TY - JOUR
T1 - Mechanism for the increase in plasma triacylglycerol concentrations after consumption of short-term, high-carbohydrate diets
AU - Mittendorfer, B.
AU - Sidossis, L. S.
PY - 2001
Y1 - 2001
N2 - Background: 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. Objective: We examined the effect of diet composition on VLDL-triacylglycerol metabolism using in vivo isotopically labeled VLDL-triacylglycerol tracers. Design: 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). Results: The plasma VLDL-triacylglycerol concentration was higher after the HC diet than after the HF diet (690 ± 186 compared with 287 ± 104 μmol/L; P < 0.05) because of higher rates of VLDL-triacylglycerol production (0.76 ± 0.12 compared with 0.45 ± 0.15 μmol·kg-1·min-1; P < 0.05) rather than diminished VLDL-triacylglycerol clearance (1.5 ± 0.5 compared with 1.7 ± 0.5 mL ·kg-1·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 μmol·kg-1·min-1; P < 0.05), which presumably increased hepatic fatty acid availability for triacylglycerol synthesis. Conclusions: 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.
AB - Background: 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. Objective: We examined the effect of diet composition on VLDL-triacylglycerol metabolism using in vivo isotopically labeled VLDL-triacylglycerol tracers. Design: 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). Results: The plasma VLDL-triacylglycerol concentration was higher after the HC diet than after the HF diet (690 ± 186 compared with 287 ± 104 μmol/L; P < 0.05) because of higher rates of VLDL-triacylglycerol production (0.76 ± 0.12 compared with 0.45 ± 0.15 μmol·kg-1·min-1; P < 0.05) rather than diminished VLDL-triacylglycerol clearance (1.5 ± 0.5 compared with 1.7 ± 0.5 mL ·kg-1·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 μmol·kg-1·min-1; P < 0.05), which presumably increased hepatic fatty acid availability for triacylglycerol synthesis. Conclusions: 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.
KW - Fatty acid
KW - High-carbohydrate diet
KW - High-fat diet
KW - Liver
KW - Stable isotopes
KW - Substrate oxidation
KW - Triacylglycerol
UR - http://www.scopus.com/inward/record.url?scp=0035052108&partnerID=8YFLogxK
U2 - 10.1093/ajcn/73.5.892
DO - 10.1093/ajcn/73.5.892
M3 - Article
C2 - 11333842
AN - SCOPUS:0035052108
SN - 0002-9165
VL - 73
SP - 892
EP - 899
JO - American Journal of Clinical Nutrition
JF - American Journal of Clinical Nutrition
IS - 5
ER -