sufficient to impair their catabolism. To measure plasma TRL residence time, intestinal TRL production was induced by a radioactive oral lipid bolus. Radioactive and total triglyceride (TG) were rapidly cleared in control mice but accumulated in plasma of transgenic mice, in relation to hapoA-II concentration. Similar plasma TG accumulations were measured in transgenic mice with or without endogenous apoA-II expression. HapoA-II (synthesized in liver) was detected in chylomicrons (produced by intestine). The association of hapoA-II with TRL in plasma was further confirmed by the absence of hapoA-II in chylomicrons and VLDL of transgenic mice injected with Triton WR 1339, which prevents apolipoprotein exchanges. We show that the association of hapoA-II with TRL occurs in the circulation and induces postprandial hypertriglyceridemia.

Postprandial increase in blood triglyceride levels is an independent risk factor for coronary artery disease, and dietary resistant starch (RS) is increasingly being considered for its contribution to disease prevention. Specifically, RS has beneficial effects on of the glycemic index, diabetes, cholesterol levels, and weight management. However, the effects of once-daily intake of RS on postprandial hypertriglyceridemia remain poorly characterized. In this study, the effects of a single administration of cornstarch-derived RS on postprandial increases in blood triglyceride levels were investigated in rats using oral fat tolerance/loading tests. Following the administration of lipid meals, increases in serum triglycerides levels were significantly reduced in rats fed corn oil containing 500 mg/mL RS. Moreover, fecal lipid volumes and wet weights following lipid meals were significantly greater in rats fed corn oil containing 500 mg/mL RS than in the corn oil only group, confirming the inhibition of dietary fat absorption. Finally, a significant positive correlation was observed between fecal lipid contents and wet weights in rats administered RS. These results suggest that RS intake with dietary fats induces defecation and confirm results of recent reports on the health-promoting potential of once-daily RS intake. [ABSTRACT FROM AUTHOR]

Background: Recent experimental studies have revealed that n-3 fatty acids, such as eicosapentaenoic acid (EPA) regulate postprandial insulin secretion, and correct postprandial glucose and lipid abnormalities. However, the effects of 6-month EPA treatment on postprandial hyperglycemia and hyperlipidemia, insulin secretion, and concomitant endothelial dysfunction remain unknown in patients with impaired glucose metabolism (IGM) and coronary artery disease (CAD). Methods and results: We randomized 107 newly diagnosed IGM patients with CAD to receive either 1800 mg/day of EPA (EPA group, n = 53) or no EPA (n = 54). Cookie meal testing (carbohydrates: 75 g, fat: 28.5 g) and endothelial function testing using fasting-state flow-mediated dilatation (FMD) were performed before and after 6 months of treatment. The primary outcome of this study was changes in postprandial glycemic and triglyceridemic control and secondary outcomes were improvement of insulin secretion and endothelial dysfunction. After 6 months, the EPA group exhibited significant improvements in EPA/arachidonic acid, fasting triglyceride (TG), and high-density lipoprotein cholesterol (HDL-C). The EPA group also exhibited significant decreases in the incremental TG peak, area under the curve (AUC) for postprandial TG, incremental glucose peak, AUC for postprandial glucose, and improvements in glycometabolism categorization. No significant changes were observed for hemoglobin A1c and fasting plasma glucose levels. The EPA group exhibited a significant increase in AUC-immune reactive insulin/AUC-plasma glucose ratio (which indicates postprandial insulin secretory ability) and significant improvements in FMD. Multiple regression analysis revealed that decreases in the TG/HDL-C ratio and incremental TG peak were independent predictors of FMD improvement in the EPA group. Conclusions: EPA corrected postprandial hypertriglyceridemia, hyperglycemia and insulin secretion ability. This amelioration of several metabolic abnormalities was accompanied by recovery of concomitant endothelial dysfunction in newly diagnosed IGM patients with CAD. [ABSTRACT FROM AUTHOR]

The aim of the present study was to determine the effect of postprandial hypertriglyceridemia on the risk of decompression stress following hyperbaric air exposures. The study involved 55 male individuals aged 20-48 years (31.47 ± 5.49 years), body mass index 20.3-33.2 kg/m² (25.5 ± 2.58 kg/m²). Blood was sampled two hours after a meal each participant had in accordance with individual dietary preferences to determine the following parameters: blood cell counts, activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), concentrations of total cholesterol and triglycerides. After each hyperbaric exposure, the presence and intensity of decompression stress were assessed using the Doppler method. Decompression stress was found in 30 individuals. Postprandial hypertriglyceridemia and hypercholesterolemia increased the risk of decompression stress after hyperbaric air exposures [ABSTRACT FROM AUTHOR]

