Postprandial Lipemia Research Articles

Fasted exercise does not improve postprandial lipemia responses to different meals in lean and obese subjects: A crossover, randomized clinical trial.

Persistent episodes of postprandial hyperlipemia (PPL) and hyperglycemia (PPG) are considered risk factors for coronary heart disease (CHD) and premature death; whereas physical exercise improves lipid profile and glucose tolerance thus decreasing cardiovascular risks. To investigate the effects of low-intensity fasted aerobic exercise on the magnitude of the PPL and PPG responses to meals with different energy content, in normal and obese subjects. The study used a randomized crossover design. Twenty-one male (Lean: n=9, BMI: 24.3±2.2; and obese: n=12, BMI 32.31±2.1) volunteers aged 20-30 years, performed three interventions, separated by 7 days each: (i) 45min at rest and isocaloric high-fat meal (60% lipids, 30% carbohydrates and 10% protein); (ii) fasted low-intensity aerobic exercise (50% VO2max) for 45min followed by an isocaloric or (iii) calorie deficit high-fat meal. Subjects were serially assessed for blood triglycerides, and glucose levels. Low-intensity fasted aerobic exercise had no acute effect on PPL in lean and obese subjects. Glucose concentrations were reduced only in lean subjects. There is a significant difference in PPL values when comparing lean to obese subjects, implying that the nutritional status influences lipid and carbohydrate after fasted low-intensity aerobic exercise. Registered under ClinicalTrials.gov Identifier no. NCT00929890.

Aerobic exercise improves postprandial inflammatory and hemostatic markers after a high-fat meal: a randomized crossover study.

Exercise intensity modulates postprandial lipemia. However, its effect on hemostatic and pro- and anti-inflammatory markers in the postprandial state is still unknown. Eleven young males performed a 2-day trial on different conditions: (i) REST: rest for 45min; (ii) MIE: moderate-intensity exercise; and (iii) HIE: heavy-intensity exercise. Experimental conditions were performed in the evening. On the following morning, blood samples were taken in the fasted state (0h) and at 1, 3, and 5h after the consumption of a high-fat meal (HFM). Interleukin-10 (IL-10) levels were higher in the HIE vs. MIE trial at 0 and 1h (p< 0.033) and IL-10 incremental area under the curve (iAUC) was greater in the MIE (p= 0.027) and HIE (p= 0.045) trials vs. REST. Lower levels of anti-coagulation factor VII (FVII) were observed at 1h in the MIE condition vs. REST (p= 0.043). In comparison with REST, MIE improved hemostatic (FVII) and anti-inflammatory markers (IL-10 iAUC) whereas HIE enhanced IL-10 in the postprandial state. Regardless of the exercise intensity, aerobic exercise mitigates the deleterious consequences of an HFM. Novelty: Prior aerobic exercise at moderate-intensity attenuates next day's postprandial FVII and IL-10 levels whereas exercise performed at heavy-intensity increases IL-10 levels. Moderate-intensity exercise may be more beneficial to improve hemostatic (FVII) and anti-inflammatory (IL-10) responses while heavy-intensity exercise may improve anti-inflammatory (IL-10) levels only.

Role of Fluid Milk in Attenuating Postprandial Hyperglycemia and Hypertriglyceridemia.

Postprandial plasma glucose and triglyceride concentrations are predictive of relative cardiovascular disease (CVD) risk, and the pathogenesis of both insulin resistance and atherosclerosis has been attributed to acute states of hyperglycemia and hypertriglyceridemia. Postprandial lipemia and hyperglycemia suppress vascular reactivity and induce endothelial dysfunction. Epidemiological studies suggest that chronically-high consumption of milk and milk products is associated with a reduced risk of type 2 diabetes, metabolic syndrome, and CVD. The addition of dairy products to meals high in carbohydrates and fat may lessen these risks through reductions in postprandial glucose and triglyceride responses. Purported mechanisms include dairy proteins and bioactive compounds, which may explain the inverse relationship between dairy consumption and cardiometabolic diseases. The current review evaluates the available literature describing the relationships between metabolic dysfunction, postprandial metabolism, and vascular dysfunction and discusses the potential role of milk and dairy products in attenuating these impairments.

