Elevated Postprandial Triglyceride Research Articles

Thirty Minutes of Moderate-Intensity Downhill or Level Running Has No Effect on Postprandial Lipemia

Elevated postprandial triglyceride (TG) concentrations are linked to a relatively high risk of cardiovascular disease. Eccentric endurance exercise, such as downhill walking and running, can provide metabolic benefits similar to concentric exercise. However, whether eccentric exercise affects postprandial lipemia remains unknown. Nine healthy young men performed level running (trial) or downhill running (DR trial, -15% slope) at 60% [INSIDE:1]O2max or rest (CON trial) for 30 min in a randomized crossover design. The participants were fed a high-fat meal the next day. Blood and expired gas samples were collected before and 0.5, 1, 2, 3, 4, 5, and 6 h after the meal. Muscle soreness was measured using a visual analog scale. The DR trial induced mild muscle damage. During the 6-h postprandial period, serum TG concentrations and area under the curve (AUC) were similar across the three trials. The DR trial had a significantly higher AUC of nonesterified fatty acid concentrations and a significantly lower AUC of glucose concentrations than the CON trial. The results suggested that neither moderate-intensity DR nor running a level surface had a significant effect on lipemia after a high-fat meal. However, DR improved the postprandial glycemic response.

Comparison of nonfasting and fasting lipoprotein subfractions and size in 15,397 apparently healthy individuals: An analysis from the VITamin D and OmegA-3 TriaL

Elevated postprandial triglycerides reflect a proatherogenic milieu, but underlying mechanisms are unclear. We examined differences between fasting and nonfasting profiles of directly measured lipoprotein size and subfractions to assess if postprandial triglycerides reflected increases in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL) and remnants, or small dense lipid depleted LDL (sdLDL) particles. We conducted a cross-sectional analysis of 15,397 participants (10,135 fasting; 5262 nonfasting [<8hours since last meal]) from the VITamin D and OmegA-3 TriaL. Baseline cholesterol subfractions were measured by the vertical auto profile method and particle subfractions by ion mobility. We performed multivariable linear regression adjusting for cardiovascular and lipoprotein-modifying risk factors. Mean age (SD) was 68.0years (±7.0), with 50.9% women. Adjusted mean triglyceride concentrations were higher nonfasting by 17.8±1.3%, with higher nonfasting levels of directly measured VLDL cholesterol (by 3.5±0.6%) and total VLDL particles (by 2.0±0.7%), specifically large VLDL (by 12.3±1.3%) and medium VLDL particles (by 5.3±0.8%), all P<.001. By contrast, lower concentrations of low density lipoprotein (LDL) and IDL cholesterol and particles were noted for nonfasting participants. sdLDL cholesterol levels and particle concentrations showed no statistically significant difference by fasting status (-1.3±2.1% and 0.07±0.6%, respectively, P>.05). Directly measured particle and cholesterol concentrations of VLDL, not sdLDL, were higher nonfasting and may partly contribute to the proatherogenicity of postprandial hypertriglyceridemia. These differences, although statistically significant, were small and may not fully explain the increased risk of postprandial hypertriglyceridemia.

Whey Protein Combined with Low Dietary Fiber Improves Lipid Profile in Subjects with Abdominal Obesity: A Randomized, Controlled Trial

Abdominal obesity is associated with elevated postprandial triglycerides (TG), an independent risk factor for cardiovascular diseases. Previous studies show that whey protein (WP) and dietary fiber may separately reduce postprandial TG. However, few studies have investigated the long-term effects of WP and dietary fiber on postprandial TG. We aimed to investigate the separate and combined long-term effects of WP and dietary fiber from wheat bran on postprandial TG and markers of lipid metabolism in subjects with abdominal obesity. We conducted a 12-week, double-blind, randomized, controlled, parallel intervention study. In a 2 × 2 factorial design, 73 adults were randomized to receive 60 g/day of either WP hydrolysate or maltodextrin (MD) combined with high-fiber wheat bran products (HiFi; 30 g dietary fiber/day) or low-fiber refined wheat products (LoFi; 10 g dietary fiber/day). A high-fat meal test was conducted before and after the intervention. Sixty-five subjects were included in the final analyses. There were no differences between intervention groups in postprandial TG assessed as incremental area under the curve (iAUC). WP-LoFi had reduced postprandial TG assessed as total area under the curve (tAUC) and reduced fasting TG compared with all other groups, and reduced fasting apolipoprotein B-48 compared with MD-LoFi. There were no changes in lipoprotein lipase activity. Total cholesterol and apolipoprotein B-100 were reduced after WP intake compared with MD. Total cholesterol was increased after HiFi intake compared with LoFi. In conclusion, intake of WP in combination with low-fiber cereal products for 12 weeks had beneficial effects on postprandial TG tAUC and fasting TG, but not on postprandial TG iAUC in subjects with abdominal obesity. Combining WP with high-fiber wheat bran products did not improve lipid profile.

