A single dose of c9,t11 or t10,c12 conjugated linoleic acid isomers perturbs vitamin A metabolism in mice.

Conjugated linoleic acid (CLA) is a polyunsaturated fatty acid that has numerous biologic activities. Previous studies in rodents demonstrated that chronic intake of CLA t10,c12 or CLA c9,t11 isomers perturbs the metabolism of retinoids (vitamin A and its derivatives). Specifically, although both isomers increased liver retinoid levels, only CLA t10,c12 also stimulated hepatic retinol secretion into the bloodstream. Given that retinoid homeostasis in mammalian serum and tissues is crucial to maintain health, it is important to gain more insights into the mode of action of this nutrient-nutrient interaction. Here we hypothesized that an acute administration of either CLA isomer may also influence vitamin A metabolism. By gavaging wild-type and retinol-binding protein knockout mice with an oral bolus of radiolabeled retinol containing 1 of these 2 isomers, we showed that both CLA t10,c12 and CLA c9,t11 rapidly enhance hepatic uptake of dietary vitamin A and its resecretion from the liver in the form of retinol bound to retinol-binding protein. Indeed, in mice lacking this protein, the sole specific carrier for retinol in the circulation, this latter effect was blunted. In addition, by using a pharmacologic inhibitor of the clearance of chylomicrons, which distribute recently ingested vitamin A and lipids throughout the body, we provided evidence that CLA intake might rapidly enhance intestinal absorption of dietary vitamin A. These data demonstrate the existence of multiple levels of interaction between dietary CLA and retinoid metabolism and warrant further studies to understand the molecular mechanisms underlying these effects and their implications for human health.