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.

Effects of a single bout of walking on postprandial triglycerides in men of Chinese, European and Japanese descent: a multisite randomised crossover trial

IntroductionElevated non-fasting triglyceride (TG) concentrations are a risk factor for cardiovascular diseases but can be reduced after acute exercise. Ethnic-based differences in the magnitude of postprandial lipaemia and the extent...

Acute Running and Coronary Heart Disease Risk Markers in Male Cigarette Smokers and Nonsmokers: A Randomized Crossover Trial.

Cigarette smoking is an independent risk factor for coronary heart disease and is associated with impaired postprandial metabolism. Acute exercise reduces postprandial lipemia and improves other coronary heart disease risk markers in nonsmokers. Less is known about responses in cigarette smokers. Twelve male cigarette smokers (mean ± SD; age = 23 ± 4 yr, body mass index = 24.9 ± 3.0 kg·m-2) and 12 male nonsmokers (age = 24 ± 4 yr, body mass index = 24.1 ± 2.0 kg·m-2) completed two, 2-d conditions (control and exercise) in a randomized crossover design. On day 1, participants rested for 9 h (0800-1700) in both conditions except a 60-min treadmill run (65% ± 7% peak oxygen uptake, 2.87 ± 0.54 MJ) was completed between 6.5 and 7.5 h (1430-1530) in the exercise condition. On day 2 of both conditions, participants rested and consumed two high-fat meals over 8 h (0900-1700) during which 13 venous blood samples and nine resting arterial blood pressure measurements were collected. Smokers exhibited higher postprandial triacylglycerol and C-reactive protein than nonsmokers (main effect group effect size [Cohen's d] ≥ 0.94, P ≤ 0.034). Previous day running reduced postprandial triacylglycerol, insulin, and systolic and diastolic blood pressure (main effect condition d ≥ 0.28, P ≤ 0.044) and elevated postprandial nonesterified fatty acid and C-reactive protein (main effect condition d ≥ 0.41, P ≤ 0.044). Group-condition interactions were not apparent for any outcome across the total postprandial period (0-8 h; all P ≥ 0.089), but the exercise-induced reduction in postprandial triacylglycerol in the early postprandial period (0-4 h) was greater in nonsmokers than smokers (-21%, d = 0.43, vs -5%, d = 0.16, respectively; group-condition interaction P = 0.061). Acute moderate-intensity running reduced postprandial triacylglycerol, insulin, and resting arterial blood pressure the day after exercise in male cigarette smokers and nonsmokers. These findings highlight the ability of acute exercise to augment the postprandial metabolic health of cigarette smokers and nonsmokers.

Postprandial triglyceridaemia is modulated by insulin resistance but not by grade of obesity in abdominal and morbid obese subjects.

Obesity is associated with high cardiovascular risk. Postprandial lipidaemia has been associated with cardiovascular disease risk. Our aim was to identify whether anthropometric parameters, insulin resistance (IR) and/or fasting plasma triglycerides may determine postprandial changes in lipoprotein concentrations in abdominal and morbid obese subjects. We have studied 20 non-diabetic, normolipidaemic subjects with abdominal obesity, 20 morbid obese subjects and 20 healthy individuals, that have similar age and gender. In all of them a standardised oral fat load test (OFLT) with unsaturated fat was performed. During the OFLT, the postprandial triglycerides response was significantly higher in subjects with abdominal obesity compared with morbid obese subjects (4hours triglycerides pick value and AUC of triglycerides). Both obese groups showed significantly higher postprandial triglycerides response compared with healthy subjects. Dividing the obesity group according to the presence of IR, we found that IR was an important factor related with postprandial lipaemia but not BMI or waist circumference. In addition, postprandial glycaemia and insulinaemia significantly decreased in all studied subjects, being the highest decrease in morbid obese subjects and in subjects with IR. Postprandial triglyceridaemia significantly correlated with IR parameters and not with anthropometric parameters in AO and MO subjects. In subjects with AO and MO, postprandial triglycerides values are higher than healthy individuals and independently predicted by fasting IR parameters. Furthermore, unsaturated fat improved IR state.

