Postprandial Lipemia Research Articles

Walking Exercise Reduces Postprandial Lipemia but Does Not Influence Postprandial Hemorheological Properties and Oxidative Stress.

A higher postprandial triglycerides response and hemorheological abnormalities may increase the incidence of metabolic disorders and negatively interfere with the aging process. A single session of preprandial endurance exercise was found to be effective in reducing triglyceride levels after a high-fat diet. However, whether the exercise-induced reduction in postprandial triglyceride levels influences hemorheological indicators remains unknown. This study aims to investigate the effects of postprandial lipemia on hemorheological properties and oxidative stress. Eight healthy young male participants completed two experimental trials. On day 1, the participants were randomly assigned to walk for 1 h at 50% VO2max (EE trial) or rest (CON trial). On day 2, participants rested and consumed a high-fat meal in the morning. Results: The postprandial area under the curve (AUC) of plasma TG concentration was significantly lower in EE compared to CON (EE: 9.2 ± 1.9; CON: 10.9 ± 1.7 mmol/L·h−1; p = 0.013; Cohen’s d = 0.036). No significant difference was observed in hemorheological properties and MDA (p > 0.05). Endurance exercise effectively decreased postprandial TG concentration but did not influence the postprandial hemorheological properties and oxidative stress indicators.

Acute response in glycemia and lipemia postprandial after resistance and concurrent training in overweight postmenopausal women

Introduction: In postmenopausal women, metabolic responses to lipids during postprandial periods following combined exercise training are unknown. Objective: To examine the acute effects of resistance training (RT) and concurrent training (CT) on postprandial lipemia and glycemia in postmenopausal women. Methods: This quasi-experimental, exposure response study, linked 27 women who were randomly divided into three groups and evaluated for anthropometry, physical fitness, and nutrition status. Two experimental groups did a session of different types of physical activities (RT or CT), and a control group did not do any training activities (only aerobic exercise). At 12 hours post-training, in fasting conditions, a hypercaloric nutritional compound equivalent to 50% of the basal metabolic rate (BMR) of each woman was supplied. Pre and post hypercaloric intake, biochemical markers (lipemia and glycemia) were determined and compared with the control group. Results: A reduction in total energy expenditure was observed due to RT and CT training (p<0.005). The changes are associated with decreased total cholesterol and low-density lipoprotein levels in the RT group, as well as decreased triglyceride levels and increased high-density lipoprotein levels in the CT and aerobic exercise groups. Conclusion: RT and CT performed 12 hours before the consumption of the hyper caloric nutritional compound can change postprandial lipid and glucose levels. Acute physical training could influence the reduction of energy expenditure and the improvement of glycaemia and lipemia in postmenopausal women. Keywords: exercise; fitness; glycemia; lipemia; nutrition; postmenopausal; trainings.

Impact Of Moderate-to-vigorous Physical Activity And Visceral Adiposity On Postprandial Triglycerides In Metabolically At-risk Adults

Postprandial lipemia occurs early in chronic disease progression. The degree of postprandial triglyceride (ppTG) is influenced by physiological and lifestyle factors such as diet, central obesity, and physical activity (PA). However, it is unclear how habitual dietary factors and PA impact ppTG in healthy adults with high central adiposity. PURPOSE: To examine the impact of habitual moderate-to-vigorous PA (MVPA), saturated fat (SF) in the habitual diet, and central adiposity on ppTG in metabolically at-risk adults. METHODS: Non-diabetic adults (n = 21) with a high waist circumference (> 35” women, >40” men) completed a high-fat meal challenge (50 g FAT, 54 g CHO, 12 g PRO), with blood collected at fasting and hourly after meal ingestion for 5 h. TG (mmol/L) was determined by lipid panels and summarized as iAUC and the change from fasting (TGmax). Habitual dietary data was collected through the online DHQ-III, with SF percentage (SF / total fat) used for analysis. Visceral adipose tissue (VAT) was determined through bioelectrical impedance analysis. Participants wore an accelerometer for 7 days (>10 h/day) and average number of MVPA bouts/day (≥ 2690 counts/min) was derived. Separate linear models for TG iAUC and TG magnitude were used to test the impact of an interaction between average MVPA bouts and VAT, accounting for habitual dietary SF. RESULTS: MVPA, VAT, and habitual dietary SF explain ~36% of variation in TG iAUC and TGmax. Average MVPA bouts and VAT jointly impacted TG iAUC (p < 0.01), with a ppTG-lowering effect observed with lower VAT and more frequent MVPA bouts and a pronounced ppTG-raising effect observed with greater VAT with frequent MVPA bouts (β = 1.1). Habitual SF did not predict TG iAUC (p = 0.68). Likewise, average MVPA bouts and VAT impacted TGmax (p = 0.03), with a TG-raising effect observed with greater VAT despite more MVPA bouts (β = 0.31). Interestingly, an inverse relationship was observed between habitual SF intake and TGmax (β = - 0.04, p = 0.02). CONCLUSION: Frequent MVPA promotes lower ppTG, a benefit that is reversed with increased VAT. These findings suggest that increased VAT promotes ppTG even with regular MVPA, stressing the importance of strategies to decrease VAT in improving regulation of postprandial lipemia in at-risk adults. Supported by USDA-ARS Pulse Crop Health Initiative 58-3060-9-040.