Postprandial lipaemia 10 and 34 hours after playing football: Does playing frequency affect the response?

Elevated postprandial triglyceride (TG) is associated with increased risk of cardiovascular disease. The time window for the last bout beneficial effect on postprandial lipaemia after football play is unknown. The aim of the present study was to examine whether playing affects postprandial TG during 1.5 day of reduced activity. Eighteen males were randomly allocated to perform either 1 (1FOOT; n = 9; age = 33.0 ± 5.0 yrs; body mass index = 24.2 ± 3.6 kg/m2) or 3 (3FOOT) consecutive days of 60-min 5 vs 5 football (n = 9; age = 32.8 ± 5.2 yrs; body mass index = 26.2 ± 4.1 kg/m2) matches across a 5-day study period. They arrived to the laboratory 10 hrs and 34 hrs after the final football session and blood samples were collected at fasted (0 min) and 45, 90, 240 and 360 min post a high fat load meal. There were non significant increase for postprandial TG AUC (9.1%; p = 0.17; 95%CI = -0.43 to 2.0; ES = -0.23) and iAUC (14.2%; p = 0.43; 95%CI = -0.92 to 1.9; ES = -0.24) between 10 and 34 hrs after the 1FOOT. For the 3FOOT, there was a non significant decrease in postprandial TG AUC (-2.7%; p = 0.73; 95%CI = -2.0 to 1.5; ES = 0.05) and iAUC (-17.5%; p = 0.41; 95%ci = -2.5 to 1.1; ES = 0.31) from 10 to 34 hrs, respectively. Performing three consecutive days of football exercise may offer no greater protective effect for postprandial TG before a period of reduced activity, compared to a single session.

The GTPase ARFRP1 affects lipid droplet protein composition and triglyceride release from intracellular storage of intestinal Caco-2 cells

Intestinal release of dietary triglycerides via chylomicrons is the major contributor to elevated postprandial triglyceride levels. Dietary lipids can be transiently stored in cytosolic lipid droplets (LDs) located in intestinal enterocytes for later release. ADP ribosylation factor-related protein 1 (ARFRP1) participates in processes of LD growth in adipocytes and in lipidation of lipoproteins in liver and intestine. This study aims to explore the impact of ARFRP1 on LD organization and its interplay with chylomicron-mediated triglyceride release in intestinal-like Caco-2 cells. Suppression of Arfrp1 reduced release of intracellularly derived triglycerides (0.69-fold) and increased the abundance of transitional endoplasmic reticulum ATPase TERA/VCP, fatty acid synthase-associated factor 2 (FAF2) and perilipin 2 (Plin2) at the LD surface. Furthermore, TERA/VCP and FAF2 co-occurred more frequently with ATGL at LDs, suggesting a reduced adipocyte triglyceride lipase (ATGL)-mediated lipolysis. Accordingly, inhibition of lipolysis reduced lipid release from intracellular storage pools by the same magnitude as Arfrp1 depletion. Thus, the lack of Arfrp1 increases the abundance of lipolysis-modulating enzymes TERA/VCP, FAF2 and Plin2 at LDs, which might decrease lipolysis and reduce availability of fatty acids for triglyceride synthesis and their release via chylomicrons.