Effect of food intake on complete blood count of healthy dogs

The present determined the hematological alterations of healthy dogs at the peak of postprandial hypertriglyceridemia. Twenty-four clinically healthy dogs had blood samples collected to perform complete blood count on three consecutive days at the same time every day: first day after a 12-hour fast; second day three hours after feeding with commercial feed, during the peak of postprandial lipemia; and third day after a 12-hour fast. Feeding led to an increase in MCHC, hemoglobin and white blood cell count due to the increase in segmented neutrophil, monocyte and eosinophil concentrations. A significant increase in total plasma protein content was also observed. Postprandial condition at the peak of hypertriglyceridemia influences hematological parameters of healthy dogs, which is an important finding, however transient, when interpreting laboratory blood tests.

Quantile-dependent expressivity of plasma adiponectin concentrations may explain its sex-specific heritability, gene-environment interactions, and genotype-specific response to postprandial lipemia.

Background“Quantile-dependent expressivity” occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g. adiponectin) is high or low relative to its distribution. We have previously shown that the heritability (h2) of adiposity, lipoproteins, postprandial lipemia, pulmonary function, and coffee and alcohol consumption are quantile-specific. Whether adiponectin heritability is quantile specific remains to be determined.MethodsPlasma adiponectin concentrations from 4,182 offspring-parent pairs and 1,662 sibships from the Framingham Heart Study were analyzed. Quantile-specific heritability from offspring-parent (βOP,h2 = 2βOP/(1 + rspouse)) and full-sib regression slopes (βFS, h2 = {(1 + 8rspouseβFS)0.05-1}/(2rspouse)) were robustly estimated by quantile regression with nonparametric significance assigned from 1,000 bootstrap samples.ResultsQuantile-specific h2 (± SE) increased with increasing percentiles of the offspring’s age- and sex-adjusted adiponectin distribution when estimated from βOP (Ptrend = 2.2 × 10−6): 0.30 ± 0.03 at the 10th, 0.33 ± 0.04 at the 25th, 0.43 ± 0.04 at the 50th, 0.55 ± 0.05 at the 75th, and 0.57 ± 0.08 at the 90th percentile, and when estimated from βFS (Ptrend = 7.6 × 10−7): 0.42 ± 0.03 at the 10th, 0.44 ± 0.04 at the 25th, 0.56 ± 0.05 at the 50th, 0.73 ± 0.08 at the 75th, and 0.79 ± 0.11 at the 90th percentile. Consistent with quantile-dependent expressivity, adiponectin’s: (1) heritability was greater in women in accordance with their higher adiponection concentrations; (2) relationships to ADIPOQ polymorphisms were modified by adiposity in accordance with its adiponectin-lowering effect; (3) response to rosiglitazone was predicted by the 45T> G ADIPOQ polymorphism; (4) difference by ADIPOQ haplotypes increased linearly with increasing postprandial adiponectin concentrations.ConclusionAdiponectin heritability is quantile dependent, which may explain sex-specific heritability, gene-environment and gene-drug interactions, and postprandial response by haplotypes.