Abstract: Postprandial hypertriglyceridemia is now established as an important risk factor for cardiovascular disease (CVD). This metabolic abnormality is principally initiated by overproduction and/or decreased catabolism of triglyceride-rich lipoproteins (TRLs) and is a consequence of predisposing genetic variations and medical conditions such as obesity and insulin resistance. Accumulation of TRLs in the postprandial state promotes the retention of remnant particles in the artery wall. Because of their size, most remnant particles cannot cross the endothelium as efficiently as smaller low-density lipoprotein (LDL) particles. However, since each remnant particle contains approximately 40 times more cholesterol compared with LDL, elevated levels of remnants may lead to accelerated atherosclerosis and CVD. The recognition of postprandial hypertriglyceridemia in the clinical setting has been severely hampered by technical difficulties and the lack of established clinical protocols for investigating postprandial lipemia. In addition, there are currently no internationally agreed management guidelines for this type of dyslipidemia. Here we review the mechanism for and consequences of excessive postprandial hypertriglyceridemia, epidemiological evidence in support of high triglycerides and remnant particles as risk factors for CVD, the definition of hypertriglyceridemia, methods to measure postprandial hypertriglyceridemia and apolipoproteins and, finally, current and future treatment opportunities. [Copyright &y& Elsevier]

Abstract: Background: Postprandial hypertriglyceridemia is a risk factor for atherosclerotic disease. However, the postprandial triglyceride (PTG) concentration fluctuates markedly and is poorly reproducible. The aim of this study was to determine whether the mean PTG (mean-PTG) concentration is a risk factor for carotid atherosclerosis in patients with type 2 diabetes. Methods: We measured the fasting and postprandial lipid concentrations, and the maximum intima-media thickness (max IMT) of carotid arteries by ultrasound in 115 diabetic patients. A carotid plaque was defined as max IMT of >1.0mm. The mean-PTG concentration was calculated from several PTG concentrations measured on different days during a 1-year follow-up period. Results: PTG concentrations showed marked intra-individual variability, and ranged from 0.29 to 6.03mmol/l. Patients with carotid plaques had higher mean-PTG concentrations than those without carotid plaques (1.51±0.57 vs. 1.29±0.47mmol/l, p =0.025). Neither fasting triglycerides nor one-point PTG concentrations differed between the two groups. Multivariate stepwise logistic regression analysis revealed that the mean-PTG concentration was significantly associated with carotid plaques [OR 1.20 (95% CI, 1.05–1.37), p =0.009], even after adjusting for traditional risk factors including HDL-cholesterol, LDL-cholesterol, age, hypertension, and duration of diabetes. Conclusions: The mean-PTG concentration is an independent risk factor for carotid atherosclerosis in patients with type 2 diabetes. [Copyright &y& Elsevier]

Several authors have reported the association of postprandial hypertriglyceridemia with oxidative stress, systemic inflammation and endothelial dysfunction. Our aim was to investigate the effect of high-calorie meal on blood markers of oxidative stress and endothelial dysfunction and the association of APOA5 -1131T/C and -250G/A hepatic lipase (HL) polymorphisms with postprandial triglyceride response. This study included 102 healthy male volunteers. All participants consumed a highcalorie meal (823 calories, 50 g fat, 28 g protein, 60 g carbohydrates). Total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, hsCRP, TAS and ICAM-1 were measured at fasting state and postprandially. APOA5 -1131T/C and -250G/A HL polymorphisms were also determined. Postprandial triglycerides were significantly increased (1.4 (1.1-2.1) vs. 2.4 (1.9-3.3) mmol/l, P<0.001). Average triglyceride increase was 1.0±0.7 mmol/l (65 %). Concentration of triglycerides, HDLcholesterol, LDL-cholesterol, TAS and ICAM-1 differed significantly between the fasting state and postprandial measurements (P<0.001). However, those differences were within the limits of analytical imprecision. Other parameters did not change 3 h after the meal. Triglycerides response did not differ respective to the APOA5 and HL polymorphisms. Family history of hypertension and acute myocardial infarction were associated with higher postprandial triglyceride concentrations. Postprandial hypertriglyceridemia is not associated with increased concentrations of hsCRP, TAS and ICAM-1. Furthermore, APOA5 -1131T/C and -250G/A HL polymorphisms are not associated with different postprandial triglyceride response. [ABSTRACT FROM AUTHOR]