Non-fat milk attenuates acute hypertriglyceridemia in obese individuals who consume a high fat diet: A randomized control trial

BackgroundRepeated exposure to elevated postprandial triglycerides, as seen with typical Western diets, contributes to atherosclerosis and vascular disease. We determined if a single serving of non-fat milk added to a high fat tolerance test could attenuate postprandial hypertriglyceridemia in individuals who consume a high fat diet. MethodsIn this placebo-controlled, randomized, crossover experimental study, 30 overweight/obese adults consumed a high-fat tolerance test meal combined with either non-fat milk, carbohydrate control drink, or caloric control drink. ResultsPlasma triglycerides increased over time with no significant differences between interventions. Peak plasma triglyceride levels during HFTT were significantly related to dietary fat intake (r = 0.30, p < 0.05). When participants were divided into tertiles based on habitual dietary fat intake, the higher fat diet group exhibited reduced triglyceride net integrated area under the curve when supplemented with non-fat milk. No significant differences in hemodynamic measures (brachial flow-mediated dilation and femoral vascular conductance) were observed between the milk and caloric control trials for either the low fat or high fat diet groups. ConclusionsA single serving of non-fat milk may attenuate acute hypertriglyceridemia in individuals who chronically consume a high fat diet, offering a simple and easily implemented option for managing elevations in postprandial triglycerides.

Pre-Meal Effect of Whey Proteins on Metabolic Parameters in Subjects with and without Type 2 Diabetes: A Randomized, Crossover Trial.

Diabetic dyslipidemia with elevated postprandial triglyceride (TG) responses is characteristic in type 2 diabetes (T2D). Diet and meal timing can modify postprandial lipemia (PPL). The impact of a pre-meal of whey proteins (WP) on lipid metabolism is unidentified. We determined whether a WP pre-meal prior to a fat-rich meal influences TG and apolipoprotein B-48 (ApoB-48) responses differentially in patients with and without T2D. Two matched groups of 12 subjects with and without T2D accomplished an acute, randomized, cross-over trial. A pre-meal of WP (20 g) or water (control) was consumed 15 min before a fat-rich meal (supplemented with 20 g WP in case of water pre-meal). Postprandial responses were examined during a 360-min period. A WP pre-meal significantly increased postprandial concentrations of insulin (P < 0.0001), glucagon (P < 0.0001) and glucose-dependent insulinotropic peptide (GIP) (P < 0.0001) in subjects with and without T2D. We detected no effects of the WP pre-meal on TG, ApoB-48, or non-esterified fatty acids (NEFA) responses to the fat-rich meal in either group. Paracetamol absorption i.e., gastric emptying was delayed by the WP pre-meal (P = 0.039). In conclusion, the WP pre-meal induced similar hormone and lipid responses in subjects with and without T2D. Thus, the WP pre-meal enhanced insulin, glucagon and GIP responses but did not influence lipid or glucose responses. In addition, we demonstrated that a WP pre-meal reduced gastric emptying in both groups.

High Intensity Versus Low Volume Resistance Exercise On Postprandial Triglycerides In Healthy College Students

Elevated postprandial triglycerides (TGs) contribute to the development of cardiovascular disease. Prior exercise is a well-established method to lower postprandial TGs; however, most exercise protocols involve prolonged aerobic or resistance training (RT) of sixty to ninety minute which is not realistically attainable by the general population. PURPOSE: The present study investigates the effect of high intensity interval training (HIIT) of twenty minutes and RT of thirty minutes on postprandial TGs. METHODS: Approval for this study was obtained from the Institutional Review Board of the College of Saint Benedict and Saint John’s University and signed informed consents were provided by all participants. Thirty healthy college-age students (5 males, 25 females) were recruited from nutrition and exercise science courses. All subjects completed the control, HIIT, and resistance protocols one week apart. Subjects performed the exercise protocols 12-16 hours prior to an oral fat tolerance test (milkshake, 1 g of fat per kg of body weight). Subjects were instructed to consume similar diets during the 24 hours prior to the milk shake. Each exercise session was supervised; HIIT consisted of four 30 second sprints with 4 minutes of walking recovery and the low-volume RT consisted of six machine-based lifts, 2 sets of 8 repetitions at 75% of one repetition maximum. Postprandial TGs were measured at baseline and three hours following consumption of the milkshake using the CardioChek PA blood analyzer (PTS Diagnostics, Indianapolis, IN). Data was analyzed using a three way repeated measures ANOVA statistical test. RESULTS: The triglyceride levels at baseline were on average less than 150 mg/dL (desirable value); however, 20% were above. The means are as follows for each treatment and time point (baseline, and postprandial respectively): Control 107 +/- 49, 140 +/- 73 mg/dL; HIIT 93 +/- 34, 122 +/- 59 mg/dL; and Resistance 108 +/- 47, 144 +/- 64 mg/dL. While there appears to be a trend that HIIT lowered both fasting and postprandial TG’s the decrease was not statistically significant (p=0.699). CONCLUSION: Twenty minutes of HIIT or thirty minutes of low-volume RT did not significantly lower postprandial triglyceride response to a high fat milkshake in a healthy, college-age population.

