Postprandial Lipid Metabolism Research Articles

Effects of interrupting sitting with different activity bouts on postprandial lipemia: A randomized crossover trial.

To determine whether interrupting prolonged sitting with three different activity breaks has both acute and chronic effects on postprandial lipid metabolism immediately after the activity-break period and on the following day, this study is a secondary analysis of an experimental research, which included 16 sedentary healthy adults (7 men, 24±3years, BMI 22.2±2.3kg/m2 ) who completed four 26-h laboratory trials. Participants spent 22.5hours in a whole room calorimeter for testing energy expenditure (EE), including a 9-h activity-break period: (a) 9-h prolonged sitting (SIT); (b) 3minutes of brisk walking (60% VO2max ) in between every 30-min sitting bout (WALK3), (c) 5minutes every 45-min (WALK5), and (d) 8minutes every 60-min (WALK8). Total area under the curve (tAUC) and incremental AUC (iAUC) for 2-h postprandial serum triglyceride (TG) levels and non-esterified fatty acid (NEFA) levels were examined immediately after the 9-h trial (post-dinner) and the next morning (post-breakfast). WALK8 reduced the post-breakfast TG tAUC by 11% (P=.041) relative to SIT, and the effect was attenuated after adjustment for EE. The tAUC and iAUC indicated no significant treatment effects on post-dinner TG and NEFA, and post-breakfast NEFA in any of the activity-break trials. EE was positively associated with the post-breakfast NEFA iAUC (unstandardized β=0.17µmol/L/MJ [0.05-0.28], P=.006). There was a chronic effect of interrupting sitting with short bouts (8minutes) of brisk walking every 60minutes on postprandial lipemia the following morning after intervention, and higher activity bout-induced EE may be more effective in sedentary, healthy adults.

High-intensity interval exercise in the cold regulates acute and postprandial metabolism.

High-intensity interval exercise (HIIE) has been shown to be more effective than moderate-intensity exercise for increasing acute lipid oxidation and lowering blood lipids during exercise and postprandially. Exercise in cold environments is also known to enhance lipid oxidation; however, the immediate and long-term effects of HIIE exercise in cold are unknown. The purpose of this study was to examine the effects cold stress during HIIE on acute exercise metabolism and postprandial metabolism. Eleven recreationally active individuals (age: 23 ± 3 yr, weight: 80 ± 9.7 kg, V̇O2peak: 39.2 ± 5.73 mL·kg-1·min-1) performed evening HIIE sessions (10 × 60 s cycling, 90% V̇O2peak interspersed with 90 s active recovery, 30% V̇O2peak) in thermoneutral (HIIE-TN, control; 21°C) and cold environment (HIIE-CO; 0°C), following a balanced crossover design. The following morning, participants consumed a high-fat meal. Indirect calorimetry was used to assess substrate oxidation, and venous blood samples were obtained to assess changes in noncellular metabolites. During acute exercise, lipid oxidation was higher in HIIE-CO (P = 0.002) without differences in V̇O2 and energy expenditure (P ≥ 0.162) between conditions. Postprandial V̇O2, lipid and CHO oxidation, plasma insulin, and triglyceride concentrations were not different between conditions (P > 0.05). Postprandial blood LDL-C levels were higher in HIIE-CO 2 h after the meal (P = 0.003). Postprandial glucose area under curve was 49% higher in HIIE-CO versus HIIE-TN (P = 0.034). Under matched energy expenditure conditions, HIIE demonstrated higher lipid oxidation rates during exercise in the cold; but only marginally influenced postprandial lipid metabolism the following morning. In conclusion, HIIE in the cold seemed to be less favorable for postprandial lipid and glycemic responses.NEW & NOTEWORTHY This is the first known study to investigate the effects of cold ambient temperatures on acute metabolism during high-intensity interval exercise, as well as postprandial metabolism the next day. We observed that high-intensity interval exercise in a cold environment does change acute metabolism compared to a thermoneutral environment; however, the addition of a cold stimulus was less favorable for postprandial metabolic responses the following day.

