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Alterations in NO availability and signaling play a pivotal role at early stages of the metabolic syndrome (MetSynd). We hypothesized that dietary α-linolenic acid (ALA, 18:3 n-3) favors NO availability by modulating amino acid metabolism, with a specific impact on the arginine-NO pathway. Mice were fed a hyperlipidic diet (285 g lipid/kg, 51.1 % energy), rich in either saturated fatty acids (SFA, provided by palm oil, PALM group) or ALA (provided by linseed oil, LIN group). We measured whole-body NO synthesis and systemic arginine hydrolysis with a tracer-based method, plasma concentration of related metabolites, and hepatic mRNA level of related enzymes, and the study was completed by a transcriptomic analysis in the liver. As expected with this model, hyperlipidic diets resulted in increased adiposity and glycemia after 5 weeks. As compared to PALM mice, LIN mice had a higher plasma nitrite and nitrate concentration, a higher whole-body conversion of arginine into NO vs urea, and a similar plasma concentration of asymmetric dimethylarginine (ADMA), despite a higher expression of the liver dimethylargininase-1. In LIN mice, there was a higher expression of genes involved in PPARα signaling, but a little impact on gene expression related to amino acids and arginine metabolism. This effect cannot be directly ascribed to changes in arginase activity in the liver or ADMA metabolism, nor to direct regulation of the related target genes. In conclusion, dietary ALA favors NO synthesis, which could contribute to rescue NO availability when jeopardized by the nutritional conditions in relation with the initiation of the MetSynd.

Background: Postprandial lipemia is a risk factor for cardiovascular disease. The potential impacts of the type/nature of dietary protein on postprandial lipemia and associated dysregulations have been insufficiently investigated., Objective: We investigated the postprandial effect of including in a high-fat meal some milk protein fractions that markedly differ in their physicochemical properties and composition [either casein (CAS), whey protein (WHE), or α-lactalbumin-enriched whey protein (LAC)]., Methods: The protein fractions were incorporated as 15% energy in a high-fat meal in a 3-period, crossover postprandial study of 10 healthy overweight men with an elevated waist circumference (>94 cm). We measured postprandial changes in plasma lipids, amino acids, glucose, and oxidative stress markers, vascular function (using pulse contour analysis), and low-grade inflammation (using plasma markers). We also characterized in vitro the meal structures, including the size of the fat globule, and possible changes during digestion., Results: The type of protein did not affect postprandial plasma glucose, amino acids, insulin, or nonesterified fatty acids, but, compared with WHE and LAC, which did not differ, CAS markedly reduced postprandial triglycerides (TGs), achieving a 22 ± 10% reduction in the 6-h area under the curve (P < 0.05). Similar trends were shown for plasma chylomicrons [apolipoprotein (apo)B-48; P < 0.05]. However, there were no significant differences between the meals regarding postprandial oxidative stress (plasma hydroperoxides and malondialdehyde), endothelial dysfunction (salbutamol-induced changes in pulse contour analysis), or low-grade inflammation. In vitro studies showed that when the pH of the meal decreased to stomach pH values, the reduction in the solubility of casein resulted in a phase separation between fat and protein, whereas the proteins in the other meals remained suspended with fat globules., Conclusion: In healthy overweight men, casein has specific physical interactions with fat that affect postprandial TGs, leading to the formation of fewer chylomicrons or an increase in chylomicron clearance. This trial was registered at clinicaltrials.gov as NCT00931151., (© 2015 American Society for Nutrition.)

The hypothesis that n-3 polyunsaturated fatty acids (PUFA) could contribute to maintain muscle mass during energy restriction aiming to weight loss was tested in the rat, with special attention paid to insulin signalling. After 10 weeks on a diet rich in lipids and sucrose, male rats were energy restricted and fed diets rich in 18:1 n-9 (OLE), 18:3 n-3 (ALA) or n-3 long-chain (LC, >18 carbons) PUFA. After 4 weeks, they were killed after an insulin injection. Red blood cells, liver, and Gastrocnemius muscle were enriched in ALA in the ALA group, and in LC-PUFA in the ALA and LC groups. The LC diet resulted in a higher weight loss, without negative impact on the muscle weight. In parallel, hepatic phosphorylation of insulin receptor and IRS1 was the highest in this group. This suggests that the trend we observed in the preservation of protein homeostasis in the LC group is mediated, at least partly, by an enhancement of the early steps of insulin signalling resulting from cell membrane enrichment in n-3 PUFA., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

In a previous study, we have demonstrated that a supplementation of a high-fat diet with a quinoa extract enriched in 20-hydroxyecdysone (QE) or pure 20-hydroxyecdysone (20E) could prevent the development of obesity. In line with the anti-obesity effect of QE, we used indirect calorimetry to examine the effect of dietary QE and 20E in high-fat fed mice on different components of energy metabolism. Mice were fed a high-fat (HF) diet with or without supplementation by QE or pure 20E for 3 weeks. As compared to mice maintained on a low-fat diet, HF feeding resulted in a marked physiological shift in energy homeostasis, associating a decrease in global energy expenditure (EE) and an increase in lipid utilization as assessed by the lower respiratory quotient (RQ). Supplementation with 20E increased energy expenditure while food intake and activity were not affected. Furthermore QE and 20E promoted a higher rate of glucose oxidation leading to an increased RQ value. In QE and 20E-treated HFD fed mice, there was an increase in fecal lipid excretion without any change in stool amount. Our study indicates that anti-obesity effect of QE can be explained by a global increase in energy expenditure, a shift in glucose metabolism towards oxidation to the detriment of lipogenesis and a decrease in dietary lipid absorption leading to reduced dietary lipid storage in adipose tissue., (Copyright © 2014 Elsevier Inc. All rights reserved.)

