Postprandial Lipid Metabolism Research Articles

Effects of fish oil replacement by a vegetable oil blend on digestibility, postprandial serum metabolite profile, lipid and glucose metabolism of European sea bass (Dicentrarchus labrax) juveniles

Effects of fish oil replacement by a vegetable oil blend on digestibility, postprandial serum metabolite profile, lipid and glucose metabolism of European sea bass (<i>Dicentrarchus labrax</i>) juveniles

Cluster-determinant 36 (CD36) impacts on vitamin E postprandial response.

A single nucleotide polymorphism in the cluster determinant 36 (CD36) gene has recently been associated with plasma α-tocopherol concentration, suggesting a possible role of this protein in vitamin E intestinal absorption or tissue uptake. To investigate the involvement of CD36 in vitamin E transport, we first evaluated the effect of CD36 on α- and γ-tocopherol transmembrane uptake and efflux using transfected HEK cells. γ-Tocopherol postprandial response was then assessed in CD36-deficient mice compared with wild-type mice, after the mice had been fully characterized for their α-tocopherol, vitamin A and lipid plasma, and tissue contents. Both α- and γ-tocopherol uptake was significantly increased in cells overexpressing CD36 compared with control cells. Compared with wild-type mice, CD36-deficient mice displayed a significantly decreased cholesterol hepatic concentration, and males exhibited significantly higher triacylglycerol contents in liver, brain, heart, and muscle. Although tissue α-tocopherol concentration after adjustment for lipid content was not modified, γ-tocopherol postprandial response was significantly increased in CD36-deficient mice compared with controls, likely reflecting the postprandial hypertriglyceridemia observed in these mice. Our findings show for the first time that CD36 participates-directly or indirectly-in vitamin E uptake, and that CD36 effect on postprandial lipid metabolism in turn modifies vitamin E postprandial response.

Effect of Gender and Body Weight on Postprandial Glucose and Lipid Metabolism in Adults with Type 2 Diabetes

The magnitude of the healthcare problem of type-2-diabetes increases according to its association with several risk factors for cardiovascular diseases such as obesity and dyslipidemia. This study took place in the north-western region of Algeria. We aimed to assess the effect of body weight and gender on postprandial lipid and glucose in type-2-diabetes patients. 93 diabetic patients (age 55.65±13.81 years) were studied. Anthropometric parameters and body mass index (BMI) were measured. Fasting and postprandial (PP) glucose and lipid (total cholesterol, HDLcholesterol, LDL-cholesterol, triglycerides, apo A-I and apo B) profiles were evaluated. There were a positive correlation between postprandial glucose and BMI in women (r2 = 0.041). Negative correlation with BMI was noticed for PP TG in both males (r2 = 0.011) and females (r2 = 0.021). A significant difference (p= 0.019) was observed for PP HDL-c in women (0.39 ± 0.10 g/L vs. men 0.33 ± 0.12 g/L) and also for PP apo A-I (women: 1.33 ± 0.27 g/L vs. men: 1.09 ± 0.34 g/L; p= 0.0003). According to gender and weight groups, our results indicated that female gender and overweight are associated with elevated PP HDL-c and PP apo A-I levels. However, obesity in women is related to high concentration of PP TG. The present study suggests that gender difference and weight classes are important factors that contribute to determining the postprandial responses, both for glucose and lipids, in type 2 diabetic patients.

Genetics of low density lipoprotein receptor-related protein 1 (lrp1) and postprandial lipaemia

Objectives: The Low density lipoprotein receptor-related protein 1 (LRP1) has been suggested to play an important role in the clearance of many molecules by the liver. These molecules are involved in various metabolic processes, including inflammation, coagulation, and energy metabolism (enzymes, clotting factors and lipoprotein particles) . LRP1 is a protein to which it has been also suggested a protective role in the development of atherosclerosis , but the exact mechanisms are not fully elucidated . Our objective was to evaluate the effect of three genetic variations (rs1800191, rs715948 and rs1799986) on postprandial lipid metabolism.