Abstract: Background: Morbidly obese patients have associated diseases, such as diabetes, hypertension, hyperlipidemia, and cardiovascular disease. Bariatric surgery improves these obesity-related co-morbidities, including insulin resistance. Evidence has shown that patients with morbid obesity have postprandial hypertriglyceridemia (HTG) and that this type of HTG is related to the degree of insulin resistance. Also, bariatric surgery produces a dramatic reduction in triglyceride levels. However, it is unknown whether patients with postprandial HTG have a different clinical evolution after bariatric surgery. The setting of our study was a university hospital. Methods: We studied 57 morbidly obese patients who had mild or severe postprandial HTG after fat overload (<30 mg/dL or >90 mg/dL increase in triglycerides, respectively). All the patients underwent bariatric surgery. After surgery, the anthropometric and biochemical variables and the Homeostasis Model Assessment of Insulin Resistance were measured for 1 year at 0, 15, 30, 45, 90, 180, and 365 days after surgery. Results: The patients with more severe postprandial HTG had a greater percentage of change in the Homeostasis Model Assessment of Insulin Resistance at 30, 90, and 180 days after surgery than the patients with less severe postprandial HTG. Multiple regression analysis showed that the postprandial triglyceride levels predict the variation in the Homeostasis Model Assessment of Insulin Resistance index, more so than did traditional variables, such as anthropometric, inflammatory, or hormonal data. Conclusion: The postprandial HTG level might be the best predictor of improved insulin resistance in morbidly obese patients after bariatric surgery. [Copyright &y& Elsevier]

Both fasting and postprandial hypertriglyceridemia have been identified as risk markers for cardiovascular disease. High-sensitivity C-reactive protein (hs-CRP), known to independently predict future cardiovascular disease, has also been reported to be a direct participant in the progression of atherosclerosis. We evaluated whether or not fasting and/or postprandial hypertriglyceridemia influence hs-CRP of men with normal glucose tolerance. According to the triglyceride (TG) level, measured before and 1 and 2 h after a meal tolerance test, subjects were classified into a normotriglyceridemic (NTG) group ( n = 86), a postprandial hypertriglyceridemia (PHTG) group ( n = 50), or a fasting hypertriglyceridemia (FHTG) group ( n = 53). Hs-CRP and HOMA-R were significantly higher in the FHTG group than in the other groups ( P < 0.01). The PHTG group had higher hs-CRP than the NTG group ( P < 0.05). No significant differences in age, BMI, LDL cholesterol, or carotid intima-media thickness were found in comparison of the three groups. Multivariate linear regression analysis showed that the area under the TG curve (AUC-TG), HbA1c, and BMI were independently correlated with hs-CRP ( P < 0.001, P = 0.016, P = 0.032, respectively). Our data suggests that a hypertriglyceridemic state is associated with hs-CRP irrespective of BMI, LDL-C, and HDL-C, indicating that hs-CRP might represent chronic inflammation induced by hypertriglyceridemia in Japanese men with normal glucose tolerance. [ABSTRACT FROM AUTHOR]

Diacylglycerol acyltransferase (DGAT) catalyzes the final step of triacylglycerol (TAG) synthesis, and is considered as a potential target to control hypertriglyceridemia or other metabolic disorders. In this study, we found that the extract of rose petals suppressed TAG synthesis in cultured cells, and that the extract showed DGAT inhibitory action in a dose-dependent manner. Fractionation of the rose extract revealed that the DGAT inhibitory substances in the extract were ellagitannins; among them rugosin B, and D, and eusupinin A inhibited DGAT activity by 96, 82, and 84% respectively, at 10 μM. These substances did not inhibit the activities of other hepatic microsomal enzymes, glucose-6-phosphatase and HMG-CoA reductase, or pancreatic lipase, suggesting that ellagitannins inhibit DGAT preferentially. In an oral fat load test using mice, postprandial plasma TAG increase was suppressed by rose extract; TAG levels 2 h after the fat load were significantly lower in mice administered a fat emulsion containing rose extract than in control mice (446.3 ± 33.1 vs 345.3 ± 25.0 mg/dL, control vs rose extract group; P < 0.05). These results suggest that rose ellagitannins or rose extract could be beneficial in controlling lipid metabolism and used to improve metabolic disorders. [ABSTRACT FROM AUTHOR]