Intestinal lipid absorption and transport in type 2 diabetes.

Postprandial hyperlipidaemia is an important feature of diabetic dyslipidaemia and plays an important role in the development of cardiovascular disease in individuals with type 2 diabetes. Postprandial hyperlipidaemia in type 2 diabetes is secondary to increased chylomicron production by the enterocytes and delayed catabolism of chylomicrons and chylomicron remnants. Insulin and some intestinal hormones (e.g. glucagon-like peptide-1 [GLP-1]) influence intestinal lipid metabolism. In individuals with type 2 diabetes, insulin resistance and possibly reduced GLP-1 secretion are involved in the pathophysiology of postprandial hyperlipidaemia. Several factors are involved in the overproduction of chylomicrons: (1) increased expression of microsomal triglyceride transfer protein, which is a key enzyme in chylomicron synthesis; (2) higher stability and availability of apolipoprotein B-48; and (3) increased de novo lipogenesis. Individuals with type 2 diabetes present with disorders of cholesterol metabolism in the enterocytes with reduced absorption and increased synthesis. The increased production of chylomicrons in type 2 diabetes is also associated with a reduction in their catabolism, mostly because of a reduction in activity of lipoprotein lipase. Modification of the microbiota, which is observed in type 2 diabetes, may also generate disorders of intestinal lipid metabolism, but human data remain limited. Some glucose-lowering treatments significantly influence intestinal lipid absorption and transport. Postprandial hyperlipidaemia is reduced by metformin, pioglitazone, alpha-glucosidase inhibitors, dipeptidyl peptidase 4 inhibitors and GLP-1 agonists. The most pronounced effect is observed with GLP-1 agonists, which reduce chylomicron production significantly in individuals with type 2 diabetes and have a direct effect on the intestine by reducing the expression of genes involved in intestinal lipoprotein metabolism. The effect of sodium-glucose cotransporter 2 inhibitors on intestinal lipid metabolism needs to be clarified.

Oral fat tolerance testing identifies abnormal pancreatic β-cell function and insulin resistance in individuals with normal glucose tolerance.

Insulin sensitivity and β-cell function are affected by lipid metabolism disorders, even before the onset of type 2 diabetes. People are in the postprandial state most of the time. Therefore, identifying postprandial hyperlipemia is important. This study aimed to assess patients with abnormalities in lipid metabolism, but with normal glucose tolerance, using oral fat tolerance testing (OFTT) to identify defects in insulin sensitivity and β-cell function. We included 248 volunteers with normal glucose tolerance who underwent OFTT. They were divided into three groups in accordance with their fasting and 4-h postprandial triglyceride (TG) concentrations. Their lipid concentrations during OFTT were compared. The disposition index (DI) was applied to estimate β-cell function, and the Matsuda insulin sensitivity index (ISIM ) was used to assess insulin sensitivity. We used multiple linear regression analysis to estimate the relationships of fasting and postprandial TG concentrations with β-cell function and insulin sensitivity . The changes in TG concentrations during OFTT were more marked than those in low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol or total cholesterol concentrations. As lipid metabolism deteriorated, the ISIM and the DI gradually decreased. Multiple linear regression analysis showed that fasting and 4-h postprandial TG concentrations affected LnISIM and LnDI. In individuals with normal glucose tolerance, β-cell function and insulin sensitivity gradually decrease with a deterioration in the lipid profile. Not only fasting TG, but also postprandial TG concentrations are independent risk factors for impaired β-cell function and insulin resistance.