Effects of a plant sterol- or stanol-enriched high-fat meal on postprandial lipid and glucose metabolism in healthy subjects

Effects of a plant sterol- or stanol-enriched high-fat meal on postprandial lipid and glucose metabolism in healthy subjects

Patients with type 1 diabetes show signs of vascular dysfunction in response to multiple high-fat meals.

BackgroundA high-fat diet promotes postprandial systemic inflammation and metabolic endotoxemia. We investigated the effects of three consecutive high-fat meals on endotoxemia, inflammation, vascular function, and postprandial lipid metabolism in patients with type 1 diabetes.MethodsNon-diabetic controls (n = 34) and patients with type 1 diabetes (n = 37) were given three high-caloric, fat-containing meals during one day. Blood samples were drawn at fasting (8:00) and every two hours thereafter until 18:00. Applanation tonometry was used to assess changes in the augmentation index during the investigation day.ResultsThree consecutive high-fat meals had only a modest effect on serum LPS-activity levels and inflammatory markers throughout the day in both groups. Of note, patients with type 1 diabetes were unable to decrease the augmentation index in response to the high-fat meals. The most profound effects of the consecutive fat loads were seen in chylomicron and HDL-metabolism. The triglyceride-rich lipoprotein remnant marker, apoB-48, was elevated in patients compared to controls both at fasting (p = 0.014) and postprandially (p = 0.035). The activities of the HDL-associated enzymes PLTP (p < 0.001), and CETP (p = 0.007) were higher and paraoxonase (PON-1) activity, an anti-oxidative enzyme bound to HDL, decreased in patients with type 1 diabetes (p = 0.027).ConclusionsIn response to high-fat meals, early signs of vascular dysfunction alongside accumulation of chylomicron remnants, higher augmentation index, and decreased PON-1 activity were observed in patients with type 1 diabetes. The high-fat meals had no significant impact on postprandial LPS-activity in non-diabetic subjects or patients with type 1 diabetes suggesting that metabolic endotoxemia may be more central in patients with chronic metabolic disturbances such as obesity, type 2 diabetes, or diabetic kidney disease.

Genetically Low Triglycerides and Mortality: Further Support for “the Earlier the Better”?

In this issue of Clinical Chemistry , Mette Thomsen and colleagues contribute another gem from the treasure trove that is the Copenhagen City Heart Study (1). This mendelian randomization study builds upon the investigators' prior work linking genetically increased circulating triglyceride concentrations (a marker of remnant lipoproteins) with higher risk of ischemic heart disease (2). The present study gives the other bookend, linking genetically lower nonfasting circulating triglyceride concentrations with lower all-cause mortality. This work at the intersection of lipidology and preventive cardiology will be of interest to those working at many different scientific and clinical levels to improve the prevention of cardiovascular disease. Strengths of the study include the long duration of follow-up spanning 2 decades and the completeness of outcome ascertainment, with 100% of patients accounted for thanks to the Danish Central Person Register. In addition, the study takes advantage of a modern epidemiologic technique—the so-called “randomized trial of biomarkers”—mendelian randomization. In linking genetic information with biomarker concentrations and clinical outcomes, this technique is thought to limit much of the bias in traditional epidemiologic approaches and allow causal inference. An additional strength of this study is the nonfasting measurement of circulating triglyceride concentrations. Indeed, we as humans spend most of our lives in a nonfasting state and nonfasting triglyceride concentrations have a stronger association with incident cardiovascular events than fasting values (3). Triglycerides measured 2–4 h postprandially have an especially strong association with cardiovascular disease risk, illuminating the importance of postprandial lipid metabolism in cardiovascular disease. The authors took a 2-pronged approach, beginning with observational analyses of 13 957 persons who were followed for 24 years with 9991 deaths. A concentration-dependent association of nonfasting triglycerides with all-cause mortality was observed. Compared to the reference group with triglycerides of 266–442 mg/dL (3–5 mmol/L), there was a graded decrease in …

