Fm. Riches et al., Reduction in visceral adipose tissue is associated with improvement in apolipoprotein B-100 metabolism in obese men, J CLIN END, 84(8), 1999, pp. 2854-2861
We investigated the effect of reduction in visceral obesity on the kinetics
of apolipoprotein B-100 (apoB) metabolism in a controlled dietary interven
tion study in 26 obese men. Hepatic secretion of very low density lipoprote
in (VLDL) apoB was measured using a primed, constant, infusion of 1-[C-13]l
eucine. In seven men receiving the reduction diet, intermediate density lip
oprotein (IDL) and low density lipoprotein (LDL) apoB kinetics were also de
termined. ApoB isotopic enrichment was measured using gas chromatography-ma
ss spectrometry, and SAAM-II was used to estimate the fractional turnover r
ates. Subcutaneous and visceral adipose tissues at the L3 vertebra were qua
ntified by magnetic resonance imaging. With weight reduction there was a si
gnificant decrease (P < 0.05) in body mass index, waist circumference, and
visceral adipose tissue. The plasma concentrations of total cholesterol, tr
iglyceride, insulin, and lathosterol also significantly decreased (P < 0.05
). Compared with weight maintenance, weight reduction significantly decreas
ed the VLDL apoB concentration, pool size, and hepatic secretion of VLDL ap
oB (Delta+2.5 +/- 4.6 vs. Delta-14.7 +/- 4.0 mg/kg fat free mass day; P = 0
.010), but did not significantly alter its fractional catabolism. Weight re
duction 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 convers
ion of VLDL to LDL apoB (11.7 +/- 2.58 vs. 56.3 +/- 11.4%; P = 0.008). A ch
ange in hepatic VLDL apoB secretion was significantly correlated with a cha
nge in visceral adipose tissue area (r = 0.59; P = 0.043), but not plasma c
oncentrations of insulin, free fatty acids, or lathosterol. The data suppor
t 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 i
ncrease the fractional catabolism of LDL apoB, but this requires further ev
aluation.