SCD1 is nutritionally and spatially regulated in the intestine and influences systemic postprandial lipid homeostasis and gut-liver crosstalk

Stearoyl-CoA desaturase-1 is an endoplasmic reticulum (ER)-membrane resident protein that inserts a double bond into saturated fatty acids, converting them into their monounsaturated counterparts. Previous studies have demonstrated an important role for SCD1 in modulating tissue and systemic health. Specifically, lack of hepatic or cutaneous SCD1 results in significant reductions in tissue esterified lipids. While the intestine is an important site of lipid esterification and assimilation into the body, the regulation of intestinal SCD1 or its impact on lipid composition in the intestine and other tissues has not been investigated. Here we report that unlike other lipogenic enzymes, SCD1 is enriched in the distal small intestine and in the colon of chow-fed mice and is robustly upregulated by acute refeeding of a high-sucrose diet. We generated a mouse model lacking SCD1 specifically in the intestine (iKO mice). These mice have significant reductions not only in intestinal lipids, but also in plasma triacylglycerols, diacylglycerols, cholesterol esters, and free cholesterol. Additionally, hepatic accumulation of diacylglycerols is significantly reduced in iKO mice. Comprehensive targeted lipidomic profiling revealed a consistent reduction in the myristoleic (14:1) to myristic (14:0) acid ratios in intestine, liver, and plasma of iKO mice. Consistent with the reduction of the monounsaturated fatty acid myristoleic acid in hepatic lipids of chow fed iKO mice, hepatic expression of Pgc-1α, Sirt1, and related fatty acid oxidation genes were reduced in chow-fed iKO mice. Further, lack of intestinal SCD1 reduced expression of de novo lipogenic genes in distal intestine of chow-fed mice and in the livers of mice fed a lipogenic high-sucrose diet. Taken together, these studies reveal a novel pattern of expression of SCD1 in the intestine. They also demonstrate that intestinal SCD1 modulates lipid content and composition of not only intestinal tissues, but also that of plasma and liver. Further, these data point to intestinal SCD1 as a modulator of gut-liver crosstalk, potentially through the production of novel signaling lipids such as myristoleic acid. These data have important implications to understanding how intestinal SCD1 may modulate risk for post-prandial lipemia, hepatic steatosis, and related pathologies.

An increased disulfide/native thiol ratio and oxidative stress index in metabolic syndrome patients with postprandial lipemia

An increased disulfide/native thiol ratio and oxidative stress index in metabolic syndrome patients with postprandial lipemia

5 days of time-restricted feeding increases fat oxidation rate but not affect postprandial lipemia: a crossover trial

Studies have revealed that time-restricted feeding affects the fat oxidation rate; however, its effects on the fat oxidation rate and hyperlipidemia following high-fat meals are unclear. This study investigated the effects of 5-day time-restricted feeding on the fat oxidation rate and postprandial lipemia following high fat meals. In this random crossover experimental study, eight healthy male adults were included each in the 5-day time-restricted feeding trial and the control trial. The meals of the time-restricted feeding trial were provided at 12:00, 16:00, and 20:00. The meals of the control trial were provided at 08:00, 14:00, and 20:00. The contents of the meals of both trials were the same, and the calories of the meals met the 24-h energy requirement of the participants. After 5 days of the intervention, the participants consumed high-fat meals on the sixth day, and their physiological changes were determined. The fasting fat oxidation rate (p < 0.001) and postprandial fat oxidation rate (p = 0.019) of the time-restricted feeding trial were significantly higher than those of the control trial. The 24-h energy consumption and postprandial triglyceride, blood glucose, insulin, glycerol, and free fatty acid concentrations of the two trials showed no significant differences (p > 0.05). The results revealed that 5 days of time-restricted feeding effectively increased the fasting and postprandial fat oxidation rate, but it did not affect postprandial lipemia.