Evaluation of circulating miR-122, miR-30c and miR-33a levels and their association with lipids, lipoproteins in postprandial lipemia

AimsPostprandial lipemia is characterized by an increase in triglyceride-rich lipoproteins after fatty meals. MicroRNAs (miRs) play important roles in lipid and lipoprotein metabolism. The aim of this study was to determine relationship between levels of plasma miR expression and lipoprotein metabolism-related proteins in subjects with normal (NPR) and high postprandial response (HPR) in postprandial period. Materials and methodsThe oral fat tolerance test was applied to 22 individuals with NPR and 22 with HPR. Key findingsIncreased expressions of miR-122 and miR-33a and miR-122/30c ratio and decreased miR-30c expression were observed in fasting and postprandial period of HPR compared with NPR. ROC curve analysis showed that miR-122/30c ratio is a good biomarker for postprandial lipemia (AUC: 0.97, p < 0.001). Levels of TG, MTTP, and Apo B-48 and chylomicron (CM) particle size were significantly higher in HPR than in NPR (p < 0.05). The miR-122/30c ratio at 2 h was positively correlated with CM particle size, and with TG, MTTP and Apo B-48 levels at 4th hour. miR-33a expression decreased in HPR and was negatively correlated with ABCA1 and Apo A-1 levels at 4th hour of the postprandial period in both groups. SignificanceIncreased miR-122 and decreased miR-30c expression levels in HPR may play critical roles in elevated or prolonged postprandial lipemia. The miR122/30c ratio exhibited good association with MTTP, Apo B-48 and TG levels, and with CM particle size, and may be a reliable marker for evaluating postprandial lipemia. miR-33a may also play a key role in decreased HDL-C in postprandial lipemia.

Acute Effects of Metformin and Vildagliptin after a Lipid-Rich Meal on Postprandial Microvascular Reactivity in Patients with Type 2 Diabetes and Obesity: A Randomized Trial.

Background: Type 2 diabetes mellitus and obesity are both related to endothelial dysfunction. Postprandial lipemia is a cardiovascular risk. Notably, it is known that a high-fat diet may elicit microvascular dysfunction, even in healthy subjects. Since anti-diabetic drugs have different mechanisms of action and also distinct vascular benefits, we aimed to compare the results of two anti-diabetic drugs after the intake of a lipid-rich meal on microcirculation in patients with type 2 diabetes and obesity. In parallel, we also investigated the metabolic profile, oxidative stress, inflammation, plasma viscosity, and some gastrointestinal peptides. Subjects/Methods: We included 38 drug-naïve patients, all women aged between 19 and 50 years, with BMI ≥ 30 kg/m2. We performed endothelial measurements and collected samples before (fasting) and after the intake of a lipid-rich meal at 30, 60, 120, and 180 min. Patients were randomized to metformin or vildagliptin, given orally just before the meal. Endothelial function was assessed by videocapillaroscopy and laser-Doppler flowmetry to investigate microvascular reactivity. Besides, we also investigated plasma viscosity, inflammatory and oxidative stress biomarkers, gastrointestinal peptides, and metabolic profile in all time points. Results: No differences at baseline were noted between groups. Vildagliptin increased glucagon-like peptide-1 compared to metformin. Paired comparisons showed that, during the postprandial period, vildagliptin significantly changed levels of insulin and glucagon-like peptide-1, and also the dipeptidyl peptidase-4 activity, while metformin had effects on plasma glucose solely. Metformin use during the test meal promoted an increase in functional capillary density, while vildagliptin kept non-nutritive microvascular blood flow and vasomotion unchanged. Conclusions: After the intake of a lipid-rich meal, the use of vildagliptin preserved postprandial non-nutritive microflow and vasomotion, while metformin increased capillary recruitment, suggesting protective and different mechanisms of action on microcirculation.

Acute Resistance Exercise Reduces Postprandial Lipemia and Oxidative Stress in Resistance-Trained Men

