Diabetes, Vol 26, Issue 1 11-21, Copyright © 1977 by American Diabetes Association

ARTICLES

Postheparin plasma lipoprotein lipase and hepatic lipase in diabetes mellitus. Relationship to plasma triglyceride metabolism

EA Nikkila, JK Huttunen and C Ehnholm

The activity of two triglyceride lipases was determined by an immunochemical method in the postheparin plasma of 60 diabetic patients and of 47 age- and sex-matched nondiabetic control subjects. The results were related to the type of diabetes, to plasma triglyceride and insulin concentrations, to removal of exogenous fat from the blood, and to turnover of VLDL-triglycerides . The mean postheparin plasma lipoprotein lipase (LPL) activity was decreased by 44 per cent (p less than 0.001) in patients with untreated ketotic diabetes and by 20 per cent (p less than 0.01) in patients with untreated mild to moderate nonketotic early-onset diabetes. Insulin treatment of ketotic diabetes resulted in a rapid increase in the activity of LPL and decrease in serum triglycerdie level, whereas sulfonylurea treatment of non-insulin-requiring diabetics did not significantly influence the enzyme activity. In insulin-treated chronic diabetics the average postheparin plasma LPL activity was not different from that of nondiabetic controls, but some of these patients had high LPL values. In normolipidemic maturity-onset-type diabetics the LPL activity was within normal range, but in those having hypertriglyceridemia the average LPL value was decreased by an average of 26 per cent (p less than 0.01). The LPL activity showed a significant negative correlation with the logarithm of serum triglyceride concentration (r = -0.62) and a positive correlation with fractional removal of Intralipid (r = +0.64) and fractional turnover of V triglyceride (r = +0.40). The activity of LPL was correlated to basal plasma insulin concen tration in the insulin-deficient diabetes r = +0.34) but not in patients with maturity-onset-type diabetes. The hepatic lipase (HL) activity of postheparin plasma was similar in diabetes and controls, with the exception of hypertriglyceridemic maturity-onset diabetics, who had higher mean HL activity than the corresponding control group (p greater than 0.01). The activity of HL was not related to triglyceride removal but showed a significant correlation to VLDL-triglyceride production rate. On the basis of these results it seems that a deficiency of LPL accounts for a great deal of the elevation of serum triglyceride in insulin-deficient human diabetes but has a smaller role in the pathogenesis of the hypertriglyceridemia that is associated with maturity-onset diabetes. The latter abnormality is caused mainly by an increased secretion of triglycerides into the blood even though a decreased LPL may contribute to development of hyperlipemia in cases with gross elevation of serum triglycerides.
CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				F. G.S. Toledo, A. D. Sniderman, and D. E. Kelley Influence of Hepatic Steatosis (Fatty Liver) on Severity and Composition of Dyslipidemia in Type 2 Diabetes Diabetes Care, August 1, 2006; 29(8): 1845 - 1850. [Abstract] [Full Text] [PDF]

				J. E. Bauer, D. Nagaoka, B. Porterpan, K. Bigley, T. Umeda, and K. Otsuji Postprandial Lipolytic Activities, Lipids, and Carbohydrate Metabolism Are Altered in Dogs Fed Diacylglycerol Meals Containing High- and Low-Glycemic-Index Starches J. Nutr., July 1, 2006; 136(7): 1955S - 1957S. [Full Text] [PDF]

				A. Carpentier, B. W. Patterson, K. D. Uffelman, A. Giacca, M. Vranic, M. S. Cattral, and G. F. Lewis The Effect of Systemic Versus Portal Insulin Delivery in Pancreas Transplantation on Insulin Action and VLDL Metabolism Diabetes, June 1, 2001; 50(6): 1402 - 1413. [Abstract] [Full Text]

				R. Frénais, H. Nazih, K. Ouguerram, C. Maugeais, Y. Zaïr, J. M. Bard, B. Charbonnel, T. Magot, and M. Krempf In Vivo Evidence for the Role of Lipoprotein Lipase Activity in the Regulation of Apolipoprotein AI Metabolism: A Kinetic Study in Control Subjects and Patients with Type II Diabetes Mellitus J. Clin. Endocrinol. Metab., May 1, 2001; 86(5): 1962 - 1967. [Abstract] [Full Text]