Deregulated Lipid Sensing by Intestinal CD36 in Diet-Induced Hyperinsulinemic Obese Mouse Model.

The metabolic syndrome (MetS) greatly increases risk of cardiovascular disease and diabetes and is generally associated with abnormally elevated postprandial triglyceride levels. We evaluated intestinal synthesis of triglyceride-rich lipoproteins (TRL) in a mouse model of the MetS obtained by feeding a palm oil-rich high fat diet (HFD). By contrast to control mice, MetS mice secreted two populations of TRL. If the smaller size population represented 44% of total particles in the beginning of intestinal lipid absorption in MetS mice, it accounted for only 17% after 4 h due to the secretion of larger size TRL. The MetS mice displayed accentuated postprandial hypertriglyceridemia up to 3 h due to a defective TRL clearance. These alterations reflected a delay in lipid induction of genes for key proteins of TRL formation (MTP, L-FABP) and blood clearance (ApoC2). These abnormalities associated with blunted lipid sensing by CD36, which is normally required to optimize jejunal formation of large TRL. In MetS mice CD36 was not downregulated by lipid in contrast to control mice. Treatment of controls with the proteosomal inhibitor MG132, which prevented CD36 downregulation, resulted in blunted lipid-induction of MTP, L-FABP and ApoC2 gene expression, as in MetS mice. Absence of CD36 sensing was due to the hyperinsulinemia in MetS mice. Acute insulin treatment of controls before lipid administration abolished CD36 downregulation, lipid-induction of TRL genes and reduced postprandial triglycerides (TG), while streptozotocin-treatment of MetS mice restored lipid-induced CD36 degradation and TG secretion. In vitro, insulin treatment abolished CD36-mediated up-regulation of MTP in Caco-2 cells. In conclusion, HFD treatment impairs TRL formation in early stage of lipid absorption via insulin-mediated inhibition of CD36 lipid sensing. This impairment results in production of smaller TRL that are cleared slowly from the circulation, which might contribute to the reported association of CD36 variants with MetS risk.

Acute and Chronic Effects of Sprint Interval Training on Postprandial Lipemia in Women At‐Risk for Metabolic Syndrome

Individuals with the metabolic syndrome (MetS) exhibit elevated postprandial triglycerides (TG). The aims of this investigation were to determine 1) the effectiveness of 6 weeks of sprint interval training (SIT) on postprandial lipemia (PPL) and 2) if the attenuation of PPL following 6‐weeks of SIT is magnified compared to a single session of SIT prior to training in women at‐risk for MetS (n = 45; 30‐65 yrs). Postprandial responses to a high‐fat meal challenge (HFMC) were assessed for 3 h at baseline (B‐HFMC; all participants) without prior exercise, paired with a single session of SIT (four 30‐s all‐out sprints with 4‐min recovery) prior to the intervention (Pre‐HFMC; SIT only), and after the 6‐week SIT intervention without prior exercise (Post‐HFMC; CON) or paired with an acute bout of SIT ~14‐18 h prior to Post‐HFMC (SIT). Responses to the HFMC were assessed by collecting venous blood samples fasted and at 0, 30, 60, 120, and 180 min postprandial. Compared to baseline, an acute bout of SIT before (Pre‐HFMC) and after the 6‐week intervention (Post‐HFMC) significantly attenuated fasted (P&lt;0.05; 16.6% and 12.3%, respectively) and postprandial area under the curve (13.1% and 9.7%, respectively; tAUC) TG responses. There was no difference in fasted or tAUC TG responses between Pre‐HFMC and Post‐HFMC. SIT is an effective mode of exercise to reduce fasting and postprandial TG concentrations in women at‐risk for MetS.