In the postprandial period, low-grade inflammation may contribute to vascular endothelial dysfunction, a hallmark of atherogenesis. Little is known about the involvement of the adipose tissue in the initiation of the postprandial inflammatory response such as obtained after a high-saturated fat meal (HFM). In the present study, we first studied the time course of appearance of systemic inflammation after a HFM in healthy rats, and then we investigated whether a HFM activates the inflammatory signaling in the visceral adipose tissue, with a focus on the key component, nuclear factor-kappaB (NF-kappaB). Two hours after the HFM, plasma IL-6 and PAI-1, but not plasma C-reactive protein and soluble intracellular adhesion molecule-1, showed a marked, transient increase. These changes were specific to the postprandial state as not observed after a control water load. Neutrophils count and activation markers CD11B and CD62L, assessed by flow cytometry, also rose significantly 2 h after the HFM, while remaining steady after the control. At the same time, the HFM decreased significantly B-cell count and expression of the activation marker CD62L. Interestingly, at the same early time after the HFM, in the visceral adipose tissue, there was a 2.2-fold increase in the activation of NF-kappaB (p65) in nuclear extract and an increase in IL-6 mRNA. As far as we know, this is the first study evidencing an acute, postprandial activation of inflammation in visceral adipose tissue. This early activation of NF-kappaB pathway after a HFM may play a triggering role in the initiation of the complex postprandial proatherogenic phenotype., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

In contrast to the quality of carbohydrates and lipids, little is known on the influence of the type of dietary protein on the development of the metabolic or insulin resistance syndrome. Cysteine intake has been recently documented to impact insulin sensitivity. The aim of this study was to determine whether rapeseed protein, an emergent cysteine-rich protein, could inhibit the onset of the metabolic syndrome. For 9 weeks, rats were fed a diet rich in saturated fats and sucrose, which also included 20 % protein either as milk protein ('Induction' diet I) or rapeseed protein (diet R). A third, control group received an isoenergetic diet containing milk protein but polyunsaturated fats and starch ('Prudent' diet P). Plasma glucose, insulin, TAG and cholesterol, and blood pressure were monitored during the study, glucose tolerance was tested at week 7 and body composition determined at week 9. Plasma glucose, insulin and TAG increased during the experiment and, at week 9, plasma insulin was significantly 34 % lower in the R group and 56 % lower in P group as compared with the I group. The insulin peak after the glucose load was significantly 28-30 % lower in R and P than in I and the insulin sensitivity index was significantly higher in R than in I. Unexpectedly, peripheral fat deposition was slightly higher in R than in I. In this model, substituting rapeseed protein for milk protein had preventive effects on the early onset of insulin resistance, similar to those achieved by manipulating the types of dietary fat and carbohydrates.

The aim of this work was to determine the effects in rats of ingesting 1 of 3 diets with normal or high protein concentrations and various carbohydrate:lipid ratios on weight gain, body composition, and the development and metabolism of white adipose tissue (WAT). For this purpose, male Wistar rats were fed for 20 or 42 d a high-carbohydrate, low-fat, normal-protein diet (76, 10, and 14% of energy as carbohydrate, lipid, and protein, respectively, carbohydrate:lipid ratio (C/L) = 7.6), a normal-carbohydrate, low-fat, high-protein diet (35, 10, and 55% of energy as carbohydrate, lipid, and protein respectively, C:L = 3.5), or a carbohydrate-free, high-fat, high-protein diet (45 and 55% of energy as fat and protein, respectively, C:L = 0). Growth, food intake, body composition, WAT cellularity, and several markers of lipogenesis including fatty acid synthase and lipoprotein lipase activities were measured in adipose tissue and liver. Lowering the C:L ratio reduced the development of WAT, weight gain, body fat mass, and adipocyte size, and in rats fed the carbohydrate-free diet (C:L = 0), the total number of adipocytes in subcutaneous WAT. These reductions in adipose tissue development with decreases in the C:L ratio of the diet seemed to be due primarily to reduced hepatic lipogenesis.

We used a previously developed compartmental model to assess the postprandial distribution and metabolism of dietary nitrogen (N) in the splanchnic and peripheral areas after the ingestion of a single meal containing milk protein either alone (MP) or with additional sucrose (SMP) or fat (FMP). The addition of fat was predicted to enhance splanchnic dietary N anabolism only transiently, without significantly affecting the global kinetics of splanchnic retention and peripheral uptake. In contrast, the addition of sucrose, which induced hyperinsulinemia, was predicted to enhance dietary N retention and anabolism in the splanchnic bed, thus leading to reduced peripheral dietary amino acid availability and anabolism. The incorporation of dietary N into splanchnic proteins was thus predicted to reach 18, 24, and 35% of ingested N 8 h after MP, FMP, and SMP, respectively. Such a model provides insight into the dynamics of the system in the nonsteady postprandial state and constitutes a useful, explanatory tool to determine the region-specific utilization of dietary N under different nutritional conditions.