A whole-grain cereal-based diet lowers postprandial plasma insulin and triglyceride levels in individuals with metabolic syndrome

Background and aimUntil recently, very few intervention studies have investigated the effects of whole-grain cereals on postprandial glucose, insulin and lipid metabolism, and the existing studies have provided mixed results. The objective of this study was to evaluate the effects of a 12-week intervention with either a whole-grain-based or a refined cereal-based diet on postprandial glucose, insulin and lipid metabolism in individuals with metabolic syndrome. Methods and resultsSixty-one men and women age range 40–65 years, with the metabolic syndrome were recruited to participate in this study using a parallel group design. After a 4-week run-in period, participants were randomly assigned to a 12-week diet based on whole-grain products (whole-grain group) or refined cereal products (control group). Blood samples were taken at the beginning and end of the intervention, both fasting and 3 h after a lunch, to measure biochemical parameters. Generalized linear model (GLM) was used for between-group comparisons. Overall, 26 participants in the control group and 28 in the whole-grain group completed the dietary intervention. Drop-outs (five in the control and two in the whole-grain group) did not affect randomization. After 12 weeks, postprandial insulin and triglyceride responses (evaluated as average change 2 and 3 h after the meal, respectively) decreased by 29% and 43%, respectively, in the whole-grain group compared to the run-in period. Postprandial insulin and triglyceride responses were significantly lower at the end of the intervention in the whole-grain group compared to the control group (p = 0.04 and p = 0.05; respectively) whereas there was no change in postprandial response of glucose and other parameters evaluated. ConclusionsA twelve week whole-grain cereal-based diet, compared to refined cereals, reduced postprandial insulin and triglycerides responses. This finding may have implications for type 2 diabetes risk and cardiovascular disease.

Exercise and dietary-mediated reductions in postprandial lipemia.

Postprandial hyperlipemia produces long-term derangements in lipid/lipoprotein metabolism, vascular endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity which are strongly linked to atherogenesis. The purpose of this review is to (1) provide a qualitative analysis of the available literature examining the dysregulation of postprandial lipid metabolism in the presence of obesity, (2) inspect the role of adiposity distribution and sex on postprandial lipid metabolism, and (3) examine the role of energy deficit (exercise- and/or energy restriction-mediated), isoenergetic low-carbohydrate diets, and omega-3 (n-3) fatty acid supplementation on postprandial lipid metabolism. We conclude from the literature that central adiposity primarily accounts for sex-related differences in postprandial lipemia and that aerobic exercise attenuates this response in obese or lean men and women to a similar extent through potentially unique mechanisms. In contrast, energy restriction produces only mild reductions in postprandial lipemia suggesting that exercise may be superior to energy restriction alone as a strategy for lowering postprandial lipemia. However, isoenergetic very low-carbohydrate diets and n-3 fatty acid supplementation reduce postprandial lipemia indicating that macronutrient manipulations reduce postprandial lipemia in the absence of energy restriction. Therefore, interactions between exercise/energy restriction and alterations in macronutrient content remain top priorities for the field to identify optimal behavioral treatments to reduce postprandial lipemia.

Early Improvement of Postprandial Lipemia After Bariatric Surgery in Obese Type 2 Diabetic Patients