Abstract: Angiopoietin-like protein family 4 (Angptl4) has been shown to regulate lipoprotein metabolism through the inhibition of lipoprotein lipase (LPL). In familial hypercholesterolemia (FH), individuals lacking low-density lipoprotein receptor (LDLR) present not only hypercholesterolemia, but also increased plasma triglyceride (TG)-rich lipoprotein remnants, and develop atherosclerosis. In addition, the most common type of dyslipidemia in individuals with diabetes is increased TG levels. We first generated LDLR−/−Angptl4−/− mice to study the effect of Angptl4 deficiency on the lipid metabolism. Fasting total cholesterol, VLDL-C, LDL-C, HDL-C and TG levels were decreased in LDLR−/−Angptl4−/− mice compared with LDLR−/−Angptl4+/+ mice. In particular, post olive oil-loaded TG excursion were largely attenuated in LDLR−/−Angptl4−/− mice compared with LDLR−/−Angptl4+/+ mice. We next introduced diabetes by streptozotocin (STZ) treatment in Angptl4−/− mice and examined the impacts of Angptl4 deficiency. Compared with diabetic Angptl4+/+ mice, diabetic Angptl4−/− mice showed the improvement of fasting and postprandial hypertriglyceridemia as well. Thus, targeted silencing of Angptl4 offers a potential therapeutic strategy for the treatment of dyslipidemia in individuals with FH and insulin deficient diabetes. [Copyright &y& Elsevier]

Abstract: Objectives : Apolipoprotein C-III (APOC3) is a component of triglyceride rich lipoproteins, and SstI polymorphism has been associated with hypertriglyceridemia. Apolipoprotein A-I (APOA1) is the major component of HDL and MspI polymorphism has been associated with APOA1 and HDL-C levels. Thus, we study the influence of these polymorphisms in the postprandial response in metabolic syndrome (MS). Design and methods : 73 MS patients and 21 healthy subjects underwent a fat overload, with measurements of their fasting and postprandial lipid profile. The APOC3 SstI and the APOA1MspI polymorphisms were genotyped. Results : No significant differences were found in the lipid profile with respect to the MspI genotype. Patients with the S2S2 APOC3 genotype had significantly higher fasting and postprandial triglyceride levels and postprandial APOC3 and chylomicron-triglyceride levels compared with the other SstI APOC3 genotypes. Conclusions : Homozygosity for the minor allele of the APOC3 SstI polymorphism was associated to a worse postprandial response in MS patients. [ABSTRACT FROM AUTHOR]

The article presents a study which examines the suppressive effect of Yamato-mana (Brassica rapa L. Oleifera Group) constituent glucosinolates. It was found that the 3-butenyl glucosinolate (gluconapin) decreases the plasma triglyceride gain induced by corn oil administration to mice. It mentions however, that phenethyl glucosinolate (sinigrin) also reduces the plasma triglyceride level which shows that alkenyl glucosinolates is useful for postprandial hypertriglyceridemia prevention.

Abstract: Angiopoietin-like protein family 4 (Angptl 4) has been shown to regulate lipoprotein metabolism through the inhibition of lipoprotein lipase (LPL). We generated ApoE−/−Angptl 4−/− mice to study the effect of Angptl 4 deficiency on lipid metabolism and atherosclerosis. Fasting and postolive oil-loaded triglyceride (TG) levels were largely decreased in ApoE−/−Angptl 4−/− mice compared with and ApoE−/−Angptl 4+/+ mice. There was a significant (75±12%) reduction in atherosclerotic lesion size in ApoE−/−Angptl 4−/− mice compared with ApoE−/− Angptl 4+/+ mice. Peritoneal macrophages, isolated from Angptl 4−/− mice to investigate the foam cell formation, showed a significant decrease in newly synthesized cholesteryl ester (CE) accumulation induced by acetyl low-density lipoprotein (acLDL) compared with those from Angptl 4+/+ mice. Thus, genetic knockout of Angptl 4 protects ApoE−/− mice against development and progression of atherosclerosis and strongly suppresses the ability of the macrophages to become foam cells in vitro. [Copyright &y& Elsevier]

