AJP - Endocrinology and Metabolism, Vol 271, Issue 6 E952-E964, Copyright © 1996 by American Physiological Society

ARTICLES

Hepatic VLDL secretion of genetically obese Zucker rats is inhibited by a high-fat diet

L. Oussadou, G. Griffaton and A. D. Kalopissis
U177 Institut National de la Sante et de la Recherche Medicale, Paris, France.

Hepatocytes from obese and lean Zucker rats adapted to a control (C) or a high-fat (HF) diet were prepared for the study of fatty acid (FA) uptake, partition between oxidation and esterification, and very low density lipoprotein (VLDL) production. A first 2-h kinetic study showed higher oleate uptake on a C diet by obese rat cells and an almost exclusive esterification to triacylglycerol (TG), VLDL secretion being 2.5-fold higher in obese rat cells and enhanced 1.4-fold in both genotypes in the presence of 0.7 mM oleate vs. 0.1 mM or no oleate. Fat feeding 1) decreased oleate uptake, esterification, incorporation into VLDL-TG, and mass VLDL-TG secretion and 2) abolished the VLDL-TG increase by 0.7 mM oleate. Similar but more pronounced effects were obtained in fat-fed lean animals. A second kinetic study using very short incubation times up to 1 h confirmed that fat feeding decreased oleate uptake and esterification, greatly stimulating its oxidation and production of acetoacetate (obese) or acetoacetate and beta-hydroxybutyrate (lean). Synthesis of lactate and pyruvate greatly decreased under HF feeding, remaining higher in obese rat cells. The drastic inhibition of labeled and total hepatic VLDL-TG secretion in obese and lean Zucker rats by the HF diet could be partly explained by decreased exogenous FA availability for VLDL-TG synthesis through its greater channeling toward oxidation and, indirectly, by the altered hepatocyte metabolic state.

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