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Am J Physiol Endocrinol Metab 262: E663-E670, 1992;
0193-1849/92 $5.00
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AJP - Endocrinology and Metabolism, Vol 262, Issue 5 E663-E670, Copyright © 1992 by American Physiological Society

ARTICLES

Lipoprotein lipase release from cardiac myocytes is increased by decavanadate but not insulin

J. E. Braun and D. L. Severson
Medical Research Council Signal Transduction Group, Faculty of Medicine, University of Calgary, Alberta, Canada.

Streptozotocin-induced diabetes reduced cellular lipoprotein lipase (LPL) activity in cardiac myocytes from rat hearts and decreased the heparin-induced release of LPL into the medium. This effect of diabetes was rapidly reversed by in vivo treatment with insulin (5 U iv for 1 h); administration of insulin in vivo to control rats also increased heparin-releasable LPL activity. In contrast, in vitro addition of insulin to control and diabetic myocytes did not alter either cellular or heparin-releasable LPL activities. Insulin stimulated glucose oxidation and protein synthesis in control and diabetic myocytes. Decavanadate (0.05-1 mM) or vanadyl ion (0.5 mM) enhanced the release of LPL into the medium. Heparin- and decavanadate-induced release of LPL was not additive, and heparin pretreatment reduced the subsequent release of LPL by decavanadate. Decavanadate displaced LPL bound to heparin-Sepharose and increased LPL release into the perfusate of hearts. Therefore, decavanadate can mimic heparin in its effect on LPL. The absence of a direct in vitro effect of insulin on LPL in cardiac myocytes suggests that insulin may require some other in vivo factor or that diabetes-induced changes in LPL activity are secondary to some other metabolic factor.


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