Aim: To explore the clinical implications of postprandial hypertriglyceridemia in postmenopausal Japanese women. Methods: Postprandial blood samples were collected from 91 women at their initial visit, with fasting blood samples collected within the following month to examine their lipid profiles. These women were grouped into normotriglyceridemia (fasting/postprandial triglycerides [TG] < 150; n = 36), mild postprandial hypertriglyceridemia (fasting TG < 150, postprandial TG ≥ 150, <225; n = 27), moderate postprandial hypertriglyceridemia (fasting TG < 150, postprandial TG ≥ 225; n = 19) and hypertriglyceridemia (fasting TG ≥ 150; n = 9) by using 225 mg/dL as the cut-off value for postprandial hypertriglyceridemia. Results: The subjects were 54.1 ± 7.8 years old; their duration of menopause, 6.0 ± 7.7 years; body mass index, 21.4 ± 4.0 kg/m2; postprandial TG concentration, 189 ± 110 mg/dL; and fasting TG concentration, 109 ± 50 mg/dL. Approximately 50% ( n = 46) of the women had normal fasting TG (fasting TG < 150), but high postprandial TG (postprandial TG ≥ 150). Approximately 10% ( n = 9) of the women had hypertriglyceridemia (fasting TG ≥ 150 mg/dL). In those with postprandial hypertriglyceridemia ( n = 46), postprandial TG negatively correlated with high-density lipoprotein cholesterol (HDL-C), while fasting TG showed no such correlation with HDL-C. Conclusion: Postprandial TG may provide a better understanding of lipid metabolism in postmenopausal women. [ABSTRACT FROM AUTHOR]

Abstract: Background and aim: A family history of myocardial infarction (MI) is an independent risk factor for future coronary events. Decreased plasma lipoprotein lipase (LPL) activity is associated with delayed clearance of triglyceride-rich lipoproteins (TRL) and low fasting HDL cholesterol. The aim of the study was to investigate the relations between plasma LPL activity, postprandial TRL and HDL cholesterol in offspring of MI patients. Methods and results: A case-control study was performed in 17 healthy middle-aged offspring of MI patients and 13 healthy age-and sex-matched controls. Fasting blood samples were collected and each subject was given a standardized oral fat load (1g fat/kg body weight) with subsequent blood samples collected for an 8-h period. Offspring of MI patients had significantly lower postheparin LPL activity (62.9mU/ml±22.8mU/ml) (mean±SD) than healthy controls (93.0mU/ml±21.7mU/ml) (p =0.002). Decreased postheparin LPL activity was accompanied by significantly increased and delayed clearance of postprandial TRL and subsequent lower fasting HDL cholesterol in offspring of MI patients. Postheparin LPL activity was associated with HDL cholesterol (r =0.40, p =0.036) and trend analysis revealed a decrease in incremental area under the curve (AUCi) for chylomicrons with increasing LPL activity (p =0.013). Conclusions: Offspring of MI patients had decreased postheparin LPL activity accompanied by increased postprandial TRL and subsequent decreased HDL cholesterol, an unfavourable lipid profile which may contribute to their increased risk for future coronary events. [Copyright &y& Elsevier]