Chronic supplementation of proanthocyanidins reduces postprandial lipemia and liver miR-33a and miR-122 levels in a dose-dependent manner in healthy rats

Elevated postprandial triglycerides are associated with an increased risk of cardiovascular disease. Acute proanthocyanidin supplementation improves postprandial lipemia. Therefore, in this study, we evaluated whether a chronic treatment (3 weeks) of grape seed proanthocyanidins (GSPE) improves tolerance to lipid overload and represses liver microRNA (miRNA)-33a and miRNA-122 and their target genes as a mechanism to soften the elevated postprandial triglycerides in healthy rats. Additionally, the minimal GSPE chronic dose required to alter miRNA levels was determined by means of a dose–response experiment using 5, 15, 25 or 50 mg of GSPE/kg body weight. GSPE repressed miR-33a and miR-122 liver expression and reduced postprandial lipemia in a dose-dependent manner. Significant effects were only observed at high levels of proanthocyanidin consumption, but moderate doses of proanthocyanidins were still able to modulate miRNA expression. Therefore, it can be suggested that a population with a normal intake of proanthocyanidin-rich foods can benefit from the modulation of miRNA expression. At the molecular level, this action can confer homeostatic robustness and will thus exert subtle changes in lipid metabolism, thereby reducing the risk associated with postprandial hyperlipemia.

Hepatic Remnant Lipoprotein Clearance by Heparan Sulfate Proteoglycans and Low-Density Lipoprotein Receptors Depend on Dietary Conditions in Mice

Chylomicron and very low-density lipoprotein remnants are cleared from the circulation in the liver by heparan sulfate proteoglycan (HSPG) receptors (syndecan-1), the low-density lipoprotein receptor (LDLR), and LDLR-related protein-1 (LRP1), but the relative contribution of each class of receptors under different dietary conditions remains unclear. Triglyceride-rich lipoprotein clearance was measured in AlbCre(+)Ndst1(f/f), Ldlr(-/-), and AlbCre(+)Lrp1(f/f) mice and mice containing combinations of these mutations. Triglyceride measurements in single and double mutant mice showed that HSPGs and LDLR dominate clearance under fasting conditions and postprandial conditions, but LRP1 contributes significantly when LDLR is absent. Mice lacking hepatic expression of all 3 receptors (AlbCre(+)Ndst1(f/f) Lrp1(f/f) Ldlr(-/-)) displayed dramatic hyperlipidemia (870 ± 270 mg triglyceride/dL; 1300 ± 350 mg of total cholesterol/dL) and exhibited persistent elevated postprandial triglyceride levels because of reduced hepatic clearance. Analysis of the particles accumulating in mutants showed that HSPGs preferentially clear a subset of small triglyceride-rich lipoproteins (≈ 20-40 nm diameter), whereas LDLR and LRP1 clear larger particles (≈ 40-60 nm diameter). Finally, we show that HSPGs play a major role in clearance of triglyceride-rich lipoproteins in mice fed normal chow or under postprandial conditions but seem to play a less significant role on a high-fat diet. These data show that HSPGs, LDLR, and LRP1 clear distinct subsets of particles, that HSPGs work independently of LDLR and LRP1, and that HSPGs, LDLR, and LRP1 are the 3 major hepatic triglyceride-rich lipoprotein clearance receptors in mice.