Rapeseed Lecithin Increases Lymphatic Lipid Output and α-Linolenic Acid Bioavailability in Rats

Soybean lecithin, a plant-based emulsifier widely used in food, is capable of modulating postprandial lipid metabolism. With arising concerns of sustainability, alternative sources of vegetal lecithin are urgently needed, and their metabolic effects must be characterized. We evaluated the impact of increasing doses of rapeseed lecithin (RL), rich in essential α-linolenic acid (ALA), on postprandial lipid metabolism and ALA bioavailability in lymph-cannulated rats. Male Wistar rats (8 weeks old) undergoing a mesenteric lymph duct cannulation were intragastrically administered 1 gof an oil mixture containing 4% ALA and 0, 1, 3, 10, or 30% RL (5 groups). Lymph fractions were collected for 6 h.Lymphlipidsandchylomicrons (CMs) were characterized. The expression of genes implicated in intestinal lipid metabolism was determined in the duodenum at 6 h.Datawasanalyzedusing either sigmoidal or linear mixed-effects models, or one-way ANOVA, where appropriate. RL dose-dependently increased the lymphatic recovery (AUC) of total lipids (1100 μg/mL·hperadditional RL%; P=0.010) and ALA (50 μg/mL·hperadditional RL%; P=0.0076). RL induced a faster appearance of ALA in lymph, as evidenced by the exponential decrease of the rate of appearance of ALA with RL (R2=0.26; P=0.0064). Although the number of CMs was unaffected by RL, CM diameter was increased in the 30%-RL group, compared to the control group (0% RL), by 86% at 3-4 h(P=0.065) and by 81% at 4-6 h(P=0.0002) following administration. This increase was positively correlated with the duodenal mRNA expression of microsomal triglyceride transfer protein (Mttp; ρ= 0.63; P=0.0052). The expression of Mttp and secretion-associated, ras-related GTPase 1 gene homolog B (Sar1b, CM secretion), carnitine palmitoyltransferase IA (Cpt1a) and acyl-coenzyme A oxidase 1 (Acox1, beta-oxidation), and fatty acid desaturase 2 (Fads2, bioconversion of ALA into long-chain n-3 PUFAs) were, respectively, 49%, 29%, 74%, 48%, and 55% higher in the 30%-RL group vs. the control group (P<0.05). In rats, RL enhanced lymphatic lipid output, as well as the rate of appearance of ALA, which may promote its subsequent bioavailability and metabolic fate.

Time-of-day and Meal Size Effects on Clinical Lipid Markers

Dyslipidemia and cardiovascular disease are common in shift workers and eating at night may contribute to this pathophysiology. To examine the effects of eating at different times of day on lipid profiles. Two 24-hour baseline days with 8 hours of sleep, 3 meals (breakfast, lunch, dinner) and a snack, followed by a 40-hour constant routine (CR) with hourly isocaloric meals. Intensive Physiological Monitoring Unit, Brigham and Women's Hospital. Twenty-one healthy adults [23.4 ± 2.7 years, 5F]. Forty-hour CR. A standard clinical lipid panel, consisting of total cholesterol, triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C), was assayed in blood samples collected 4-hourly across ~4 days. When participants ate at night, levels of TG were similar to eating during the day, however, these levels at night were reached with consuming approximately half the calories. Additionally, 24-hour levels of TG were 10% higher when meals were consumed hourly across 24 hours compared to consuming a typical 3-meal schedule while awake during the day and sleeping at night. The endogenous circadian rhythms of TG, which peaked at night, were shifted earlier by ~10 hours under baseline conditions, whereas the rhythms in total cholesterol, HDL-C, and LDL-C remained unchanged and peaked in the afternoon. The time-of-day dependency on postprandial lipid metabolism, which leads to hypersensitivity in TG responses when eating at night, may underlie the dyslipidemia and elevated cardiovascular disease risk observed in shift workers.

Body composition, but not insulin resistance, influences postprandial lipemia in patients with Turner's syndrome.

