Diabetes, Vol 37, Issue 9 1271-1278, Copyright © 1988 by American Diabetes Association

ARTICLES

Interrelationships among insulin's antilipolytic and glucoregulatory effects and plasma triglycerides in nondiabetic and diabetic patients with endogenous hypertriglyceridemia

H Yki-Jarvinen and MR Taskinen
Second Department of Medicine, University of Helsinki, Finland.

We tested the hypothesis that the previously observed association among hypertriglyceridemia, hyperinsulinemia, and insulin resistance could be explained by a defect in insulin's antilipolytic effect. Insulin action was measured in 10 nondiabetic and 8 diabetic patients with hypertriglyceridemia (fasting plasma triglyceride 800 +/- 154 and 1105 +/- 445 mg/dl, respectively, P NS; fasting plasma glucose 99 +/- 3 and 161 +/- 12 mg/dl, respectively, P less than .001) and in 8 weight-matched normolipemic nondiabetic individuals (fasting plasma triglyceride and glucose 110 +/- 21 and 91 +/- 3 mg/dl). The slope of the decay in plasma free fatty acid (FFA) during insulin infusion was used as an index of insulin's antilipolytic effect. Insulin stimulation of glucose uptake in vivo during intravenous hyperinsulinemic clamp and in vitro in adipocytes were measures of insulin's glucoregulatory action. Both glucoregulatory and antilipolytic effects were similarly reduced in both hypertriglyceridemic groups compared with normal subjects. The plasma triglyceride concentration correlated positively with the slope of FFA suppression by insulin (r = .81, P less than .0001) and the fasting FFA concentration (r = .65, P less than .0001). In multiple linear regression analysis, insulin's antilipolytic effect and the fasting FFA concentration explained 83% of the variation in the plasma triglyceride concentration. These associations were independent of insulin's glucoregulatory effect and the fasting plasma insulin concentration. The data indicate that patients with endogenous hypertriglyceridemia are resistant to both the antilipolytic and glucoregulatory actions of insulin and that increased flux of FFA as a result of the latter, rather than hyperinsulinemia, is responsible for elevation of very-low-density lipoprotein production.(ABSTRACT TRUNCATED AT 250 WORDS)
CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				Z. Sun and P. Ernsberger Marked Insulin Resistance in Obese Spontaneously Hypertensive Rat Adipocytes Is Ameliorated by in Vivo but Not in Vitro Treatment with Moxonidine J. Pharmacol. Exp. Ther., February 1, 2007; 320(2): 845 - 852. [Abstract] [Full Text] [PDF]

				I. Yokoyama, Y. Inoue, T. Moritan, K. Ohtomo, and R. Nagai Simple Quantification of Skeletal Muscle Glucose Utilization by Static 18F-FDG PET J. Nucl. Med., October 1, 2003; 44(10): 1592 - 1598. [Abstract] [Full Text] [PDF]

				J. Vakkilainen, S. Makimattila, A. Seppala-Lindroos, S. Vehkavaara, S. Lahdenpera, P.-H. Groop, M.-R. Taskinen, and H. Yki-Jarvinen Endothelial Dysfunction in Men With Small LDL Particles Circulation, August 15, 2000; 102(7): 716 - 721. [Abstract] [Full Text] [PDF]

				A. Laws, H.M. Hoen, J.V. Selby, M.F. Saad, S.M. Haffner, and B.V. Howard Differences in Insulin Suppression of Free Fatty Acid Levels by Gender and Glucose Tolerance Status: Relation to Plasma Triglyceride and Apolipoprotein B Concentrations Arterioscler. Thromb. Vasc. Biol., January 1, 1997; 17(1): 64 - 71. [Abstract] [Full Text]

				S. Gupta, A. de Belder, and L. O Hughes Avoiding premature coronary deaths in Asians in Britain BMJ, October 21, 1995; 311(7012): 1035 - 1036. [Full Text]