Mécanisme d’absorption intestinale des acides gras à longue chaîne : rôle émergent du CD36

Abstract

Excessive lipid intake, associated with a qualitative imbalance, favors the development of obesity and associated diseases. From organs involved in the 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. Over the two last decades, cloning of lipid binding proteins (LBP), proteins involved in trafficking and metabolic fate of LCFA in gut have provided new insights on cellular and molecular mechanisms involved in fat absorption. The synthesis of recent literature indicates that 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 apolipoproteins. CD36 could operate as a lipid sensor responsible for a transducing signal related to the lipid content of the diet at the origin of this intestinal adaptation. This lipid-mediated metabolic response may lead to the formation of large chylomicrons rapidly degraded in the blood. All together, these new data indicate that this intestinal lipid sensing mechanism may be a therapeutic target for reducing the postprandial hypertriglyceridemia and associated cardiovascular risks.

Keywords

• intestine
• CD36
• lipid-binding proteins
• intestinal adaptation
• sensing
• lipid absorption
• postprandial hypertriglyceridemia