The aim of the present study was to examine the influence of body composition and insulin resistance on the magnitude of postprandial lipemia in patients with Turner's syndrome receiving oral versus transdermal estrogen replacement. Twenty-five patients with Turner's syndrome receiving oral or transdermal estrogen replacement were evaluated for body mass index, waist-to-hip and waist-to-height ratios, fasting glycemia, insulin, body composition (dual-energy X-ray absorptiometry), and postprandial lipid metabolism. For statistical analysis, we used parametric tests to compare numeric variables between the two subgroups. We observed no difference in postprandial triglyceride levels between patients receiving oral versus transdermal hormone replacement therapy. The postprandial triglycerides increment correlated positively with the percentage of total fat mass (p=0.02) and android fat mass (p=0.02) in the transdermal group. In the oral estrogen group, a positive correlation was observed between the increment in postprandial triglycerides and waist-to-hip (p=0.15) and waist-to-height (p=0.009) ratios. No association was observed between the estrogen replacement route and insulin resistance evaluated by the homeostatic model assessment-insulin resistance (HOMA-IR) index (p=0.19 and p=0.65 for the oral and transdermal groups, respectively). We concluded that body composition and anthropometric characteristics possibly affect the extent of postprandial lipemia independently from the route of estrogen replacement.

The Impact of Dietary Glycemic Index and Glycemic Load on Postprandial Lipid Kinetics, Dyslipidemia and Cardiovascular Risk.

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

Acute and chronic improvement in postprandial glucose metabolism by a diet resembling the traditional Mediterranean dietary pattern: Can SCFAs play a role?

Postprandial metabolic abnormalities are considered important and independent risk factors for cardiovascular diseases. However, the effects of the Mediterranean diet on postprandial metabolism and the mechanism underpinning the effects on clinical variables have not been exhaustively explored. Therefore, the aims of the present study were to evaluate the acute and medium-term effects (8 weeks) on postprandial glucose and lipid metabolism of a diet resembling a typical Mediterranean diet (Med-D) compared to a western-type diet (Control-D), and the mechanisms underlying those effects. Twenty-nine overweight/obese individuals of both genders, aged 20-60 years, were enrolled and randomly assigned to two isoenergetic dietary interventions: 1) a Med-D (n=16), and 2) a Control-D (n=13). Adherence to the dietary interventions was assessed by a 7-day food record. A meal test resembling the assigned diet was performed at baseline and after 8 weeks of intervention. Blood samples at fasting and over 4-h after the meal were collected to assess metabolic parameters and short chain fatty acid (SCFA) levels. Fecal samples were also collected to evaluate the microbiota composition. Glucose and insulin responses were significantly reduced at baseline after the Med test meal compared to the Control meal (p<0.05) and this effect was strengthened after 8 weeks of intervention with the Mediterranean diet (p<0.05); together with an improvement in OGIS. At the end of the intervention, postprandial plasma butyric acid incremental area under the curve (IAUC) was significantly increased in the Med-D group (p=0.019) and correlated inversely with plasma insulin IAUC and directly with oral glucose insulin sensitivity (OGIS) (r:-0.411, p=0.046 and r: 0.397, p=0.050 respectively). These metabolic changes were accompanied by significant changes in gut microbiota, such as an increase in the relative abundance of Intestinimonas butyriciproducens and Akkermansia muciniphila (p<0.05) in the Med-D compared to Control-D group. Our study provides strong evidence that a diet resembling the traditional Med-D improves postprandial glucose metabolism and insulin sensitivity. Furthermore, the study highlights a possible involvement of gut microbiota metabolites - such as butyric acid, and of dietary fiber as a precursor - in improving glucose metabolism and insulin sensitivity.

Differential Metabolic Impact of Natural Food-Grade Emulsifiers Rich in Alpha-Linolenic Acid