Abstract: Background: Postprandial hypertriglyceridemia is known to cause endothelial dysfunction and increased oxidative stress. Oral supplements of l-arginine have been found to improve endothelial function. However, the effects of supplements of l-arginine on the influences of postprandial hypertriglyceridemia were not studied before. Methods: Forty young healthy men without any risk factors were equally divided into two groups. l-arginine group (age 22±1 years, body mass index 23.5±1.2 kg/m2) received a standard high-fat meal with 15 g oral l-arginine. Control group (age 22±1 years, body mass index 23.8±0.9 kg/m2) received a standard high-fat meal with placebo. A standard high-fat meal consisted of 900 kcal and 50 g of fat. Flow-mediated vasodilation (FMD), von Willebrand factor (vWF), p-Selectin, and glutathione peroxidase (GSH-Px) were measured before and 2 h after the high-fat meal. Results: Serum triglyceride levels were significantly increased 2 h after the high-fat meal in both groups. In the control group, FMD (10.5±1.2% vs. 6.8±1.4%, p <0.001) and GSH-Px (23.5±6.2 vs. 21.9±5.0 μg/ml, p =0.029) were significantly decreased after the high-fat meal. P-Selectin (20.0±7.7 vs. 25.9±10.5 mg/l, p =0.025) and vWF (731.2±131.5 vs. 934.9±133.8 mU/ml, p <0.001) were significantly increased after the high-fat meal. In the l-arginine group, FMD (10.3±1.3 vs. 9.3±0.9%, p <0.001) was slightly but significantly decreased after the high-fat meal but not GSH-Px (23.6±3.6 vs. 23.0±4.8%, p =0.468). P-Selectin (20.1±5.9 vs. 25.7±10.2 mg/l, p =0.001) and vWF (793.2±146.0 vs. 944.4±136.8 mU/ml, p <0.001) were significantly increased after the high-fat meal. Degree of FMD attenuation following the high-fat meal was significantly less in the l-arginine group (1.0±0.9 vs. 3.8±1.5%, p <0.001). Conclusions: Concomitant supplements of l-arginine improved endothelial dysfunction and oxidative stress induced by postprandial hypertriglyceridemia. However, changes of p-Selectin and vWF were not affected by supplements of l-arginine with the high-fat meal. [Copyright &y& Elsevier]

Abstract: Objective: We compared the levels of biomarkers of oxidative stress before and after a fat overload in three groups. Materials and methods: 17 controls and two groups with hypertriglyceridemia: 43 without the metabolic syndrome (TG-non-MS) and 29 with the metabolic syndrome (TG-MS). All subjects underwent a 60 g fat overload. Baseline measurements included glucose, BMI (body mass index), waist circumference and HOMA IR (homeostasis model assessment insulin resistance). Cholesterol, triglycerides, HDL (high density lipoprotein) cholesterol, TNF-alpha (tumor necrosis factor) and IL-6 (interleukin-6), lipoperoxide (LPO), carbonylated proteins, reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione peroxidase (GSH-PX), glutathione reductase (GSH-Rd), catalase and glutathione transferase (GST) were measured at baseline and 3 h after fat overload. Results: Compared to the controls, the two patient groups had higher plasma levels at baseline and after overload of cholesterol, triglycerides and apolipoprotein B, LPO, carbonylated proteins and GSSG, and lower levels of antioxidants at baseline and after the fat overload. Conclusion: The two patient groups had the same degree of oxidative stress. [Copyright &y& Elsevier]

Background: We examined the influence of cholesteryl ester transfer protein TaqIB polymorphism on triglyceride (TG) response to an oral fat tolerance test (OFTT) in patients heterozygous for familial hypercholesterolemia (hFH). Methods: We genotyped 67 hFH patients (32 men and 35 postmenopausal women) who were subjected to an OFTT. Results: All B1 allele carriers had lower high-density lipoprotein cholesterol (HDL-C) levels (p=0.013) and higher postprandial TG response at 6 and 8 h (p=0.05 and p=0.04, respectively) compared to B2 allele carriers. Multiple regression analysis showed that in the hFH group with a positive response, the presence of the B2 allele was significantly related to lower levels of TG-area under the curve (AUC) (p<0.01) compared to B1, adjusting for age, gender and body mass index. In the hFH group with a negative response, although age and female gender had a significant effect on TG-AUC levels (p<0.01 for both), the allele type was not significantly related to the TG-AUC levels (p=0.99). Conclusions: B2 carriers had a lower postprandial TG response compared to B1 carriers. There were no differences in TG levels between B1 and B2 carriers in patients with a negative OFTT response. Therefore, at higher TG concentration, the B2 allele may protect against an exaggerated postprandial TG increase and subsequent lowering of HDL-C. Clin Chem Lab Med 2007;45:1190–8. [ABSTRACT FROM AUTHOR]

The article evaluates the suppressive effects of oolong tea extract and oolong tea-polymerized polyphenols (OTTP) on postprandial hypertriglyceridemia in rats and mice. According to the authors, lymphatic recovery of triglycerides in rats cannulated in the thoracic duct was delayed by the administration of oolong tea extract and more effectively than with green tea extract. They add OTTP also suppressed postprandial hypertriglyceridemia after administration of olive oil in mice.