Acute Effects of White Button and Shiitake Mushroom Powder Supplementation on Postprandial Lipemia and Glycemia Following a High-Fat Meal

ObjectivesTo determine the acute effects on postprandial lipemia (PPL) and glycemia (PPG) by supplementing a high-fat meal with either White Button (WB) or Shiitake (SH) mushroom powder. MethodsNine healthy participants (5 female and 4 male, 23.3 ± 1.3 yr, 17.8 ± 6% body fat, 56.2 ± 11.4 kg fat free mass) were randomized to receive three different meals in a double-blind fashion. Each meal consisted of an 8 oz. cooked beef patty and a bun (883 kcal, 47 g fat, 37.5 g carbohydrate, 73.2 g protein). The control meal was not supplemented with any mushroom powder. The other two meals had 14 g of either WB or SH dried mushroom powder incorporated into the beef patty prior to cooking. Participants fasted for 12 hours and avoided vigorous exercise the day prior to eating a treatment or control meal. Blood was drawn before meal consumption (Time = 0 hours) and every two hours after consumption for a total of six hours (Time = 2, 4, 6 hours). Lipid and glucose panels were performed following meal consumption. Data were analyzed using linear mixed effects models on the outcomes triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and glucose. Fixed effects were gender, meal type, time, and meal type by time interaction, while a random intercept accounted for the variability in the outcomes among the participants. ResultsLDL levels were significantly lower for both SH and WB meals compared to the control meal (p = 0.0007) over the course of six hours. Meal type did not affect triglyceride, HDL, and glucose levels. Gender affected triglyceride and HDL levels over the treatment course. Triglyceride levels were significantly higher in males (p = 0.0084) and HDL levels were significantly lower in females (p = 0.0005). Triglyceride and glucose levels were significantly higher, (p < 0.001 and p < 0.0001 respectively), during the postprandial time course (Time = 0, 2, 4, 6 hours). ConclusionsBoth SH and WB mushrooms may be important to supplement in the diet to lower serum LDL levels. Future studies are needed to evaluate which of the two treatments is the more potent. Funding SourcesDedicated to Matthew J Morris, deceased, whose contributions were crucial to this work.

Body Composition Measures Associated With Postprandial Triglyceride Concentrations

ObjectivesA large increase in triglyceride (TG) concentrations following a high-fat meal (i.e., postprandial lipemia) is an independent cardiovascular disease risk factor. However, little is known regarding individual factors that are associated with or determine postprandial triglycerides. We aimed to identify body composition measures that are associated with postprandial triglyceride concentrations following a high-fat meal. MethodsWe conducted a secondary analysis of data from 5 previously conducted studies in our laboratory, each utilizing identical methods. Postprandial TG were measured at baseline and 4 hours after a high-fat shake (73% fat; 9 kcal/kg). In addition to body mass index (BMI) and waist circumference (WC), body composition variables – relative body fat (BF%), relative muscle mass (MM%), and visceral adipose tissue (VAT) – were measured via bioelectrical impedance. ResultsAcross 5 studies, complete data from 156 participants (age: 44.9 ± 21.0 years; sex: 83F/73M; BMI: 27.3 ± 5.5 kg/m2; fasting glucose: 98.6 ± 7.8 mg/dL; fasting TG: 94.6 ± 45.3 mg/dL; fasting total cholesterol: 170.8 ± 34.5 mg/dL) were compiled for this secondary analysis. Postprandial TG were correlated with age (r = 0.24, p = 0.003) but no difference between sexes was observed (p = 0.06). Significantly associated with 4-hr TG were BMI (r = 0.29, p < 0.0001), WC (r = 0.33, p < 0.0001), BF% (r = 0.23, p = 0.004), MM% (r = 0.23, p = 0.004), and VAT (r = 0.35, p < 0.0001). In a backward elimination regression (R2 = 0.15), the variables most predictive of 4-hr TG were MM% (β = 0.21, p = 0.009), VAT (β = 0.25, p = 0.004), and BF% (β = 0.16, p = 0.064). ConclusionsIn a secondary analysis of 156 participants across 5 studies, we identified MM%, VAT, and BF% as being the most predictive of 4-hr TG. Although the strength of the relationship may be weak to moderate, body composition appears to influence postprandial triglycerides. Further research could determine preventative measures regarding body composition to lower the risk of cardiovascular disease associated with postprandial triglycerides. Funding SourcesOklahoma Center for the Advancement of Science and Technology (HR20-027), American Society for Nutrition, Donna Cadwalader Research and Development Grant, Oklahoma State University Office of the Vice President for Research.