Abstract Objectives Dietary synthetic emulsifiers have recently been shown to promote metabolic syndrome and considerably alter gut microbiota. Conversely, natural emulsifiers such as milk polar lipids (PL) are associated with beneficial metabolic effects. The effects of plant PL remain, however, poorly described. Our objective was to evaluate, using two complimentary rodent models, the impact of nutritional doses of lecithin (≤10%) of vegetal sources alternative to soy on gut microbiota, postprandial lipid metabolism, and the bioavailability of an essential plant lipid, alpha-linolenic acid (ALA). Methods For 5 days, male Swiss mice (n = 60) were fed normolipidic diets (identical ALA content) containing 0, 1, 3 or 10% rapeseed lecithin (RL) or 10% soy lecithin. Following an overnight fast, the mice were force-fed the same oil mix and euthanised after 90 min. As a mechanistic study, male Wistar rats (n = 30) with mesenteric duct cannulation were fed 5 oil mixtures containing 0 to 20% RL. Lymph fractions were collected up to 6 h post-gavage. Plasma and lymph lipid composition was determined using GC-FID, chylomicron (CM) size using light-scattering spectroscopy, and intestinal gene expression and faecal microbiota composition by RT-qPCR. Results In mice, the consumption of lecithin significantly increased levels of faecal Clostridium leptum (P &amp;lt; 0.001), regardless of lecithin origin or dose. The partial replacement of oil with lecithin did not significantly alter plasma total lipids nor the expression of genes of intestinal lipid absorption. The percentage of ALA in plasma triglycerides was significantly higher in the 10% RL group compared to other groups (P &amp;lt; 0.05). In rats, RL significantly and dose-dependently increased the rate of appearance (P &amp;lt; 0.01) and concentration of ALA in lymph (P &amp;lt; 0.01). 20% RL additionally increased CM size and expression of genes of CM secretion (Mttp, Sar1b; P &amp;lt; 0.05). Conclusions Our results reveal that, whereas both rapeseed and soy lecithin improved gut microbiota composition by increasing the anti-inflammatory Clostridium leptum bacterial group, only rapeseed lecithin enhanced ALA bioavailability. This study illustrates the importance of considering the use of natural emulsifiers, especially rapeseed lecithin, as plant-based food ingredients with potential health benefits. Funding Sources ANRT and UMT ACTIA BALI.

Bile acid treatment and FXR agonism lower postprandial lipemia in mice.

Postprandial dyslipidemia is a common feature of insulin-resistant states and contributes to increased cardiovascular disease risk. Recently, bile acids have been recognized beyond their emulsification properties as important signaling molecules that promote energy expenditure, improve insulin sensitivity, and lower fasting lipemia. Although bile acid receptors have become novel pharmaceutical targets, their effects on postprandial lipid metabolism remain unclear. Here, we investigated the potential role of bile acids in regulation of postprandial chylomicron production and triglyceride excursion. Healthy C57BL/6 mice were given an intraduodenal infusion of taurocholic acid (TA) under fat-loaded conditions, and circulating lipids were measured. Targeting of bile acid receptors was achieved with GW4064, a synthetic agonist to the farnesoid X receptor (FXR), and deoxycholic acid (DCA), an activator of the Takeda G-protein-coupled receptor 5. TA, GW4064, and DCA treatments all lowered postprandial lipemia. FXR agonism also reduced intestinal triglyceride content and activity of microsomal triglyceride transfer protein, involved in chylomicron assembly. Importantly, TA (but not DCA) effects were largely lost in FXR knockout mice. These bile acid effects are reminiscent of the antidiabetic hormone glucagon-like peptide-1 (GLP-1). Although the GLP-1 receptor agonist exendin-4 retained its ability to acutely lower postprandial lipemia during bile acid sequestration and FXR deficiency, it did raise hepatic expression of the rate-limiting enzyme for bile acid synthesis. Bile acid signaling may be an important mechanism of controlling dietary lipid absorption, and bile acid receptors may constitute novel targets for the treatment of postprandial dyslipidemia.NEW & NOTEWORTHY We present new data suggesting potentially important roles for bile acids in regulation of postprandial lipid metabolism. Specific bile acid species, particularly secondary bile acids, were found to markedly inhibit absorption of dietary lipid and reduce postprandial triglyceride excursion. These effects appear to be mediated via bile acid receptors, farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5). Importantly, bile acid signaling may trigger glucagon-like peptide-1 (GLP-1) secretion, which may in turn mediate the marked inhibitory effects on dietary fat absorption.

Effects of Lactobacillus plantarum Q180 on Postprandial Lipid Levels and Intestinal Environment: A Double-Blind, Randomized, Placebo-Controlled, Parallel Trial.

