TY - JOUR
T1 - Influence of obesity on the metabolism of apolipoprotein B in humans
AU - Egusa, G.
AU - Beltz, W. F.
AU - Grundy, Scott M
AU - Howard, B. V.
PY - 1985
Y1 - 1985
N2 - The influence of obesity on the metabolism of apolipoprotein B (apo B) in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) was investigated in nine obese and seven nonobese Pima Indian men. Kinetics of VLDL-apo B (VLDL-B), VLDL-triglycerides, IDL-B and LDL-B were studied after injection of autologous 131I-VLDL, [3H]glycerol, and autologous 125I-LDL. Specific activities were measured in apo B isolated from all lipoprotein fractions and in triglyceride isolated from VLDL. Transport rates and fractional catabolic rates for apo B in VLDL, IDL, and LDL and triglyceride in VLDL were determined by multicompartmental analysis. This method also allowed the estimation of rates of interconversions of the lipoproteins. The two groups had similar mean ages and heights, but the obese group had a higher total body weight (131 ± 14 vs. 66 ± 3 kg ± SEM) and fat free mass (81 ± 5 vs. 54 ± 2 kg) than lean controls. Plasma total lipids were similar for the two groups and apo B concentrations in VLDL, IDL, and LDL were similar in obese and lean subjects. In spite of similarity in concentrations, obese subjects compared to lean subjects had higher synthetic rates of VLDL-triglyceride (62.6 ± 15 vs. 26.2 ± 7 g/d, P < 0.01), VLDL-B (2,241 ± 215 vs. 1,113 ± 72 mg/d, P < 0.001), and LDL-B (1,234 ± 87 vs. 802 ± 83 mg/d, P < 0.01). Furthermore, in obese subjects significantly higher amounts of VLDL-B were removed from the circulation without conversion to LDL-B (1,078 ± 159 vs. 460 ± 34 mg/d, P < 0.05), and obese subjects had a higher fractional catabolic rate for LDL than the lean controls (0.48 ± 0.02 vs. 0.41 ± 0.02 d-1, P < 0.05). The rapid catabolism of LDL and increased metabolism of VLDL without conversion to LDL in obese individuals may be mechanisms for maintenance of LDL at normal levels despite the overproduction of its precursor.
AB - The influence of obesity on the metabolism of apolipoprotein B (apo B) in very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) was investigated in nine obese and seven nonobese Pima Indian men. Kinetics of VLDL-apo B (VLDL-B), VLDL-triglycerides, IDL-B and LDL-B were studied after injection of autologous 131I-VLDL, [3H]glycerol, and autologous 125I-LDL. Specific activities were measured in apo B isolated from all lipoprotein fractions and in triglyceride isolated from VLDL. Transport rates and fractional catabolic rates for apo B in VLDL, IDL, and LDL and triglyceride in VLDL were determined by multicompartmental analysis. This method also allowed the estimation of rates of interconversions of the lipoproteins. The two groups had similar mean ages and heights, but the obese group had a higher total body weight (131 ± 14 vs. 66 ± 3 kg ± SEM) and fat free mass (81 ± 5 vs. 54 ± 2 kg) than lean controls. Plasma total lipids were similar for the two groups and apo B concentrations in VLDL, IDL, and LDL were similar in obese and lean subjects. In spite of similarity in concentrations, obese subjects compared to lean subjects had higher synthetic rates of VLDL-triglyceride (62.6 ± 15 vs. 26.2 ± 7 g/d, P < 0.01), VLDL-B (2,241 ± 215 vs. 1,113 ± 72 mg/d, P < 0.001), and LDL-B (1,234 ± 87 vs. 802 ± 83 mg/d, P < 0.01). Furthermore, in obese subjects significantly higher amounts of VLDL-B were removed from the circulation without conversion to LDL-B (1,078 ± 159 vs. 460 ± 34 mg/d, P < 0.05), and obese subjects had a higher fractional catabolic rate for LDL than the lean controls (0.48 ± 0.02 vs. 0.41 ± 0.02 d-1, P < 0.05). The rapid catabolism of LDL and increased metabolism of VLDL without conversion to LDL in obese individuals may be mechanisms for maintenance of LDL at normal levels despite the overproduction of its precursor.
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U2 - 10.1172/JCI112011
DO - 10.1172/JCI112011
M3 - Article
C2 - 4031064
AN - SCOPUS:0021990235
SN - 0021-9738
VL - 76
SP - 596
EP - 603
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 2
ER -