High DHA dosage from algae oil improves postprandial hypertriglyceridemia and is safe for type-2 diabetics

Postprandial refers to diet induced changes in plasma concentrations of sugars, amino acids and fats be- tween 0 and 6 h following a meal. This review details the fat transport through lipoprotein particles and triglyceride frac- tions in the postprandial plasma. The long-chain omega-3 fatty acid docosahexaenoic acid (DHA) is more active in postprandial plasma and is more abundantly incorporated into the surface phospholipid fraction of lipoproteins. A survey of controlled clinical trials in the literature demon- strates that 1,000 mg to 2,000 mg DHA daily is effective to treat hypertriglyceridemia (HTG), mixed dyslipidemia and most effectively controls elevated postprandial triglycerides (TG). TG is a marker for total fat in circulation. Omega-3 fatty acids lower fasting and postprandial TG, an activity first discovered in 1971 in Greenlandic Inuits. Low TG and high DHA were coincident with the absence of type 2 diabetes. It is now known that DHA is the major structural and functional omega-3 component of lipoproteins in hu- man plasma. DHA is the omega-3 to most substantially increase by mass in the phospholipid fraction of very low- density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL). DHA is most effective at raising HDL levels and improves the omega-3 index in red blood cells (RBC). DHA intake also correlates with greater than 25 % reductions of fasting TG and greater than 40 % reductions in postprandial TG. Postprandial HTG is common in the type 2 diabetes; therefore, we considered the safety of DHA from Schizochytrium sp. algae oil and the evidence for risk reduction of coronary vascular disease (CVD) and type 2 diabetes. Recent clinical trials suggest high DHA intake from Chromista algae controls plasma TG, but does not appear to control glucocentric markers or cholesterol levels. DHA directly affects postprandial TG transport, but has little effect on insulin function and insulin resistance. Applications for use in South Asian diabetics are considered. 1,200 mg algae DHA daily over 3 months is an optimized program for direct control of postprandial HTG and is safe for type 2 diabetics.

Effects of omega-3 fatty acids on postprandial triglycerides and monocyte activation

ObjectiveEpidemiologic studies suggest that elevated postprandial triglycerides (ppTG) are associated with future cardiovascular events. Monocyte activation plays an important role in vascular diseases. Omega-3 fatty acids (n3-FA) lower fasting TG levels. The effects of n3-FA on ppTG and the role of ppTG for monocyte activation are insufficiently understood. Methods and results23 healthy volunteers and 30 non-diabetic patients with documented coronary artery disease were subjected to an oral TG tolerance test (OTTT) consisting of 80 g cream fat or to water as control (H2O). Patients were treated with 4 g n3-FA/day or placebo for 3 weeks in a randomized, placebo-controlled, double-blind, crossover study. Relative postprandial TG increase reached its maximum 4 h after fat intake (185.1 ± 10.9% of baseline). n3-FA reduced fasting TG from 137.1 ± 12.9 to 112.2 ± 8.6 mg/dl (p < 0.05), and maximum ppTG concentrations from 243.6 ± 24.6 to 205.8 ± 17.1 mg/dl (p < 0.05), while relative TG increase (192.8 ± 12.7%) was comparable to placebo. Relative monocytopenia and neutrophilia were detected following fat intake, which was unaffected by n3-FA and also detectable in the H2O group. Serum chemotactic cytokine (MCP1 and fractalkine) concentrations and monocyte migration were not affected by fat intake or n3-FA. Monocyte activation markers CD11b and CD14, monocyte subpopulations CD16+CD14high and CD16+CD14low, sICAM serum levels and markers of oxidative stress remained unchanged by fat intake or n3-FA. ConclusionThe postprandial TG increase does not stimulate monocytes beyond their circadian activation patterns. n3-FA reduce fasting TG and the postprandial TG increase. n3-FA may therefore allow to prospectively study whether selected patients benefit from TG-lowering independent of LDL- and HDL-cholesterol.

Abstract 16791: Elevated Post-Prandial Triglyceride Concentrations Are Associated with an Unfavorable Cardiometabolic Risk Factor Profile in Patients with Coronary Artery Disease