Abstract: Background: Oxidative stress has been implicated in vascular complications of diabetes mellitus (DM). This study aims to evaluate the relationship between postprandial hypertriglyceridemia (PP-HTG) and oxidative stress in Indian patients of type 2 DM with macrovascular complications. Methods: Plasma triglycerides (TG), thiobarbituric acid reactive substances (TBARS), erythrocyte reduced glutathione (GSH) and superoxide dismutase (SOD) were measured in fasting and postprandial (PP) state at 2, 4, 6 and 8 h after a high fat meal challenge in controls (Group I) and patients of type 2 DM without (Group II) and with macrovascular complications (Group III). Results: Postprandial TGs increased significantly in patients with type 2 DM, which showed an exaggerated response to high fat meal challenge in Group III as compared to Group II. Highest PP-TBARS were also observed in Group III which correlated positively with TG. However, GSH and SOD were lower in both groups of diabetics as compared to controls. Conclusions: The magnitude of PP-HTG appears to be the major determinant of oxidative stress in type 2 DM, which along with a compromised antioxidant status may lead to endothelial dysfunction and macrovascular complications. [Copyright &y& Elsevier]

Abstract: Hypertriglyceridemia is an important risk factor for coronary heart disease (CHD) and in the development of atherosclerosis, especially in subgroups of the population like those with type 2 diabetes. Although triglycerides are generally increased in the postprandial period, the association between postprandial triglyceride (ppTG) levels and atherosclerosis has not been investigated in north Indian type 2 diabetic subjects known to have a very high prevalence rate of premature CHD and insulin resistance. To investigate the role of ppTG levels in atherosclerosis in type 2 diabetes, we examined the correlation between ppTG levels and carotid intima–media thickness (IMT). Carotid IMT was determined by high resolution B-mode ultrasonography in 86 newly detected type 2 diabetic subjects (1–12 months duration) having good glycemic control (HbA1C &#60;7%) and 45 non-diabetic subjects matched according to age and body mass index (BMI). Plasma glucose, insulin, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were measured after overnight fasting. Plasma insulin and glucose were also measured 2h and plasma triglycerides 4h after breakfast. The mean carotid IMT in diabetic subjects was higher than those in non-diabetic subjects (0.77±0.15mm versus 0.53±0.16mm, P &#60;0.001). Based on the fasting and postprandial triglyceride levels, the diabetic subjects were divided into three groups: normo–normo (NN); normo–hyper (NH); hyper–hyper (HH) [NN: fTG&#60;1.70mmol/L and ppTG&#60;2.30mmol/L; NH: fTG&#60;1.70mmol/L and ppTG>2.30mmol/L; HH: fTG>1.70mmol/L and ppTG>2.30mmol/L]. Carotid IMT was significantly increased in the NH (0.79±0.09mm) and HH (0.82±0.06mm) groups compared with the NN group (0.59±0.09mm, P &#60;0.001). Although ppTG, age, fasting LDL-cholesterol, HOMA-estimated insulin resistance, HbA1C were all independently correlated with carotid IMT, age and ppTG levels had the strongest statistical influence (P &#60;0.002). [Copyright &y& Elsevier]

Examines the effect of tea catechins on postprandial hypertriglyceridemia in rats. Administration of a lipid emulsion; Effect of tea catechins on plasma triacylglycerol; Dose-dependent suppression of postprandial hypertriglyceridemia; Role of catechins with a galloyl moiety as agents for suppressing dietary fat absorption through the small intestine.

Abstract: Improvement of gastrointestinal transit was thought to be a new tactic to treat postprandial hypertriglyceridemia in diabetic individuals with gastroparesis. Diabetic gastroparesis, lipid load testing, and the effect of domperidone or aqueous extract of rhizomes of Rheum palmatum L. on postprandial hypertriglyceridemia were evaluated in alloxan-induced diabetic rats. Alloxan diabetic animals had a slow gastrointestinal transit, together with delayed and exaggerated postprandial hypertriglyceridemia, after oral administration of olive oil, which was significantly improved after oral administration of domperidone or R. palmatum L. However, atropine could prevent the effects of R. palmatum L. The reduced postprandial hypertriglyceridemia was highly correlated with the improvement in gastrointestinal transit. These results suggest that promotion of gastrointestinal transit may be useful for the treatment of postprandial hypertriglyceridemia in diabetic patients with gastroparesis. R. palmatum L. may become a new choice for these patients since it has more potential benefits than domperidone. [Copyright &y& Elsevier]