Effects of dapagliflozin on postprandial lipid metabolism in type 2 diabetes mellitus.

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) modulate lipid metabolism and improve cardiovascular morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). The exact cardioprotective mechanism of SGLT2i is unclear. We evaluated the effects of SGLT2i on postprandial lipids, lipoprotein concentrations, glucose and fatty acids. A placebo-controlled randomized, proof-of-concept study. Fourteen male patients with T2DM on intensive insulin regimen were randomly and double-blind allocated to 12 weeks dapagliflozin (10 mg) or placebo. Postprandial effects were assessed with an 8-h standardized oral fat loading test. Mean glycated A1c did not change by dapagliflozin, but the mean daily insulin dose was significantly reduced. Although dapagliflozin did not affect fasting or postprandial levels of glucose and insulin, it increased the postprandial levels of glucagon. While fasting levels of free fatty acids and beta-hydroxybutyrate (bHBA) were unchanged, dapagliflozin significantly increased the postprandial bHBA response. This was seen in the context of increased postprandial glucagon levels by dapagliflozin, without influencing postprandial insulin or glucose levels. Dapagliflozin did not affect fasting or postprandial plasma cholesterol and triglycerides nor postprandial inflammatory markers. Fasting apolipoprotein B48 was decreased without affecting the postprandial response. Markers of inflammation and vascular function did not change. Treatment with dapagliflozin of patients with T2DM led to a reduction of fasting chylomicron remnants and increased postprandial ketone bodies compared to placebo suggesting enhanced hepatic fatty acid oxidation. The latter may have been caused by decreasing the insulin-glucagon ratio. The beneficial clinical effects seen in the trials using dapagliflozin most likely are not due to effects on postprandial inflammation nor postprandial lipemia.

Effect of Acute Intake of Fermented Orange Juice on Fasting and Postprandial Glucose Metabolism, Plasma Lipids and Antioxidant Status in Healthy Human.

Higher postprandial plasma glucose and lipemia, and oxidative and inflammatory responses, are considered important cardiovascular risk factors. Fermentation of fruits has generated products with high concentrations of bioactive compounds. The aim of this study was to evaluate the potential acute effects that fermented orange juice (FOJ) can exert in healthy humans by modulating postprandial response, and inflammatory/antioxidant status, compared with orange juice (OJ). Nine volunteers were recruited for a randomized, controlled, and crossover study. Participants ingested 500 mL of FOJ. At 4 h post intake, subjects consumed a standardized mixed meal. Blood samples were collected at 0–8 h hours post intake. The subjects repeated the protocol with OJ following a 2-week washout period. Glucose and lipid metabolism, plasma antioxidant capacity (ORAC, FRAP), endogenous antioxidants (albumin, bilirubin, uric acid), C-reactive protein and fibrinogen were measured in plasma samples. There was a trend of a smaller increase in LDL-C after FOJ intake compared with OJ, a significant decrease in apo-B and significant increase in ORAC. The glycemic and triglyceride response of meal was attenuated with FOJ. No differences were obtained in endogenous antioxidants and inflammation status between the treatments. The acute consumption of FOJ could play a protective role against cardiovascular risk factors.

Prior arm-crank exercise has no effect on postprandial lipaemia in nondisabled adults

