Effects of acute hyperinsulinemia on VLDL triglyceride and VLDL apoB production in normal weight and obese individuals

• Published in: Diabetes (New York, N.Y.) Vol. 42; no. 6; pp. 833 - 842
• Main Authors: Lewis, G. F., Uffelman, K. D., Szeto, L. W., Steiner, G.
• Format: Journal Article
• Language: English
• Published: American Diabetes Association 01-06-1993
• ISSN: 0012-1797; 1939-327X; 0012-1797
• DOI: 10.2337/diabetes.42.6.833

Effects of acute hyperinsulinemia on VLDL triglyceride and VLDL apoB production in normal weight and obese individuals.
G F Lewis ,
K D Uffelman ,
L W Szeto and
G Steiner
Department of Medicine, University of Toronto, Ontario, Canada.
Abstract
The effects of short-term hyperinsulinemia on the production of both VLDL triglyceride and VLDL apoB were determined semiquantitatively
before and during a 6-h euglycemic hyperinsulinemic clamp (40 mU.m-2 x min-1) in 17 women (8 chronically hyperinsulinemic
obese, BMI = 35.7 kg/m2; 9 normal weight, BMI = 22.5 kg/m2). During acute hyperinsulinemia, plasma FFA decreased by approximately
95% within 1 h in both groups. VLDL triglyceride production decreased 66% in the control subjects (P = 0.0003) and 67% in
obese subjects (P = 0.0003). ApoB production decreased 53% in control subjects (P = 0.03) but only 8% in obese (NS). Plasma
triglycerides decreased by 40% from baseline in control subjects (P < 0.0001) but only by 10% in obese subjects (P = NS).
Despite the similar decrease in triglyceride and apoB production in control subjects, VLDL particle size (triglyceride-to-apoB
ratio) decreased with hyperinsulinemia (P = 0.003). In obese subjects, despite a decrease in triglyceride production similar
to that in control subjects but no change in apoB production, VLDL size did not change appreciably. Acute hyperinsulinemia
in humans: 1) suppresses plasma FFA equally in control and obese subjects at this high dose of insulin; 2) inhibits VLDL triglyceride
production equally in control and obese subjects, perhaps secondary to the decrease in FFA; 3) inhibits VLDL apoB production
in control but less so in obese subjects, suggesting that obese subjects may be resistant to this effect of insulin; 4) decreases
plasma triglyceride and VLDL particle size in control subjects, reflecting either stimulation of LPL activity or a greater
relative decrease in triglyceride to apoB production; and 5) does not decrease plasma triglyceride or VLDL size in obese subjects
to the same extent as it does in control subjects. Thus, the insulin resistance of obesity affects some but not all aspects
of VLDL metabolism.