Bariatric surgery (BS) is able to positively influence fasting lipid profile in obese type 2 diabetic patients (T2DM), but no data is available on the impact of BS on postprandial lipid metabolism neither on its relation with incretin hormones. We evaluated the short-term (2 weeks) effects of BS on fasting and postprandial lipid metabolism in obese T2DM patients and the contribution of changes in active GLP-1. We studied 25 obese T2DM patients (age = 46 ± 8 years, BMI = 44 ± 7 kg/m2), of which 15 underwent sleeve gastrectomy and 10 underwent gastric bypass. Lipid and incretin hormone concentrations were evaluated for 3 h after ingestion of a liquid meal before and 2 weeks after BS. After BS, there was a significant reduction in body weight (p < 0.001), fasting plasma glucose (p < 0.001), fasting plasma insulin (p < 0.05), HOMA-IR (p < 0.001), and fasting plasma lipids (p < 0.05). The meal response of plasma triglycerides, total cholesterol, and HDL cholesterol was significantly lower compared to pre-intervention (p < 0.05, p < 0.001). In particular, the incremental area under the curve (IAUC) of plasma triglycerides decreased by 60% (p < 0.005). The meal-stimulated response of active GLP-1 increased, reaching a statistical significance (p < 0.001). BS leads to an early improvement of fasting and postprandial lipemia. The fall in fasting triglycerides is associated with an improvement of insulin resistance, while the reduction of postprandial lipemia is likely related to reduced intestinal lipid absorption consequent to bariatric surgery.

Short-Term Effect of Pitavastatin Treatment on Glucose and Lipid Metabolism and Oxidative Stress in Fasting and Postprandial State Using a Test Meal in Japanese Men

Introduction. The objective of this study was to clarify how pitavastatin affects glucose and lipid metabolism, renal function, and oxidative stress. Methods. Ten Japanese men (average age of 33.9 years) were orally administered 2 mg of pitavastatin for 4 weeks. Postprandial glucose, lipoprotein metabolism, and oxidative stress markers were evaluated at 0 and 4 weeks of pitavastatin treatment (2 mg once daily) with a test meal consisting of total calories: 460 kcal, carbohydrates: 56.5 g (226 kcal), protein: 18 g (72 kcal), lipids: 18 g (162 kcal), and NaCl: 1.6 g. Metabolic parameters were measured at 0, 60, and 120 minutes after test meal ingestion. Results. After administration of pitavastatin, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, arachidonic acid, insulin, and adjusted urinary excretion of uric acid decreased, whereas creatinine clearance (C Cr) and uric acid clearance (C UA) increased. And postprandial versus fasting urine 8-hydroxydeoxyguanosine remained unchanged, while postprandial versus fasting isoprostane decreased after pitavastatin treatment. Next, we compared postprandial glucose and lipid metabolism after test meal ingestion before and after pitavastatin administration. Incremental areas under the curve significantly decreased for triglycerides (P < 0.05) and remnant-like particle cholesterol (P < 0.01), while those for apolipoprotein E (apoE), glucose, insulin, and high-sensitivity C-reactive protein remained unchanged. Conclusion. Pitavastatin improves postprandial oxidative stress along with hyperlipidemia.

Walnut-enriched diet reduces fasting non-HDL-cholesterol and apolipoprotein B in healthy Caucasian subjects: A randomized controlled cross-over clinical trial

BackgroundWalnut consumption is associated with reduced risk of coronary heart disease (CHD). ObjectiveWe assessed the effect of walnuts on lipid and glucose metabolism, adipokines, inflammation and endothelial function in healthy Caucasian men and postmenopausal women ≥50years old. DesignForty subjects (mean±SEM: age 60±1years, BMI 24.9±0.6kg/m2; 30 females) were included in a controlled, cross-over study and randomized to receive first a walnut-enriched (43g/d) and then a Western-type (control) diet or vice-versa, with each lasting 8weeks and separated by a 2-week wash-out. At the beginning and end of each diet phase, measurements of fasting values, a mixed meal test and an assessment of postprandial endothelial function (determination of microcirculation by peripheral artery tonometry) were conducted. Area under the curve (AUC), incremental AUC (iAUC) and treatment×time interaction (shape of the curve) were evaluated for postprandial triglycerides, VLDL-triglycerides, chylomicron-triglycerides, glucose and insulin. ResultsCompared with the control diet, the walnut diet significantly reduced non-HDL-cholesterol (walnut vs. control: −10±3 vs. −3±2mg/dL; p=0.025) and apolipoprotein-B (−5.0±1.3 vs. −0.2±1.1mg/dL; p=0.009) after adjusting for age, gender, BMI and diet sequence. Total cholesterol showed a trend toward reduction (p=0.073). Fasting VLDL-cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides and glucose, insulin, HOMA-IR, and HbA1c did not change significantly. Similarly, fasting adipokines, C-reactive protein, biomarkers of endothelial dysfunction, postprandial lipid and glucose metabolism and endothelial function were unaffected. ConclusionDaily consumption of 43g of walnuts for 8weeks significantly reduced non-HDL-cholesterol and apolipoprotein-B, which may explain in part the epidemiological observation that regular walnut consumption decreases CHD risk.

