Bile acids suppress the secretion of very-low-density lipoprotein by human hepatocytes in primary culture
Abstract
The existence of a relationship between bile acid and triacylglycerol metabolism in humans has been established, but the underlying mechanism and its physiological relevance have remained unclear. We have studied the effects of bile acids on the secretion of very-low-density lipoprotein (VLDL)-associated triacylglycerol, using [3H]glycerol labeling technique, and apolipoprotein B (apoB) in human hepatocytes in primary culture. Human hepatocytes secrete nascent VLDL with an average diameter of about 40 nm. Lipid composition of the particles resembles that reported for plasma VLDL, with the exception of a markedly lower cholesterylester content. In 24-hour cultured human hepatocytes, physiological (i.e., portal) concentrations of taurocholic acid (10 to 200 mumol/L) suppressed [3H]triacylglycerol secretion dose dependently. The degree of inhibition highly correlated (r = .87, P < .01) with taurocholic acid content of the cells of different preparations (n = 7). ApoB secretion was inhibited by taurocholic acid to a similar extent as [3H]triacylglycerol secretion (r = .93, P < .01). Lipid composition of secreted VLDL particles did not change during taurocholic acid-induced suppression. No effects on intracellular apoB, [3H]triacylg...Continue Reading
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