Probiotics can improve the intestinal environment by enhancing beneficial bacteria to potentially regulate lipid levels; however, the underlying mechanisms remain unclear. The aim of this study was to investigate the effect of Lactobacillus plantarum Q180 (LPQ180) on postprandial lipid metabolism and the intestinal microbiome environment from a clinical perspective. A double-blind, randomized, placebo-controlled study was conducted including 70 participants of both sexes, 20 years of age and older, with healthy blood triacylglyceride (TG) levels below 200 mg/dL. Treatment with LPQ180 for 12 weeks significantly decreased LDL-cholesterol (p = 0.042) and apolipoprotein (Apo)B-100 (p = 0.003) levels, and decreased postprandial maximum concentrations (Cmax) and areas under the curve (AUC) of TG, chylomicron TG, ApoB-48, and ApoB-100. LPQ180 treatment significantly decreased total indole and phenol levels (p = 0.019). In addition, there was a negative correlation between baseline microbiota abundance and lipid marker change, which was negatively correlated with metabolites. This study suggests that LPQ180 might be developed as a functional ingredient to help maintain healthy postprandial lipid levels through modulating gut environment.

Effects of Chocolate Containing D-allulose on Postprandial Lipid and Carbohydrate Metabolism in Young Japanese Women

Effects of Chocolate Containing D-allulose on Postprandial Lipid and Carbohydrate Metabolism in Young Japanese Women

A single bout of resistance exercise improves postprandial lipid metabolism in overweight/obese men with prediabetes.

Prediabetes is associated with postprandial hypertriacylglycerolaemia. Resistance exercise acutely lowers postprandial plasma triacylglycerol (TG); however, the changes in lipid metabolism that mediate this reduction are poorly understood. The aim of this study was to identify the constitutive metabolic mechanisms underlying the changes in postprandial lipid metabolism after resistance exercise in obese men with prediabetes. We evaluated the effect of a single bout of whole-body resistance exercise (seven exercises, three sets, 10-12 repetitions at 80% of one-repetition maximum) on postprandial lipid metabolism in ten middle-aged (50 ± 9years), overweight/obese (BMI: 33 ± 3kg/m2), sedentary men with prediabetes (HbA1c >38 but <48mmol/mol [>5.7% but <6.5%]), or fasting plasma glucose >5.6mmol/l but <7.0mmol/l or 2h OGTT glucose >7.8mmol/l but <11.1mmol/l). We used a randomised, crossover design with a triple-tracer mixed meal test (ingested [(13C4)3]tripalmitin, i.v. [U-13C16]palmitate and [2H5]glycerol) to evaluate chylomicron-TG and total triacylglycerol-rich lipoprotein (TRL)-TG kinetics. We used adipose tissue and skeletal muscle biopsies to evaluate the expression of genes regulating lipolysis and lipid oxidation, skeletal muscle respirometry to evaluate oxidative capacity, and indirect calorimetry to assess whole-body lipid oxidation. The single bout of resistance exercise reduced the lipaemic response to a mixed meal in obese men with prediabetes without changing chylomicron-TG or TRL-TG fractional clearance rates. However, resistance exercise reduced endogenous and meal-derived fatty acid incorporation into chylomicron-TG and TRL-TG. Resistance exercise also increased whole-body lipid oxidation, skeletal muscle mitochondrial respiration, oxidative gene expression in skeletal muscle, and the expression of key lipolysis genes in adipose tissue. A single bout of resistance exercise improves postprandial lipid metabolism in obese men with prediabetes, which may mitigate the risk for cardiovascular disease and type 2 diabetes.

The Role of the Gut Microbiota in Lipid and Lipoprotein Metabolism.

Both environmental and genetic factors contribute to relative species abundance and metabolic characteristics of the intestinal microbiota. The intestinal microbiota and accompanying microbial metabolites differ substantially in those who are obese or have other metabolic disorders. Accumulating evidence from germ-free mice and antibiotic-treated animal models suggests that altered intestinal gut microbiota contributes significantly to metabolic disorders involving impaired glucose and lipid metabolism. This review will summarize recent findings on potential mechanisms by which the microbiota affects intestinal lipid and lipoprotein metabolism including microbiota dependent changes in bile acid metabolism which affects bile acid signaling by bile acid receptors FXR and TGR5. Microbiota changes also involve altered short chain fatty acid signaling and influence enteroendocrine cell function including GLP-1/GLP-2-producing L-cells which regulate postprandial lipid metabolism.