Effects of breads of varying carbohydrate quality on postprandial glycaemic, incretin and lipidaemic response after first and second meals in adults with diet-controlled type 2 diabetes

Bread formulations of sprouted grain, whole grain and sourdough fermentation can influence metabolism. Postprandial carbohydrate and lipid metabolism in type 2 diabetes (T2D) is aberrant, rationalising identification of breads to improve these responses. The effect of breads of varying carbohydrate quality on postprandial glycaemic and lipid parameters was examined before and after a first and second meal. Twelve adults with diet-controlled T2D consumed 50g of available carbohydrate from 4 breads (3-grain sprouted sourdough (SPR), whole-grain sourdough (WG), white sourdough (SD), control white (WB)), in a randomised crossover design. Blood glucose incremental area-under-the-curve (iAUC) was significantly lower after SPR compared to all breads. Second meal plasma insulin iAUC was significantly lower after SPR compared to SD and WB; serum apolipoprotein B-100 iAUC was lower with SD compared to WB; but no other significant differences were found. Bread made from sprouted grains can improve postprandial glycaemic responses in adults with T2D.

Glucose-dependent insulinotropic polypeptide has impaired effect on abdominal, subcutaneous adipose tissue metabolism in obese subjects

Glucose-dependent insulinotropic polypeptide (GIP) appears to have a role in lipid metabolism. Recently, we showed that GIP in combination with hyperinsulinemia and hyperglycemia increases triglyceride uptake in abdominal, subcutaneous adipose tissue in lean humans. It has been suggested that increased GIP secretion in obesity will promote lipid deposition in adipose tissue. In light of the current attempts to employ GIP antagonists in the treatment and prevention of human obesity, the present experiments were performed in order to elucidate whether the adipose tissue lipid metabolism would be enhanced or blunted during a GIP, hyperinsulinemic and hyperglycemic (HI-HG) clamp in obese subjects with either normal glucose tolerance (NGT) or impaired glucose tolerance (IGT). Sixteen obese (BMI>30 kg m(-2)) subjects were divided into two groups, based on their plasma glucose response to an oral glucose challenge: (i) NGT and (ii) IGT. Abdominal, subcutaneous adipose tissue lipid metabolism was studied by conducting measurements of arteriovenous concentrations of metabolites and regional adipose tissue blood flow (ATBF) during GIP (1.5 pmol kg(-1) min(-1)) in combination with a HI-HG clamp. In both groups, ATBF responses were significantly lower than what we have found previously in healthy, lean subjects (P<0.0001). The flow response was significantly lower in the IGT group than in the NGT group (P=0.03). It was not possible to show any increase in the lipid deposition in adipose tissue under the applied experimental conditions and likewise the circulating triglyceride (TAG) concentrations remained constant. The applied GIP, HI-HG clamp did not induce any changes in TAG uptake in adipose tissue in obese subjects. This may be due to a blunted increase in ATBF. These experiments therefore suggest that GIP does not have a major role in postprandial lipid metabolism in obese subjects.