McAllister, MJ, Steadman, KS, Renteria, LI, Case, MJ, Butawan, MB, Bloomer, RJ, and McCurdy, KW. Acute resistance exercise reduces postprandial lipemia and oxidative stress in resistance-trained men. J Strength Cond Res 36(8): 2139-2146, 2022-Acute ingestion of a high-fat meal (HFM) results in significant increases in postprandial triacylglycerols (TAG) and markers of oxidative stress (OS). Combined aerobic and resistance exercise can attenuate postprandial lipemia; however, it is not clear if acute resistance exercise alone can reduce postprandial OS. The purpose of this study was to determine if acute resistance exercise can attenuate postprandial OS and to compare the effects of moderate versus high-intensity resistance exercise in this regard. Nine ( n = 9) moderately resistance-trained individuals completed 3 testing conditions in a randomized order as follows: (a) rest (no exercise), (b) moderate intensity (3 sets of 10 repetitions at 68% 1 repetition maximum [RM]), and (c) high-intensity resistance exercise (4 sets of 6 repetitions at 85% 1RM). Exercises included barbell back squat, bench press, straight leg deadlift, lat pull-down, upright row, and sit-ups. A HFM was ingested 12 hours after each condition. Blood samples were collected immediately before as well as 2 and 4 hours after ingestion and analyzed for TAG, cholesterol (CHOL), insulin, malondialdehyde (MDA), total nitrate/nitrite (NOx), glutathione (GSH), and advanced oxidation protein products (AOPP). When comparing 4 hour area under curve (AUC) data between conditions, AOPP demonstrated a significantly lower AUC after the moderate-intensity condition compared with resting condition. In addition, resistance exercise resulted in significantly higher plasma NOx concentrations as well as lower TAG and CHOL concentrations after HFM ingestion. Resistance exercise also prevented a decline in GSH that was induced by the HFM. These results demonstrate that acute resistance exercise can attenuate postprandial OS.

Postprandial Metabolism and Vascular Function: Impact of Aging and Physical Activity Level.

The consumption of a high-fat meal can induce postprandial lipemia and endothelial dysfunction. The authors assessed the impact of age and physical activity on metabolic and vascular outcomes following meal consumption in healthy adults. The authors recruited four groups: younger active (age 22.1 ± 1.4years; n = 9), younger inactive (age 22.6 ± 3.7years; n = 8), older active (age 68.4 ± 7.7years; n = 8), and older inactive (age 67.7 ± 7.2years; n = 7). The metabolic outcomes were measured at the baseline and hourly for 6hr post high-fat meal consumption (12kcal/kg; 63% fat). Flow-mediated dilation was measured at the baseline, 2hr, and 4hr postmeal. The total area under the curve for triglycerides was significantly lower in the more active groups, but did not differ based on age (younger active = 6.5 ± 1.4mmol/L × 6hr, younger inactive = 11.7 ± 4.8, older active = 6.8 ± 2.7, older inactive = 12.1 ± 1.7; p = .0004). After adjusting for artery diameter, flow-mediated dilation differed between groups at the baseline (younger active = 4.8 ± 1.6%, younger inactive = 2.5 ± 0.5, older active = 3.4 ± 0.9, older inactive = 2.2 ± 0.4; p < .001) and decreased significantly across groups 4hr postmeal (mean difference = 0.82; 95% CI [0.02, 1.6]; p = .04). These findings highlight the beneficial effect of regular physical activity on postprandial lipemia, independent of age.

The Effects of Teneligliptin on Lipid Profile: A Prospective Study for Comparison of Biomarkers Before and After a Meal

Background: In the treatment of diabetes mellitus, it is important to prevent dyslipidemia, which is one of the complications. However, no study has examined the long-term effects of teneligliptin on the blood parameters of apolipoprotein B (apoB) after a meal in patients with type 2 diabetes. Methods: The effects of teneligliptin on blood glucose and lipids were examined by measurement of biomarkers before and after a meal. We gathered data before and after 6-month treatment in diabetic patients. Results: After treating 31 patients with teneligliptin for 6 months, the blood level of apoB-48, expressed as total area under the curve (tAUC), was significantly decreased. A multiple regression analysis of factors affecting the decreases in apoB-48 tAUC indicated that apoB-48 is more likely to decrease if it is higher at the start of testing, and that the apoB-48 tAUC value is more likely to fall in women than in men. Conclusions: Teneligliptin may be beneficial for the treatment of postprandial hyperlipidemia in diabetic patients. J Endocrinol Metab. 2020;10(3-4):79-88 doi: https://doi.org/10.14740/jem679

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.