A single bout of cycling or running performed in the evening can reduce postprandial lipaemia (PPL) the following morning, although this is currently unknown for upper-body exercise. The aim of this study was to determine if a bout of arm crank exercise (high-intensity interval [HIIE] or moderate-intensity continuous [MICE]), can attenuate PPL in non-injured individuals. Eleven healthy and recreationally active participants (eight males, three females; age: 27 ± 7 yr; body mass index: 23.5 ± 2.5 kg · m-2) volunteered to participate in three trials: HIIE (10 x 60 s at 80% peak power output), MICE (50% peak power output of isocaloric duration), and a no-exercise control condition. Each exercise bout was performed at 18:00, and participants consumed a standardized evening meal at 20:00. Following an overnight fast, a 5-h mixed-macronutrient tolerance test was performed at 08:00. There were no significant differences in triglyceride incremental area under the curve between HIIE (192 ± 94 mmol. L-1 per 300 min), MICE (184 ± 111 mmol. L-1 per 300 min), and the no-exercise condition (175 ± 90 mmol. L-1 per 300 min) (P=0.46). There were no significant differences in incremental area under the curve for glucose (P=0.91) or insulin (P=0.59) between conditions. Upper-body MICE and HIIE performed in the evening do not influence PPL the following morning, in normotriglyceridemic individuals. Clinical Trials Registration: NCT04277091 Novelty: • Arm crank exercise has no effect on PPL when performed the evening prior to a mixed-macronutrient meal test • Upper-body sprint interval exercise should be investigated as a potential solution to reduce PPL.

Effects of Acute Partial Sleep Deprivation and High-Intensity Interval Exercise on Postprandial Network Interactions.

Introduction: High-intensity interval exercise (HIIE) is deemed effective for cardiovascular and autonomic nervous system (ANS) health-related benefits, while ANS disturbance increases the risk for cardiovascular disease (CVD). Postprandial lipemia and acute-partial sleep deprivation (APSD) are considered as CVD risk factors due to their respective changes in ANS. Exercising in the morning hours after APSD and have a high-fat breakfast afterwards may alter the interactions of the cardiovascular, autonomic regulation, and postprandial lipemic systems threatening individuals' health. This study examined postprandial network interactions between autonomic regulation through heart rate variability (HRV) and lipemia via low-density lipoprotein (LDL) cholesterol in response to APSD and HIIE. Methods: Fifteen apparently healthy and habitually good sleepers (age 31 ± 5.2 SD yrs) completed an acute bout of an isocaloric HIIE (in form of 3:2 work-to-rest ratio at 90 and 40% of VO2 reserve) after both a reference sleep (RSX) and 3-3.5h of acute-partial sleep deprivation (SSX) conditions. HRV time and frequency domains and LDL were evaluated in six and seven time points surrounding sleep and exercise, respectively. To identify postprandial network interactions, we constructed one correlation analysis and one physiological network for each experimental condition. To quantify the interactions within the physiological networks, we also computed the number of links (i.e., number of significant correlations). Results: We observed an irruption of negative links (i.e., negative correlations) between HRV and LDL in the SSX physiological network compared to RSX. Discussion: We recognize that a correlation analysis does not constitute a true network analysis due to the absence of analysis of a time series of the original examined physiological variables. Nonetheless, the presence of negative links in SSX reflected the impact of sleep deprivation on the autonomic regulation and lipemia and, thus, revealed the inability of HIIE to remain cardioprotective under APSD. These findings underlie the need to further investigate the effects of APSD and HIIE on the interactions among physiological systems.

Sliced versus formulated potato chips – Does food structure alter lipid digestion?

A knowledge gap exists in understanding the role of food structure on the lipid digestion of formulated foods. Simulated in-vitro digestion using the TNO Gastro-Intestinal Model-1 (TIM-1), coupled with optical microscopy, tracked structural changes throughout digestion while measuring free fatty acid (FFA) hydrolysis. The cumulative FFA bioaccessibility is the same for sliced and formulated chips matrices, but the absolute FFA bioaccessibility, as a function of digestive time, is significantly different in the jejunal and ileal compartments. Between 180 and 360 min, FFA release of sliced chips rises until the end of digestion while formulated chips peak at ~ 240–300 min in both the jejunum and ileum. The cumulative bioaccessibility of saturated FFA is higher for sliced chips, while unsaturated FFA is greater for formulated chips. Formulated chips have a loosely packed matrix that quickly disintegrates, exposing discrete lipid droplets followed by coalescence; conversely, sliced chips contain a relatively intact cellular structure where lipids surround parenchyma cell walls. Lipid droplets decrease in sliced chips (from 15 to 10 µm) and formulated chips (from 14 to 12 µm) during 90–180 min of digestion, corresponding to rapid lipolysis. This research aims to correlate physical structure with the in-vitro FFA bioaccessibility. • Potato chips with like macronutrients but different structures alter lipid digestion. • The food structure of potato chips changes the peak lipolysis time. • Altered FFA release during digestion potentially varies postprandial lipemia.

