Mechanism for the increase in plasma triacylglycerol concentrations after consumption of short-term, high-carbohydrate diets

Abstract

High-carbohydrate (HC) diets are recommended for lowering the risk of coronary heart disease because they decrease plasma LDL-cholesterol concentrations. However, an unfavorable effect of HC diets is an increase in plasma triacylglycerol concentrations. The underlying mechanisms of this effect are still unclear. We examined the effect of diet composition on VLDL-triacylglycerol metabolism using in vivo isotopically labeled VLDL-triacylglycerol tracers. Six healthy subjects were studied on 2 occasions: after 2 wk of an HC diet (75% carbohydrates, 10% fat, and 15% protein) and after 2 wk of an isoenergetic high-fat (HF) diet (30% carbohydrates, 55% fat, and 15% protein). The plasma VLDL-triacylglycerol concentration was higher after the HC diet than after the HF diet (690 +/- 186 compared with 287 +/- 104 micromol/L; P < 0.05) because of higher rates of VLDL-triacylglycerol production (0.76 +/- 0.12 compared with 0.45 +/- 0.15 micromol x kg(-1) x min(-1); P < 0.05) rather than diminished VLDL-triacylglycerol clearance (1.5 +/- 0.5 compared with 1.7 +/- 0.5 mL x kg(-1) x min(-1) after the HC diet than after the HF diet, respectively). The increase in VLDL-triacylglycerol production was probably mediated by a decrease in hepatic fatty acid oxidation after the HC diet (0.13 +/- 0.02 compared with 0.69 +/- 0.24 micromol x kg(-1) x min(-1); P < 0.05), which presumably increased hepatic fatty acid availability for triacylglycerol synthesis. The increase in fasting plasma triacylglycerol concentrations in response to short-term HC diets is due to accelerated VLDL-triacylglycerol secretion. Increased hepatic fatty acid availability, resulting from reduced hepatic fatty acid oxidation, is most likely responsible for the observed increase in VLDL-triacylglycerol secretion.