Postprandial Apolipoprotein B48 is Associated with Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis.

Objective: To describe postprandial lipemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis measured as carotid intima-media thickness (cIMT). Methods: We performed an observational study of 40 patients with RA and 40 sex and age-matched controls. Patients with dyslipidemia were excluded. Pathologically increased cIMT was defined as a carotid thickness greater than the 90th percentile (>p90) for age and sex. Fasting and postprandial plasma lipids, cholesterol, triglycerides, apolipoprotein B48 (ApoB48), and total ApoB were evaluated. The other variables included were clinical and laboratory values, Framingham score, and the 28-joint Disease Activity Score (DAS28). Two multivariate models were constructed to identify factors associated with pathologic cIMT in patients with RA. Results: Fasting lipid values were similar in patients with RA and controls, although those of postprandial ApoB48 were higher (median (IQR), 14.4 (10.8–12.1) vs. 12.1 (2.3–9,8); p = 0.042). Pathologic cIMT was recorded in 10 patients with RA (25%) and nine controls (22.5%). In patients with RA, pathologic cIMT was associated with postprandial ApoB48 (OR (95% CI), 1.15 (1.0–1.3)) and total ApoB (OR [95% CI], 1.12 [1.1–1.2]). The second model revealed a mean increase of 0.256 mm for cIMT in patients with elevated anticitrullinated protein antibodies (ACPAs). Conclusion: Postprandial ApoB48 levels in patients with RA are higher than in controls. Postprandial ApoB48 and total ApoB levels and markers of severity, such as ACPAs, are associated with pathologic cIMT in patients with RA. Our findings could indicate that these atherogenic particles have a negative effect on the endothelium.

Circulating Rather Than Intestinal PCSK9 (Proprotein Convertase Subtilisin Kexin Type 9) Regulates Postprandial Lipemia in Mice.

Increased postprandial lipemia (PPL) is an independent risk factor for atherosclerotic cardiovascular diseases. PCSK9 (Proprotein convertase subtilisin kexin type 9) is an endogenous inhibitor of the LDLR (low-density lipoprotein receptor) pathway. We previously showed that PCSK9 inhibition in mice reduces PPL. However, the relative contribution of intracellular intestinal PCSK9 or liver-derived circulating PCSK9 to this effect is still unclear. Approach and Results: To address this issue, we generated the first intestine-specific Pcsk9-deficient (i-Pcsk9-/-) mouse model. PPL was measured in i-Pcsk9-/- as well as in wild-type and streptozotocin-induced diabetic mice following treatment with a PCSK9 monoclonal antibody (alirocumab). Blocking the circulating form of PCSK9 with alirocumab significantly reduced PPL, while overexpressing human PCSK9 in the liver of full Pcsk9-/- mice had the opposite effect. Alirocumab regulated PPL in a LDLR-dependent manner as this effect was abolished in Ldlr-/- mice. In contrast, i-Pcsk9-/- mice did not exhibit alterations in plasma lipid parameters nor in PPL. Finally, PPL was highly exacerbated by streptozotocin-induced diabetes mellitus in Pcsk9+/+ but not in Pcsk9-/- mice, an effect that was mimicked by the use of alirocumab in streptozotocin-treated Pcsk9+/+ mice. Taken together, our data demonstrate that PPL is significantly altered by full but not intestinal PCSK9 deficiency. Treatment with a PCSK9 monoclonal antibody mimics the effect of PCSK9 deficiency on PPL suggesting that circulating PCSK9 rather than intestinal PCSK9 is a critical regulator of PPL. These data validate the clinical relevance of PCSK9 inhibitors to reduce PPL, especially in patients with type 2 diabetes mellitus.

