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Reduction in Visceral Adipose Tissue Is Associated with Improvement in Apolipoprotein B-100 Metabolism in Obese Men¹

University Department of Medicine and Western Australia Heart Research Institute (F.M.R., G.F.W.), University of Western Australia, and the Department of Radiology (J.H.), Royal Perth Hospital, Perth, Western Australia 6001; the Faculty of Science (G.R.S.), University of Western Australia, Nedlands, Western Australia 6009; Lipoprotein Team (R.P.N.), Medical Research Council Clinical Sciences Center, Imperial College of Medicine, Hammersmith Hospital, London W12 0NN, United Kingdom; and the Department of Bioengineering, University of Washington (P.H.R.B.), Seattle, Washington 98195

Address all correspondence and requests for reprints to: A/Prof G. F. Watts, University Department of Medicine, Royal Perth Hospital, Box X2213, GPO, Perth, Western Australia 6001, Australia. E-mail: gfwatts{at}cyllene.uwa.edu.au

We investigated the effect of reduction in visceral obesity on the kinetics of apolipoprotein B-100 (apoB) metabolism in a controlled dietary intervention study in 26 obese men. Hepatic secretion of very low density lipoprotein (VLDL) apoB was measured using a primed, constant, infusion of 1-[¹³C]leucine. In seven men receiving the reduction diet, intermediate density lipoprotein (IDL) and low density lipoprotein (LDL) apoB kinetics were also determined. ApoB isotopic enrichment was measured using gas chromatography-mass spectrometry, and SAAM-II was used to estimate the fractional turnover rates. Subcutaneous and visceral adipose tissues at the L3 vertebra were quantified by magnetic resonance imaging. With weight reduction there was a significant decrease (P < 0.05) in body mass index, waist circumference, and visceral adipose tissue. The plasma concentrations of total cholesterol, triglyceride, insulin, and lathosterol also significantly decreased (P < 0.05). Compared with weight maintenance, weight reduction significantly decreased the VLDL apoB concentration, pool size, and hepatic secretion of VLDL apoB (+2.5 ± 4.6 vs. -14.7 ± 4.0 mg/kg fat free mass·day; P = 0.010), but did not significantly alter its fractional catabolism. Weight reduction was also associated with an increased fractional catabolic rate of LDL apoB (0.24 ± 0.07 vs. 0.54 ± 0.10 pools/day; P = 0.002) and conversion of VLDL to LDL apoB (11.7 ± 2.5% vs. 56.3 ± 11.4%; P = 0.008). A change in hepatic VLDL apoB secretion was significantly correlated with a change in visceral adipose tissue area (r = 0.59; P = 0.043), but not plasma concentrations of insulin, free fatty acids, or lathosterol. The data support the hypothesis that a reduction in visceral adipose tissue is associated with a decrease in the hepatic secretion of VLDL apoB, and this may be due to a decrease in portal lipid substrate supply. Weight reduction may also increase the fractional catabolism of LDL apoB, but this requires further evaluation.

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