A computational model of postprandial adipose tissue lipid metabolism derived using human arteriovenous stable isotope tracer data.

Given the association of disturbances in non-esterified fatty acid (NEFA) metabolism with the development of Type 2 Diabetes and Non-Alcoholic Fatty Liver Disease, computational models of glucose-insulin dynamics have been extended to account for the interplay with NEFA. In this study, we use arteriovenous measurement across the subcutaneous adipose tissue during a mixed meal challenge test to evaluate the performance and underlying assumptions of three existing models of adipose tissue metabolism and construct a new, refined model of adipose tissue metabolism. Our model introduces new terms, explicitly accounting for the conversion of glucose to glyceraldehye-3-phosphate, the postprandial influx of glycerol into the adipose tissue, and several physiologically relevant delays in insulin signalling in order to better describe the measured adipose tissues fluxes. We then applied our refined model to human adipose tissue flux data collected before and after a diet intervention as part of the Yoyo study, to quantify the effects of caloric restriction on postprandial adipose tissue metabolism. Significant increases were observed in the model parameters describing the rate of uptake and release of both glycerol and NEFA. Additionally, decreases in the model’s delay in insulin signalling parameters indicates there is an improvement in adipose tissue insulin sensitivity following caloric restriction.

Metabolomics Reveal Altered Postprandial Lipid Metabolism After a High-Carbohydrate Meal in Men at High Genetic Risk of Diabetes

The transcription factor 7-like 2 (TCF7L2) gene confers one of the strongest genetic predispositions to type 2 diabetes, but diabetes development can be modified by diet. The aim of our study was to evaluate postprandial metabolic alterations in healthy men with a high genetic risk of diabetes, after two meals with varying macronutrient content. The study was conducted in 21 homozygous nondiabetic men carrying the high-risk (HR, n=8, age: 31.2±6.3 y, body mass index (BMI, kg/m2) 28.5±8.1) or low-risk (LR, n=13, age: 35.2±10.3 y, BMI: 28.1±6.4) genotypes at the rs7901695 locus. During two meal challenge test visits subjects received standardized isocaloric (450 kcal) liquid meals: high-carbohydrate (HC, carbohydrates: 89% of energy) and normo-carbohydrate (NC, carbohydrates: 45% of energy). Fasting (0 min) and postprandial (30, 60, 120, 180 min) plasma samples were analyzed for metabolite profiles through untargeted metabolomics. Metabolic fingerprinting was performed on an ultra-high-performance liquid chromatography (UHPLC) system connected to an iFunnel quadrupole-time-of-flight (Q-TOF) mass spectrometer. In HR-genotype men, after the intake of an HC-meal, we noted a significantly lower area under the curves (AUCs) of postprandial plasma concentrations of most of the phospholipids (-37% to -53%, variable importance in the projection (VIP)=1.2-1.5), lysophospholipids (-29% to -86%, VIP=1.1-2.6), sphingolipids (-32% to -47%, VIP=1.1-1.3), as well as arachidonic (-36%, VIP=1.4) and oleic (-63%, VIP=1.3) acids, their metabolites: keto- and hydoxy-fatty acids (-38% to -78%, VIP=1.3-2.5), leukotrienes (-65% to -83%, VIP=1.4-2.2), uric acid (-59%, VIP=1.5), and pyroglutamic acid (-65%, VIP=1.8). The AUCs of postprandial sphingosine concentrations were higher (125-832%, VIP=1.9-3.2) after the NC-meal, AUCs of acylcarnitines were lower (-21% to -61%, VIP=1.1-2.4), and AUCs of fatty acid amides were higher (51-508%, VIP=1.7-3.1) after the intake of both meals. In nondiabetic men carrying the TCF7L2 HR genotype, subtle but detectable modifications in intermediate lipid metabolism are induced by an HC-meal. This trial was registered at www.clinicaltrials.gov as NCT03792685.

Prolonged monitoring of postprandial lipid metabolism after a western meal rich in linoleic acid and carbohydrates.

