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.
Highlights
L’apport excessif de lipides, associe a un desequilibre qualitatif, contribue a l’augmentation de la prevalence de l’obesite et a l’apparition des maladies associees (Bray et al, 2004 ; de Wit et al, 2011)
CD36 est donc la premiere etape d’un mecanisme qui conduit a une adaptation postprandiale du metabolisme enterocytaire des lipides permettant de prendre en charge de grandes quantites de lipides alimentaires
La recherche du ro^le physiologique des lipid-binding proteins (LBP) membranaires au niveau intestinal necessite la prise en compte de la specificite intestinale
Summary
L’alimentation apporte de 30 a 40 % de l’energie sous forme de lipides, principalement des triglycerides (TG). Du fait de leur caractere hydrophobe, l’absorption des TG au niveau intestinal est un processus complexe comportant plusieurs etapes (Niot et al, 2009) (figure 1) : le captage des AGLC, le trafic intracellulaire, la synthese et la secretion des chylomicrons. A l’arrivee dans la lumiere intestinale, les lipides alimentaires, principalement des TG sont hydrolyses en monoglyceride (MG) et AGLC gr^ace aux lipases gastriques et pancreatiques. Ces produits sont ensuite associes au cholesterol, aux phospholipides, aux sels biliaires et forment des micelles mixtes (voir l’article presente dans ce numero par Beaslas et al, 2012). Il est admis que les AGLC sont absorbes preferentiellement au niveau jejunal (Mariadason et al, 2005) par les enterocytes hautement differencies se trouvant dans les deux tiers superieurs des villosites intestinales (Niot et al, 2009)
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