The Arg82Cys Polymorphism of the Protein Nepmucin Implies a Role in HDL Metabolism.

ContextBlood lipid levels are linked to the risk of cardiovascular disease and regulated by genetic factors. A low-frequency polymorphism Arg82Cys (rs72836561) in the membrane protein nepmucin, encoded by CD300LG, is associated with lower fasting concentration of high-density lipoprotein cholesterol (HDLc) and higher fasting triglycerides. However, whether the variant is linked to postprandial lipids and glycemic status remains elusive.ObjectiveHere, we augment the genetic effect of Arg82Cys on fasting plasma concentrations of HDL subclasses, postprandial lipemia after a standardized high-fat meal, and glycemic status to further untangle its role in HDL metabolism.MethodsWe elucidated fasting associations with HDL subclasses in a population-based cohort study (Oxford BioBank, OBB), including 4522 healthy men and women. We investigated fasting and postprandial consequences on HDL metabolism in recall-by-genotype (RbG) studies (fasting: 20 carrier/20 noncarrier; postprandial: 7 carrier/17 noncarrier), and shed light on the synergistic interaction with glycemic status.ResultsA lower fasting plasma concentration of cholesterol in large HDL particles was found in healthy male carriers of the Cys82 polymorphism compared to noncarriers, both in the OBB (P = .004) and RbG studies (P = .005). In addition, the Cys82 polymorphism was associated with low fasting plasma concentrations of ApoA1 (P = .008) in the OBB cohort. On the contrary, we did not find differences in postprandial lipemia or 2-hour plasma glucose levels.ConclusionTaken together, our results indicate an association between the Arg82Cys variant and a lower concentration of HDL particles and HDLc, especially in larger HDL subclasses, suggesting a link between nepmucin and HDLc metabolism or maturation.

Effects of Postprandial Lipemia Combined With Disturbed Blood Flow on the Flow-Mediated Dilation, Oxidative Stress, and Endothelial Microvesicles in Healthy Subjects.

AimsBoth postprandial lipemia (PPL) and disturbed blood flow (DBF) induce endothelial dysfunction. However, the interactive effect of these stimuli on endothelial function is currently unknown. In the present study, we tested whether PPL plus DBF causes a greater reduction in flow-mediated dilation (FMD) than PPL and if this response is associated with elevations in oxidative stress and endothelial microvesicles (EMVs).MethodsEighteen individuals (aged 28 ± 1yrs, 3 females, and BMI 24.43 ± 0.8kg/m2) randomly underwent two experimental sessions: PPL and PPL plus DBF. FMD and venous blood samples were obtained at baseline and 30, 70, and 110 min after stimulation. PPL was induced by fat overload via mozzarella pizza ingestion and DBF by forearm cuff inflation to 75 mm Hg per 30 min. Lipidic profile, oxidative stress (thiobarbituric acid reactive substances, TBARS; ferric reducing/antioxidant power, FRAP; hydrogen peroxide, H2O2) and EMVs were measured in blood samples.ResultsHypertriglyceridemia was observed in both sessions. Retrograde shear rate and oscillatory index responses were significantly higher in the PPL plus DBF compared with PPL. PPL plus DBF evoked a greater reduction in FMD than did PPL and EMVs, NADPH oxidase, and H2O2 similarly increased in both sessions, but TBARS and FRAP did not change.ConclusionThese data indicate that the association of PPL plus DBF additively impairs endothelium-dependent function in 110 min after stimulus in healthy individuals, despite a similar increase in oxidative stress and EMVs. Further studies are needed to understand the mechanisms associated with the induced-endothelial dysfunction by association of PPL and DBF.

Identification of the Chinese Population That Can Benefit Most From Postprandial Lipid Testing: Validation of the Use of Oral Fat Tolerance Testing in Clinical Practice.