Today, awareness has been raised regarding high consumption of n-6 polyunsaturated fatty acids (PUFA) in western diets. A comprehensive analysis of total and individual postprandial fatty acids profiles would provide insights into metabolic turnover and related health effects. After an overnight fast, 9 healthy adults consumed a mixed meal comprising 97 g carbohydrate and 45 g fat, of which 26.4 g was linoleic acid (LA). Nonesterified fatty acids (NEFA), phospholipid fatty acids (PL-FA) and triacylglycerol fatty acids (TG-FA) were monitored in plasma samples, at baseline and hourly over a 7-h postprandial period. Total TG-FA concentration peaked at 2 h after the meal and steadily decreased thereafter. LA from TG18:2n-6 and behenic acid from TG22:0 showed the highest response among TG-FA, with a biphasic response detected for the former. PL-FA exhibited no change. Total NEFA initially decreased to nadir at 1 h, then increased to peak at 7 h. The individual NEFA showed the same response curve except LA and some very-long-chain saturated fatty acids (VLCSFA, ≥20 carbon chain length) that markedly increased shortly after the meal intake. The similarities and dissimilarities in lipid profiles between study subjects at different time points were visualized using nonmetric multi-dimensional scaling. Overall, the results indicate that postprandial levels of LA and VLCSFA, either as NEFA or TG, were most affected by the test meal, which might provide an explanation for the health effects of this dietary lifestyle characterized by high intake of mixed meals rich in n-6 PUFA.

Hypoglycemia Abrogates the Vascular Endothelial Protective Effect of Exenatide in Type 2 Diabetes Mellitus.

Glucagon-like peptide-1 (GLP-1) receptor agonists improve postprandial glucose, lipid metabolism, and vascular endothelial function. However, little is known about the effect of hypoglycemia on vascular endothelial function in patients on GLP-1 receptor agonist therapy. The aim of the present study was to determine the effect of hypoglycemia on vascular endothelial function in patients with type 2 diabetes mellitus (T2DM) treated with exenatide. Seventeen patients with T2DM underwent a meal tolerance test to examine the changes in vascular endothelial function and in glucose metabolism, both without exenatide and after a single subcutaneous injection of 10 μg exenatide. Vascular endothelial function was evaluated using reactive hyperemia index (RHI) measured by peripheral arterial tonometry before and 120 min after the meal loading test. The primary endpoint was the difference in changes in postprandial vascular endothelial function between the baseline and exenatide test. The results were analyzed in relation to the presence of absence of hypoglycemia. The natural logarithmically scaled RHI (L_RHI) was significantly lower after the baseline meal test but not in the exenatide test. Administration of exenatide caused symptomatic hypoglycemia in two patients during the meal tolerance test. The difference in the change in L_RHI was 0.125 ± 0.085 in the non-hypoglycemic group, whereas it was lower, − 0.487 ± 0.061, in the hypoglycemic group. The results of this study also suggest that the presence of hypoglycemia induces vascular endothelial dysfunction even during GLP-1 receptor agonist therapy.Trial registration: UMIN000015699.Electronic supplementary materialThe online version of this article (10.1007/s13300-019-0596-4) contains supplementary material, which is available to authorized users.

Impact of a Usual Serving Size of Flavanol-Rich Cocoa Powder Ingested with a Diabetic-Suitable Meal on Postprandial Cardiometabolic Parameters in Type 2 Diabetics-A Randomized, Placebo-Controlled, Double-Blind Crossover Study.

