6533b7d0fe1ef96bd125b5a3

RESEARCH PRODUCT

La teneur en lipides du régime affecte les capacitésd'absorption intestinale et la triglycéridémie postprandiale: contribution du récepteur nucléaire PPARβ ?

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The dietary long chain fatty acid have crucial functions into the organism such as energysource, eicosanoïdes synthesis, gene regulation). The fat disposal is essential and depend onintestinal barrier. It is well known that intestinal fat absorption is efficient. However, we don'tif the high triglycerides bioavailability of gut is attributable to inborn properties or to acquiredproperties. To answer this question, mice were subjected to a high-fat diet (40%, w/w) during21 days. We have shown that high-fat induces : 1) intestinal LCFA uptake, 2) intestinalmitotic index which leads to an increase of intestinal relative mass, 3) expression of genesinvolved in fatty uptake (Fatty Acid Transport Protein 4, FATP-4), trafficking (Fatty AcidTransporter, FAT; Intestinal and Liver Fatty Acid-Binding Protein, I et L-FABP) andlipoprotein synthesis (Microsomal Triglyceride transfer Protein, MTP et apolipoprotein AIV).These changes were lipid-mediated, in that they were fully abolished in mice refed thecontrol diet. Moreover, these changes induces a higher efficiency of triglycerides clearance inblood. The molecular mechanism at the origin of this intestinal adaptation could be thenuclear receptor, Peroxisome Proliferator-Activated Receptor β (PPARβ). To explore thishypothesis, we have generated by the Cre-lox strategy a transgenic mouse model thatoverexpressed specifically PPARβ in the small intestine. We have shown that theoverexpression of PPARβ led to a low fat-mediated adaptation. According to our hypothesis,this data might result from an alteration of cell differentiation.