Scope Enhanced adiposity and metabolic inflammation are major features of obesity associated with altered gut microbiota and intestinal barrier. How these metabolic outcomes can be impacted by milk polar lipids (MPL), naturally containing 25% of sphingomyelin, is investigated in mice fed a mixed high‐fat (HF) diet . Methods and results Male C57Bl/6 mice receive a HF‐diet devoid of MPL (21% fat, mainly palm oil, in chow), or supplemented with 1.1% or 1.6% of MPL (HF‐MPL1; HF‐MPL2) via a total‐lipid extract from butterserum concentrate for 8 weeks. HF‐MPL2 mice gain less weight versus HF (p < 0.01). Diets do not impact plasma markers of inflammation but in the liver, HF‐MPL2 tends to decrease hepatic gene expression of macrophage marker F4/80 versus HF‐MPL1 (p = 0.06). Colonic crypt depth is the maximum in HF‐MPL2 (p < 0.05). In cecal microbiota, HF‐MPL1 increases Bifidobacterium animalis versus HF (p < 0.05). HF‐MPL2 decreases Lactobacillus reuteri (p < 0.05), which correlates negatively with the fecal loss of milk sphingomyelin‐specific fatty acids (p < 0.05). Conclusion In mice fed a mixed HF diet, MPL can limit HF‐induced body weight gain and modulate gut physiology and the abundance in microbiota of bacteria of metabolic interest. This supports further exploration of how residual unabsorbed lipids reaching the colon can impact HF‐induced metabolic disorders.

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Gammopathies were found to be present in 25 0.3%) of 192 HIV-negative renal transplant recipients ~Ith more than 30 months follow-up prospectively inves-?gated for monoclonal or oligoclonal immunoglobulins Emlg) by agarose gel electrophoresis and immunofixation. 1 leven patients had only one monoclonal band, whereas 4 had two or more bands. Of these bands, 60% were IgG kappa, 29% IgG lambda and 11 % IgM lambda or kappa, and 90% did not exceed 2 g/1. Most gammopathies occurred early post-transplant (median 5 months) and they Were always transient. Some predisposing factors for mig ~mergence could be identified: 1. age, but only in women, :duration of dialysis, 3. occurrence of prior cytomegalo-Vtru~ infection, and 4. immunosuppressive regimen in-l~dmg cyclosporine. Serological evidence for active EBV } 0 e~tion was obtained in ten patients, but in six cases in-ec~ton occurred subsequent to the finding of mig. In eight

Although UHT heat treatment is being optimized to improve the stability and functional properties of dairy products, its metabolic effects remain scarcely known. As such, we studied the effect of the type of UHT process on lipid metabolism, intestinal barrier, and inflammation in mice. Nine-week-old male C57Bl/6J mice were fed a diet composed of nonlipidic powder mixed with different UHT dairy creams (final: 13% milkfat) for 1 or 4 wk. All creams contained 0.02% of thickener (carrageenan) and were treated via either (1) classical indirect heating process (Th), (2) indirect process at higher temperature (Th+), or (3) direct process by steam injection (ThD). Plasma, epididymal adipose tissue (EAT), and intestine were analyzed. Multivariate principal component analyses were used to identify differential effects of processes. Th+ differed by a globally higher liver damage score compared with that of the other creams. After 4 wk, the duodenal expression of lipid absorption genes fatty acid binding protein 4 (Fatp4) and microsomal triglycerides transfer protein (Mttp) was lower in the Th+ versus Th group. Expression in the colon of tight junction protein zonula occludens 1 (Zo1) and of some endoplasmic reticulum stress markers was lower in both Th+ and ThD versus the Th group. In EAT, ThD had lower gene expression of several inflammatory markers after 4 wk. Some differential effects may be related to heat-induced physicochemical changes of creams. The type of cream UHT process differentially affected metabolic parameters in mice after a 4-wk fat-rich diet, partly due to cream structure. Altogether, direct steam injection process induced the lowest early markers of high-fat-induced metabolic inflammation in EAT.