Randomized controlled trials indicate that flavanol-rich cocoa intake may improve postprandial glucose and lipid metabolism in patients with type 2 diabetes (T2D), based on studies with meals that impose a strong metabolic load. Hence, the aim of the present study was to investigate whether flavanol-rich cocoa powder ingested as part of a diabetic-suitable meal may beneficially affect glucose, lipid metabolism, and blood pressure (BP) in patients with T2D. Twelve adults with T2D, overweight/obesity, and hypertension ingested capsules with 2.5 g of flavanol-rich cocoa or microcrystalline cellulose with a diabetic-suitable breakfast in a randomized, placebo-controlled, double-blind crossover study. BP was measured and blood samples were taken before, 2 and 4 h after breakfast and capsule intake. Cocoa treatment did not affect glucose, insulin, homeostasis model assessment for insulin resistance (HOMA-IR), triglycerides, total cholesterol, low density lipoprotein-cholesterol, high density lipoprotein-cholesterol, and BP. For glucose, insulin and HOMA-IR, only effects by time were observed after both treatments. Thus, 2.5 g of flavanol-rich cocoa powder ingested as part of a diabetic-suitable meal does not seem to affect postprandial glucose and lipid metabolism and BP in stably-treated diabetics. Nevertheless, future studies with close-meshed investigations are desirable, providing realistic amounts of cocoa together with realistic meals rich in carbohydrates to subjects with T2D or metabolic syndrome, which do not afford pharmacological treatment.

Effect of Ingesting Resistant Maltodextrin on Postprandial Hyperlipidemia Induced by Fructose in Young Women

Aim: Our previous study demonstrated that the ingestion of fructose with fat exacerbated and delayed postprandial lipid metabolism (J Atheroscler Thromb 2013; 20: 591). Herein, we investigated the effect of ingesting a water-soluble dietary fiber, resistant maltodextrin (RMD), which has been reported to be effective for ameliorating postprandial glycemia and lipidemia, on fructose-induced postprandial hyperlipidemia in healthy young women. Methods: Healthy young Japanese women with apolipoprotein E3/3 phenotype were enrolled. They underwent 4 test trials in a randomized crossover design: fat cream (0.35 g/kg of fat; F trial), fat cream with RMD (5 g; FR trial), fat cream with fructose (0.5 g/kg; FFr trial), and fat cream with fructose and RMD (FFrR trial). Blood samples were taken before (0) and at 0.5, 1, 2, 4, and 6 h after ingestion. Results: The serum glucose and insulin concentrations peaked at 0.5 h in the FFr and FFrR trials, and no difference was observed between these trials. There was no increase in glucose concentration in the F or FR trials. The serum triglyceride and apolipoprotein B48 concentrations peaked at 4 h in all trials. In the F and FR trials (but not in the FFr and FFrR trials), the serum triglyceride concentration returned to the fasting level at 6 h. In all trials, the apolipoprotein B48 concentration did not return to baseline at 6 h. Conclusion: Co-ingestion of RMD did not significantly inhibit fructose-induced postprandial hyperlipidemia.

Pancreatic and mucosal enzymes in choline phospholipid digestion.

The digestion of choline phospholipids is important for choline homeostasis, lipid signaling, postprandial lipid and energy metabolism, and interaction with intestinal bacteria. The digestion is mediated by the combined action of pancreatic and mucosal enzymes. In the proximal small intestine, hydrolysis of phosphatidylcholine (PC) to 1-lyso-PC and free fatty acid (FFA) by the pancreatic phospholipase A2 IB coincides with the digestion of the dietary triacylglycerols by lipases, but part of the PC digestion is extended and must be mediated by other enzymes as the jejunoileal brush-border phospholipase B/lipase and mucosal secreted phospholipase A2 X. Absorbed 1-lyso-PC is partitioned in the mucosal cells between degradation and reacylation into chyle PC. Reutilization of choline for hepatic bile PC synthesis, and the reacylation of 1-lyso-PC into chylomicron PC by the lyso-PC-acyl-CoA-acyltransferase 3 are important features of choline recycling and postprandial lipid metabolism. The role of mucosal enzymes is emphasized by sphingomyelin (SM) being sequentially hydrolyzed by brush-border alkaline sphingomyelinase (alk-SMase) and neutral ceramidase to sphingosine and FFA, which are well absorbed. Ceramide and sphingosine-1-phosphate are generated and are both metabolic intermediates and important lipid messengers. Alk-SMase has anti-inflammatory effects that counteract gut inflammation and tumorigenesis. These may be mediated by multiple mechanisms including generation of sphingolipid metabolites and suppression of autotaxin induction and lyso-phosphatidic acid formation. Here we summarize current knowledge on the roles of pancreatic and mucosal enzymes in PC and SM digestion, and its implications in intestinal and liver diseases, bacterial choline metabolism in the gut, and cholesterol absorption.