Energy utilisation and postprandial responses during sitting interrupted by regular activity breaks

ABSTRACT Interrupting sedentary behaviour with regular activity breaks benefits glycaemic control; however, the influence of the energy utilised during these activity breaks on postprandial metabolic response is relatively unknown. Therefore, the aim of this study was to investigate whether the energy utilisation of regular (every 30 min) short (1 min 40 s or 2 min) activity breaks was associated with the lowering of postprandial glycaemia, insulinemia and lipidemia. Using separate data from two previously performed studies (ALPhA Study n = 65, age 25.7 (5.2) y, 40% male, BMI 23.6 (4.1) kg · m−2. ABPA study n = 35, age 25.1 (3.7) y, 31% male, BMI 23.4 (3.2) kg · m−2) we investigated the association between energy utilisation (measured by indirect calorimetry) and postprandial glucose, insulin and triglycerides during prolonged sitting, and regular activity breaks.Results Mixed effects regression models indicated that energy utilisation was not consistently associated with postprandial glucose, insulin or triglyceride responses (p > 0.05 for all). Additionally, there was some indication that energy utilisation was obscuring (mildly suppressing) the effects of regular activity breaks on glucose, insulin and triglyceride iAUC.Conclusions If energy utilisation does not mediate the association between regular activity breaks and postprandial glycaemic response, it is possible that it is the frequency of the activity breaks that is beneficial.

Dietary Impact on Postprandial Lipemia.

Abnormalities in postprandial lipemia (PPL), particularly those related to triglyceride-rich lipoproteins, are considered an independent cardiovascular risk factor. As diet is known to be one of the main modulators of PPL, the aim of this review was to summarize and discuss current knowledge on the impact of diet and its components on PPL in humans; specifically, the impact of weight loss, different nutrients (quantity and quality of dietary fats, carbohydrates, and proteins), alcohol and other bioactive dietary components (i.e., polyphenols), as well as the effect of different dietary patterns. The possible mechanisms behind the metabolic effects of each dietary component were also discussed.

Galactose Ingested with a High-Fat Beverage Increases Postprandial Lipemia Compared with Glucose but Not Fructose Ingestion in Healthy Men

ABSTRACTBackgroundFructose ingestion with a high-fat beverage increases postprandial lipemia when compared with glucose. It is unknown whether other sugars, such as galactose, also increase postprandial lipemia.ObjectivesThe objective was to assess whether galactose ingestion within a high-fat beverage increases postprandial lipemia relative to glucose or fructose.MethodsTwo experiments were conducted, which contrasted different test drinks under otherwise standardized conditions. In Experiment 1, 10 nonobese men (age: 22 ± 1 y; BMI, 23.5 ± 2.2 kg/2) ingested either galactose or glucose (0.75 g supplemented carbohydrate per⋅kilogram body mass) within a high-fat test drink (0.94 g fat per kilogram body mass). In Experiment 2, a separate group of 9 nonobese men (age: 26 ± 6 y; BMI: 23.5 ± 2.6 kg/m2) ingested either galactose or fructose (identical doses as those in Experiment 1) within the same high-fat test drink. Capillary blood was sampled before and at frequent intervals after ingestion of the test drinks for a 300-min period to determine plasma triacylglycerol, glucose, lactate, nonesterified fatty acid, and insulin concentrations. Paired t tests and 2-way, repeated-measures ANOVA were used to compare conditions within each experiment.ResultsThe incremental AUC for triacylglycerol was greater following galactose ingestion compared with glucose (127 ± 59 compared with 80 ± 48 mmol⋅L−1 × 300 min, respectively; P = 0.04) but not compared with fructose (136 ± 74 compared with 133 ± 63 mmol⋅L−1 ×300 min, respectively; P = 0.91). Plasma lactate concentrations also increased to a greater extent with galactose compared with glucose ingestion (time–condition interaction: P < 0.001) but not fructose ingestion (time–condition interaction: P = 0.17).ConclusionsGalactose ingestion within a high-fat beverage exacerbates postprandial lipemia and plasma lactate concentrations compared with glucose but not fructose in nonobese men. These data suggest that galactose metabolism may be more similar to fructose than to glucose, providing a rationale to reassess the metabolic fate of galactose ingestion in humans. This trial was registered at clinicaltrials.gov as NCT03439878.