Novel Insights Into the Regulation of Postprandial Lipemia by Glucagon-Like Peptides: Significance for Diabetes

Glucagon-like peptide-1 (GLP-1) and GLP-2 are peptide hormones encoded by the proglucagon gene that are cosecreted in equimolar amounts from enteroendocrine L-cells of the intestine in response to nutrients, primarily carbohydrates and fats (1). Most is known about GLP-1, which stimulates the pancreatic secretion of insulin in a glucose-dependent manner while inhibiting the secretion of glucagon, gastric emptying, and satiety. This tonic effect maintains glucose homeostasis and is chiefly controlled by the enzymatic degradation of the peptide in the circulation by dipeptidyl peptidase-4 (DPP-4) (2). This has led to the development of new therapies for diabetes, including GLP-1 receptor analogs and inhibitors of DPP-4 (3). By contrast to GLP-1, the physiological and therapeutic roles of GLP-2 are less clear. GLP-2 inhibits postprandial gastric motility/secretion and intestinal hexose transport and has a trophic effect on intestinal epithelium that implies a specific role in intestinal repair processes (4). GLP-2 may antagonize the effects of GLP-1 on glucose homeostasis by enhancing the pancreatic release of glucagon but could also have a cooperative, short-term effect on satiety. Its biological actions are mediated by a specific G-protein–coupled receptor. Recent studies have also suggested that GLP-1 and possibly GLP-2 may be involved in regulating fat absorption and chylomicron biogenesis (5–8), pointing to a regulatory role in postprandial lipid metabolism. This has implications for atherogenesis and vascular disease in diabetes and insulin-resistant states. GLP-1 may improve while GLP-2 may aggravate postprandial lipemia, but exactly how these biological actions are intertwined in health and disease remains unclear. In this issue of Diabetes , Adeli and colleagues …

Effects of milk and milk constituents on postprandial lipid and glucose metabolism in overweight and obese men

Studies have suggested that two major milk constituents, casein and Ca, favourably affect postprandial responses. However, effects of milk on postprandial metabolism are unknown. We therefore investigated effects of using milk with a fat-containing meal on lipid and glucose responses in overweight men. To identify the constituent responsible for possible effects, we also studied responses to Ca and protein. A total of sixteen men (BMI .27 kg/m2) participated in four postprandial tests. They consumed a breakfast (44 g of fat) plus a drink: a control drink, low-fat milk or a protein and Ca drink (500 ml). Blood samples were taken before the meals and at regular time points during 6 h thereafter. Compared with control, the incremental AUC (iAUC) for serum TAG was increased by 44% after the protein meal (P¼0·015). Although the iAUC were not different (P¼0·051), peak glucose concentrations were reduced by 24% after protein intake, as compared with control (P¼0·021). The decrease of 18% after milk intake did not reach statistical significance. Compared with the milk meal, the iAUC for insulin was 52% lower after the control meal (P¼0·035) and 51% after the protein meal (P¼0·005). The present results indicate that the intake of milk with a fat-containing meal enhances postprandial TAG and insulin responses and may blunt glucose increases. The protein fraction of milk seems to be the main determinant for the effects on TAG and glucose. Ca did not change any of the postprandial responses.

Effects of miglitol &lt;i&gt;versus&lt;/i&gt; sitagliptin on postprandial glucose and lipoprotein metabolism in patients with type 2 diabetes mellitus

Postprandial hyperglycemia and/or hyperlipidemia can contribute to development of atherosclerosis in patients with type 2 diabetes mellitus (T2DM). The objective of this study was to compare the effects of miglitol and sitagliptin on postprandial glucose and lipid metabolism in patients with T2DM. Thirty-five patients with T2DM were randomized to 2 groups receiving miglitol (150 mg/day) or sitagliptin (50 mg/day). Serum variables related to glucose and lipid metabolism were measured before and after treatment for 10 weeks and at 0, 60, and 120 min using a cookie-loading test (CLT). After 10 weeks of treatment, miglitol (n = 16) and sitagliptin (n = 18) caused a similarly significant decrease in hemoglobin A1c (mean: 7.6% to 7.3% versus 8.0% to 7.6%) and a significant increase in fasting insulin levels, with a greater increase observed in the miglitol group than in the sitagliptin group (p=0.03). In addition, a significant decrease in the change in glucose levels after the CLT was observed in both groups, with a greater decrease observed in the miglitol group than in the sitagliptin group (p=0.02). The miglitol group also showed a greater decrease in the change in insulin levels after the CLT than the sitagliptin group (p<0.01). The lipid and lipoprotein levels did not show any significant differences between the groups after the CLT. Our results suggested that miglitol and sitagliptin treatment resulted in similar glycemic control but that a greater decrease in postprandial glucose and insulin levels was observed with miglitol compared with sitagliptin in patients with T2DM.