Background: The role of the post-prandial triglyceride (ppTG) metabolism for cardiovascular risk has not been studied prospectively. Study design: The cohort of this prospective study consisted of N=514 consecutive patients with documented stable coronary artery disease (CAD) (83% male, 17% female, age 66±0.4 years), who were subjected to a novel sequential oral triglyceride and glucose tolerance test (OTT / OGT). The test protocol (75g cream fat given 3 hours prior to 75g glucose) was previously characterized and validated. Results: Patients with normal glucose tolerance (N=126) had the lowest fasting (fTG) (108±4mg/dl) and ppTG (195±7mg/dl) concentrations, whereas patients with pathologic glucose tolerance (n=150; fTG 167±10mg/dl vs. ppTG 293±14mg/dl) and patients with diabetes (n=238; fTG 175±11mg/dl vs. ppTG 297±12mg/dl) were characterized by elevated fTG and ppTG. The mean relative TG increase (% vs. baseline) was comparable between subgroups. However, patients showed a large inter-individual variability with respect to ppTG metabolism within each group. Patients in the upper compared to the lower ppTG tertile were younger and had a more severe cardiovascular risk profile (e.g. more active smokers, higher blood pressure, higher body mass index and waist-to-hip-ratio). There were no differences in the angiographic extent of CAD, heart rate or medication. Patients in the upper ppTG tertile had higher concentrations of fasting glucose and insulin, HbA1c, total and LDL cholesterol, whereas HDL was lower. Markers of ppTG metabolism including area under the curve and maximal TG increase per hour were significantly elevated in these patients (p&lt;0.01, Chi 2 or ANOVA where indicated). Underscoring these findings, 53% of patients in ppTG tertile 3 vs. 38% in tertile 1 had diabetes and 76% vs. 32% in tertile 1 met the WHO definition criteria of the metabolic syndrome. Conclusions: Elevated ppTG concentrations characterize CAD patients with a high burden of cardiometabolic risk factors. Interestingly, patients differed strongly in the individual ppTG response. Multivariable analyses of cardiovascular events after the 12-months follow-up show that assessment of ppTG metabolism improves risk stratification in CAD patients.

Postprandial Lipemia and Fitness Status

Elevated postprandial triglycerides (postprandial lipemia; PPL) are a risk factor for the development of coronary artery disease. Chronic exercise training and the maintenance of high levels of aerobic fitness may lead to an attenuated PPL response. However, some research indicates this is due to the effects of recent exercise as acute bouts of exercise can attenuate the postprandial rise in triglycerides in active and sedentary individuals. Furthermore, to induce the PPL response, most research utilizes high-fat meal challenges which may not represent typical eating habits. PURPOSE: To investigate the role of aerobic fitness status on PPL after a 60-hr period of exercise avoidance and following the ingestion of a mixed-macronutrient nutritional beverage (360 kcal; 15% Protein, 50% Carbohyrdate, 35% Fat). METHODS: Sixteen healthy, young (22 ± 3 yrs) men participated in this IRB approved investigation. The men were categorized according to aerobic fitness (VO2max: 42.50 ± 4.0 ml/kg/min for the low group, n=8, and 58.0 ± 3.2 ml/kg/min for the high group, n=8). Plasma triglyceride levels were measured at baseline and hourly for four hours following ingestion of the meal. All data reported as mean ± standard deviation. Area under the curve (AUC) and subject characteristic data were analyzed with independent t-tests and group x time interactions of select variables were analyzed using a repeated-measures ANOVA model. Statistical significance was accepted at P < 0.05. RESULTS: Following ingestion of the meal, the four-hour incremental AUC was greater in the low aerobic fitness group than in the high aerobic fitness group (1608.37 ± 863.86 vs. 791.05 ± 234.38 mmol/l/480min; p = 0.022). CONCLUSION: In this sample of men, those with high aerobic fitness displayed an attenuated postprandial lipemic response as compared to those with low aerobic fitness after 60-hr of exercise avoidance. Funded in part by the Office of Research and Sponsored Programs at Ohio University

Elevated post-prandial triglyceride concentrations accord to the activity of intestinal alkaline phosphataseisozyme in human−Concerning with the ABO blood group secretor and their non-secretor−

Elevated post-prandial triglyceride concentrations accord to the activity of intestinal alkaline phosphataseisozyme in human−Concerning with the ABO blood group secretor and their non-secretor−