Aim. Type 2 diabetic (T2D) patients present risk factors for atherothrombosis such as fasting hypertriglyceridemia and platelet hyperactivity. Our objective was to determine the effect of large triglyceride-rich lipoproteins (large TGRL) from fasting T2D patients on platelet aggregation and, if any, to identify the signaling pathway involved. Methods. Large TGRL were isolated from the plasma of 25 T2D patients by ultra-centrifugation (d<1.000). Platelets were isolated from healthy blood donors and suspended in buffer. Platelets were preincubated in the presence or absence of TGRL and stimulated with either collagen or thrombin. Platelet aggregation and the arachidonic acid (AA) signaling pathway were studied. Results. Fasting T2D large TGRL were mostly of hepatic origin (ApoB-100/ApoB-48 ratio of 42 ± 7) and were enriched in TG (TG/total ApoB ratio of 4.2 ± 0.5). They potentiated agoniststimulated platelet aggregation (collagen: +68%, p<0.05, thrombin: +771%, p<0.05). It should be mentioned that TGRL from the plasma of healthy blood donors (n=7) had no effect on platelet aggregation. T2D large TGRL increased thromboxane B 2 (TxB 2) concentration in platelets stimulated with collagen (+34%, p<0.05) or thrombin (+37%, p<0.05) compared to platelets stimulated with one or the other agonists alone. Phosphorylation of p38 MAPK and cytosolic phospholipase A 2 (cPLA 2) was enhanced after incubation of platelets with T2D TGRL and thrombin (+87% and +32%, respectively, p<0.05) compared to platelets incubated with thrombin. Conclusion. Large TGRL from fasting T2D patients may play a role in the development of atherothrombosis by increasing platelet aggregation and activating platelet AA signaling pathway.

The aim of this study is to examine whether postprandial (PP) triglyceride-rich lipoproteins (TGRL) secreted after a moderate fat intake would activate platelets differently according to their fatty acid (FA) composition. Methods and results: In a parallel single-blind randomized trial, 30 women with type 2 diabetes are assigned a breakfast containing 20 g lipids from butter versus hazelnut-cocoa spread (HCS) rich in palm oil. Blood samples are collected at fasting and 4 h PP. FA composition of fasting and PP TGRL and their effects on the activation of platelets from healthy blood donors are assessed. Both breakfasts similarly increase plasma ApoB-48, plasma, and TGRL triglycerides (p < 0.05). TGRL mean diameter increases after both breakfasts and is greater after the butter breakfast. Both breakfasts are rich in palmitic acid, and the HCS breakfast contains 45% oleic acid. TGRL FA composition reflects the dietary FA composition. Pre-incubation of platelets with fasting and PP TGRL increases collagen-stimulated aggregation (p < 0.01 vs control). Fasting and PP TGRL similarly increase agonist-induced thromboxane B 2 concentrations, and this effect is concentration-dependent for PP TGRL. Conclusion: PP TGRL from type 2 diabetic women after a palm-oil spread versus butter-based mixed meal induce similar acute in vitro platelet activation.

Scope Synthetic emulsifiers have recently been shown to promote metabolic syndrome and considerably alter gut microbiota. Yet, data are lacking regarding the effects of natural emulsifiers, such as plant lecithins rich in essential α‐linolenic acid (ALA), on gut and metabolic health. Methods and Results For 5 days, male Swiss mice are fed diets containing similar amounts of ALA and 0, 1, 3, or 10% rapeseed lecithin (RL) or 10% soy lecithin (SL). Following an overnight fast, they are force‐fed the same oil mixture and euthanized after 90 minutes. The consumption of lecithin significantly increased fecal levels of the Clostridium leptum group (p = 0.0004), regardless of origin or dose, without altering hepatic or intestinal expression of genes of lipid metabolism. 10%‐RL increased ALA abundance in plasma triacylglycerols at 90 minutes, reduced cecal bile acid hydrophobicity, and increased their sulfatation, as demonstrated by the increased hepatic RNA expression of Sult2a1 (p = 0.037) and cecal cholic acid‐7 sulfate (CA‐7S) concentration (p = 0.05) versus 0%‐lecithin. Conclusion After only 5 days, nutritional doses of RL and SL modified gut bacteria in mice, by specifically increasing C. leptum group. RL also increased postprandial ALA abundance and induced beneficial modifications of the bile acid profile. ALA‐rich lecithins, especially RL, may then appear as promising natural emulsifiers.