The strange and critical intersection of hepatitis C and lipoprotein metabolism: “C-zing” the oil

Since its discovery in 1989, a substantial amount of research has emerged regarding the close association of hepatitis C virus (HCV) replication and hepatic lipoprotein metabolism. Even before the identification of the HCV virus, a link to fat metabolism was suspected based on clinical observations regarding steatosis as a common feature of what used to be known as “non-A, non-B hepatitis.”1 This relationship was later extended in studies that revealed that HCV-infected patients with steatosis often lack common risk factors for fatty liver, such as obesity.2 These early observations, along with subsequent studies that identified circulating viral particles in low-density, more-buoyant plasma fractions (partitioned with plasma centrifugation in sucrose or iodixanol gradients), fueled a now extensive and growing body of literature on this key aspect of HCV replication.3 Investigations performed over the past 23 years have defined replicative pathways of HCV involving mechanisms and biochemical pathways right out of the “play book” of fatty liver disease (FLD).

Dietary fat manipulation has a greater impact on postprandial lipid metabolism than the apolipoprotein E (epsilon) genotype–insights from the SATgenε study

Our aim was to determine the effects of chronic dietary fat manipulation on postprandial lipaemia according to apolipoprotein (APO)E genotype. Men (mean age 53 (SD 9) years), prospectively recruited for the APOE genotype (n = 12 E3/E3, n = 11 E3/E4), were assigned to a low fat (LF), high fat, high-saturated fat (HSF), and HSF diet with 3.45 g/day docosahexaenoic acid (HSF-DHA), each for an 8-week period in the same order. At the end of each dietary period, a postprandial assessment was performed using a test meal with a macronutrient profile representative of that dietary intervention. A variable postprandial plasma triacylglycerol (TAG) response according to APOE genotype was evident, with a greater sensitivity to the TAG-lowering effects of DHA in APOE4 carriers (p ≤ 0.005). There was a lack of an independent genotype effect on any of the lipid measures. In the groups combined, dietary fat manipulation had a significant impact on lipids in plasma and Svedberg flotation rate (S(f) ) 60-400 TAG-rich lipoprotein fraction, with lower responses following the HSF-DHA than HSF intervention (p < 0.05). Although a modest impact of APOE genotype was observed on the plasma TAG profile, dietary fat manipulation emerged as a greater modulator of the postprandial lipid response in normolipidaemic men.

Update on perilipin polymorphisms and obesity

Perilipin proteins were discovered in the adipocyte, where they regulate lipid storage and lipolysis. Animal knockout models provided initial evidence of the critical role of perilipin 1, the most abundant of the adipocyte proteins, in energy and glucose metabolism. During a decade of study, genetic variation in perilipin 1 has been consistently but not invariably associated with body weight and obesity-related complications. Related phenotypes such as postprandial lipid metabolism and aerobic fitness are also modulated by perilipin 1 genotype, consistent with earlier metabolic studies. Investigations of gene-diet interactions, together with gene expression studies, have yielded increased understanding, but important questions about causal variants and mechanisms remain. The newest work examines perilipin 4, an adipocyte regulator of triglyceride synthesis and packaging. The novel discovery that a perilipin 4 variant creates a binding site for regulation of the perilipin gene (PLIN) by microRNA suggests intriguing new possibilities for additional mechanistic investigations of other perilipin proteins.