0000000000177049
AUTHOR
Thi Thu Trang Tran
showing 8 related works from this author
Postprandial adaptation of intestinal lipid metabolism : role of CD36 and PPAR beta
2011
Postprandial hypertriglyceridemia is an emerging risk factor for cardiovascular diseases and is associated with metabolic syndrome, obesity and insulin resistance. The small intestine participates in the postprandial triglyceridemia since both the size and number of secreted chylomicrons modulate lipoprotein lipase activity (LPL). Chylomicron synthesis is a complex mechanism in which the lipidation of Apolipoprotein B48 (ApoB48) by the Microsomal Triglyceride Transfer Protein (MTP) and the transfer between reticulum and Golgi in which the Liver Fatty Acid Binding Protein (L -FABP) is involved are limiting steps. An intestinal fat-mediated adaptation in postprandial period has been demonstra…
P059 Le lipido-récepteur intestinal CD36 et sa cascade de signalisation ERK1/2 dépendante contrôle la synthèse des chylomicrons
2013
International audience; Introduction et but de l’étude. – L’intestin est capable d’adapter sa capacité d’absorption à la teneur en lipide du régime. Cette adaptation implique un système de détection des lipides au niveau entérocytaire. Le CD36, qui est une glycoprotéine transmembranaire liant avec une forte affinité les acides gras à longue chaîne (AGLC), pourrait jouer ce rôle. En effet, ex vivo, la présence d’AGLC est associée à une activation de la voie ERK1/2 et conduit à l’induction de protéines clés du métabolisme intestinal des lipides : l’ApoB48 et la MTP. Cette régulation est CD36 dépendante (Tran et al. 2011). De plus, la déficience de CD36 est associée chez l’Homme et l’animal à …
CD36 Displays Features of a Lipid-Sensor Involved in Chylomicron Processing in the Rodent Small Intestine
2010
International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long-chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms.In this report, we provide novel insights into the potential underlying mechanisms. Our in vivo data demonstrated that CD36 gene deletion in mice did not affect LCFA uptake and their subsequent esterification into triglycerides by the intestinal mucosa at micellar LCFA concentrations prevailing in the intestine. In rodents, CD36 protein early disappeared from the luminal side of intestinal villi during the post-prandial period but only whe…
Mécanisme d’absorption intestinale des acides gras à longue chaîne : rôle émergent du CD36
2012
International audience; Excessive lipid intake, associated with a qualitative imbalance, favors the development of obesity and associated diseases. Among the organs involved in lipid homeostasis, the small intestine remains the most poorly known although it is responsible for the lipid bioavailability and largely contributes to the regulation of postprandial hypertriglyceridemia. The mechanism of long chain fatty acid (LCFA) intestinal absorption is not totally elucidated. The synthesis of recent literature indicates that the intestine is able to adapt its absorption capacity to the fat content of the diet. This adaptation takes place through a fat-coordinated induction of LBP and apolipopr…
Deregulated Lipid Sensing by Intestinal CD36 in Diet-Induced Hyperinsulinemic Obese Mouse Model
2016
International audience; The metabolic syndrome (MetS) greatly increases risk of cardiovascular disease and diabetes and is generally associated with abnormally elevated postprandial triglyceride levels. We evaluated intestinal synthesis of triglyceride-rich lipoproteins (TRL) in a mouse model of the MetS obtained by feeding a palm oil-rich high fat diet (HFD). By contrast to control mice, MetS mice secreted two populations of TRL. If the smaller size population represented 44% of total particles in the beginning of intestinal lipid absorption in MetS mice, it accounted for only 17% after 4 h due to the secretion of larger size TRL. The MetS mice displayed accentuated postprandial hypertrigl…
From fatty-acid sensing to chylomicron synthesis: Role of intestinal lipid-binding proteins
2013
International audience; Today, it is well established that the development of obesity and associated diseases results, in part, from excessive lipid intake associated with a qualitative imbalance. Among the organs involved in lipid homeostasis, the small intestine is the least studied even though it determines lipid bioavailability and largely contributes to the regulation of postprandial hyperlipemia (triacylglycerols (TG) and free fatty acids (FFA)). Several Lipid-Binding Proteins (LBP) are expressed in the small intestine. Their supposed intestinal functions were initially based on what was reported in other tissues, and took no account of the physiological specificity of the small intes…
Short Term Palmitate Supply Impairs Intestinal Insulin Signaling via Ceramide Production
2016
International audience; The worldwide prevalence of metabolic diseases is increasing, and there are global recommendations to limit consumption of certain nutrients, especially saturated lipids. Insulin resistance, a common trait occurring in obesity and type 2 diabetes, is associated with intestinal lipoprotein overproduction. However, the mechanisms by which the intestine develops insulin resistance in response to lipid overload remain unknown. Here, we show that insulin inhibits triglyceride secretion and intestinal microsomal triglyceride transfer protein expression in vivo in healthy mice force-fed monounsaturated fatty acid-rich olive oil but not in mice force-fed saturated fatty acid…
Luminal Lipid Regulates CD36 Levels and Downstream Signaling to Stimulate Chylomicron Synthesis
2011
International audience; The membrane glycoprotein CD36 binds nanomolar concentrations of long chain fatty acids (LCFA) and is highly expressed on the luminal surface of enterocytes. CD36 deficiency reduces chylomicron production through unknown mechanisms. In this report, we provide novel insights into some of the underlying mechanisms. Our in vivo data demonstrate that CD36 gene deletion in mice does not affect LCFA uptake and subsequent esterification into triglycerides by the intestinal mucosa exposed to the micellar LCFA concentrations prevailing in the intestine. In rodents, the CD36 protein disappears early from the luminal side of intestinal villi during the postprandial period, but …