Postprandial hypertriglyceridaemia in type 2 diabetic subjects

Postprandial hyperlipidemia is a major risk factor for cardiovascular diseases in type 2 diabetes. The dyslipidemia of diabetes in the postprandial phase is a major determinant of the atherogenicity of LDL. This study was done to study the postprandial triglyceride levels in patients with type 2 diabetes mellitus; to assess the relationship between fasting and postprandial triglyceride levels and postprandial triglyceride levels and fasting blood sugar values in type 2 diabetes; and to analyze the relationship between postprandial hypertriglyceridaemia and conventional coronary risk factors. One hundred type 2 diabetic subjects (M:F - 67:33, mean age 56.6 ± 11.9 years, mean body mass index 24.83 kg/m 2 ) were studied and compared with controls. Fasting and 2-hour postprandial responses with respect to plasma glucose and triglycerides (TG) were measured after a breakfast meal, usually consumed by the patient with usual dose of insulin or oral hypoglycemic drugs. Postprandial hypertriglyceridaemia was taken as a postprandial TG value greater than 15% of the corresponding fasting TG value. There was signi› cant postprandial hypertriglyceridaemia in diabetics in comparison to controls. FBG was signi›cantly related to fasting and postprandial triglycerides. As FBG increased, both fasting and postprandial TG increased. Fasting TG was signi›cantly related to postprandial TG. As fasting TG increased, postprandial TG increased. There was no correlation between postprandial TG and age, sex, smoking, hypertension, total and LDL cholesterol*. is attributable in part to specific disorders of lipoprotein metabolism. These include disordered metabolism of VLDL and chylomicrons that may be atherogenic. The dyslipidemia of diabetes in the postprandial phase is a major determinant of the atherogenicity of LDL, which may account for the up to fivefold increase in atherosclerosis in the diabetic patient. Elevated postprandial triglycerides, peak postprandial triglyceridaemia have been associated in clinical trials with both early coronary artery and carotid artery atherosclerosis for persons with hyperlipidemia, independent of established risk factors. [4,5] Various clinical trials both in India (Chennai) and the West (Spain, USA, Sweden) have shown that postprandial hypertriglyceridaemia is common in type 2 DM. Normalization of the postprandial phase in diabetes will yield important cardiovascular benefits.

The pathophysiology of lipid metabolism and diabetes

Summary Patients with diabetes often present with abnormal lipid profiles because insulin regulates several of the steps of lipid metabolism. Patients with type 1 diabetes that exhibit effective glycaemic control do not have quantitative lipoprotein abnormalities, but may exhibit qualitative abnormalities, mainly an increase in smaller, more atherogenic very low-density lipoprotein (VLDL) particles. Furthermore, in the Diabetes Control and Complications Trials (DCCT) study, the group of patients with type 1 diabetes that were characterised by consistent weight gain, exhibited lipid profiles more typical of type 2 diabetes (T2D). Dyslipidaemia in T2D is characterised by several strictly linked abnormalities: elevated fasting and postprandial triglycerides (TG), a significant decrease in high-density lipoprotein (HDL) cholesterol and an increase in smaller low-density lipoprotein (LDL) and HDL particles. The increase in plasma TG is largely explained by the increased production of TG-rich; large-sized VLDL in particular. The insulin resistant liver fails to inhibit lipid attachment to pre-VLDL molecules and synthesises larger-sized VLDL at a greater rate. Large TG-rich; VLDL enhances the transfer of core lipids between VLDL, LDL, and HDL with increased formation of smaller LDL and HDL. Also, the elevated postprandial TG that are often present in patients with T2D may be linked to insulin resistance. Therefore, the abatement of hyperglycaemia and insulin resistance should be one of the main treatment objectives to address dyslipidaemia in patients with diabetes.

Postprandial dyslipidemia: an atherogenic disorder common in patients with diabetes mellitus

The increased risk of coronary artery disease among patients with diabetes mellitus is attributable, in part, to specific disorders of lipoprotein metabolism that are common in this population. These include disordered metabolism of very-low-density lipoprotein and/or chylomicrons that may be proatherogenic. Elevated postprandial triglycerides, peak postprandial triglyceridemia, and late postprandial triglyceride levels have been associated in clinical trials with both early coronary artery and carotid artery atherosclerosis for persons with normal lipid profiles and those with mild-to-moderate hyperlipidemia, independently of established risk factors. If hyperlipidemia cannot be managed through better glycemic control, diet, and exercise, then hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, fibric acid derivatives, and omega-3 fatty acids are safe and effective lipid-altering agents that can be used to correct these disorders.