BackgroundDyslipidemia has become increasingly prevalent in recent decades. Blood lipid concentrations are significantly influenced by diet; however, postprandial triglyceride concentration (PTG) is not often measured. PTG can reflect the risks of diabetes and cardiovascular disease, but not all individuals would benefit from PTG testing.ObjectiveThe aim of the present study was to determine the PTG response in a Chinese cohort and identify who would benefit from diagnostic PTG measurement.MethodsA total of 400 Chinese adults were enrolled and underwent oral fat tolerance test (OFTT), which was well tolerated. The participants were assigned to groups according to their fasting triglyceride concentration to evaluate the usefulness of PTG testing. A PTG concentration > 2.5 mmol/L was defined as high (HPTG).ResultsOf the 400 participants, 78.9% showed an undesirable PTG response. Those with FTG ≥1.0 mmol/L had a delayed PTG peak and higher peak values. Seventy-five percent of those with 1.0 mmol/L ≤FTG <1.7 mmol/L had HPTG, of whom 18.6% had impaired glucose tolerance.ConclusionsThe present data confirm the previously reported predictive value of PTG testing. Moreover, the findings indicate that Chinese people with FTGs of 1.0 -1.7 mmol/L may benefit most from the identification of postprandial hyperlipidemia through OFTT because more than half of them have occult HPTG, which may require treatment. Thus, the detection of HPTG using an OFTT represents a useful means of identifying dyslipidemia and abnormal glucose metabolism early.Clinical Trial Registration[http://www.chictr.org.cn/index.aspx], identifier ChiCTR1800019514.

Postprandial Hyperlipidemia: Association with Inflammation and Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis.

Objective: To describe postprandial lipidemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis and inflammatory activity. Methods: Observational study of 80 cases of RA and 80 sex- and age-matched controls. We excluded individuals with dyslipidemia. Postprandial hyperlipidemia (PPHL) was defined as postprandial triglycerides >220 mg/dL and/or postprandial ApoB48 levels >75th percentile (>p75). Plasma lipids, cholesterol, triglycerides, ApoB48, and total ApoB were evaluated at baseline and after a meal. Other variables analyzed included subclinical atherosclerosis (defined as presence of carotid atheromatous plaque), inflammatory activity (disease activity score (DAS28-ESR)), cytokines, apolipoproteins, and physical activity. A multivariate analysis was performed to identify factors associated with PPHL in patients with RA. Results: A total of 75 patients with RA and 67 healthy controls fulfilled the inclusion criteria. PPHL was more frequent in patients with RA than controls (No. (%), 29 (38.70) vs. 15 (22.40); p = 0.036), as was subclinical atherosclerosis (No. (%), 22 (30.10) vs. 10 (14.90); p = 0.032). PPHL in patients with RA was associated with subclinical atherosclerosis (OR (95% CI) 4.69 (1.09–12.11); p = 0.037), TNF-α (OR (95% CI) 2.00 (1.00–3.98); p = 0.048), high-sensitivity C-reactive protein (OR (95% CI) 1.10 (1.01–1.19); p = 0.027), and baseline triglycerides (OR (95% CI) 1.02 (1.00–1.04); p = 0.049). Conclusion: PPHL was more frequent in patients with RA than in controls. PPHL in patients with RA was associated with inflammation and subclinical atherosclerosis.

The Effect of GLP-1 Receptor Agonists on Postprandial Lipaemia.

To review the currently available data on the effect of Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) on postprandial lipaemia. Out of the available studies that examined the respective lipid parameter, exenatide reduced postprandial triacyglycerol (TAG) in 4/6, apolipoprotein B-48 in 3/3, non-esterified fatty acids in 2/2, and apolipoprotein C-III and very low-density lipoprotein cholesterol (VLDL-C) in 1/1 studies. Liraglutide reduced postprandial TAG in 2/2, apolipoprotein B-48 in 3/3 and apolipoprotein C-III, chylomicron-TAG and VLDL1-TAG in 1/1 studies. Lixisenatide reduced postprandial chylomicron-TAG and apolipoprotein B-48 in 1 study. Semaglutide reduced postprandial TAG, apolipoprotein B-48 and VLDL in 1 study. Dulaglutide reduced postprandial apolipoprotein B-48 in 1 study. GLP-1 RAs have consistent beneficial effects on postprandial lipaemia with most of the data coming from studies with exenatide and liraglutide. Reduction of postprandial lipaemia might be one of the mechanisms behind the pleiotropic effects of GLP-1 RAs.