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Research Article Free access | 10.1172/JCI116039

Regulation of lipoprotein lipase in the diabetic rat.

K Tavangar, Y Murata, M E Pedersen, J F Goers, A R Hoffman, and F B Kraemer

Department of Medicine, Stanford University School of Medicine, California 94305.

Find articles by Tavangar, K. in: PubMed | Google Scholar

Department of Medicine, Stanford University School of Medicine, California 94305.

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Department of Medicine, Stanford University School of Medicine, California 94305.

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Department of Medicine, Stanford University School of Medicine, California 94305.

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Department of Medicine, Stanford University School of Medicine, California 94305.

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Department of Medicine, Stanford University School of Medicine, California 94305.

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Published November 1, 1992 - More info

Published in Volume 90, Issue 5 on November 1, 1992
J Clin Invest. 1992;90(5):1672–1678. https://doi.org/10.1172/JCI116039.
© 1992 The American Society for Clinical Investigation
Published November 1, 1992 - Version history
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Abstract

Diabetes mellitus is associated with a reduction of lipoprotein lipase (LPL) activity and development of hypertriglyceridemia. In the current experiments the mechanisms involved in the regulation of LPL have been examined in control rats, streptozocin-induced diabetic rats, and diabetic rats treated chronically or with a single injection of insulin. Diabetes decreased adipose tissue LPL activity partially by decreasing immunoreactive LPL protein and the steady-state levels of LPL mRNA, but primarily by reducing the catalytic activity of LPL. Both chronic and acute insulin increased adipose tissue LPL activity by correcting the defect in the catalytic activity of LPL and increasing immunoreactive LPL protein; however, only chronic insulin restored LPL mRNA levels to normal. In the heart, LPL activity tended to be elevated with diabetes in parallel to an increase in immunoreactive LPL protein even though levels of LPL mRNA declined. Both chronic and acute insulin normalized LPL activity and immunoreactive LPL protein, while only chronic insulin corrected the levels of LPL mRNA. No changes in the catalytic activity of LPL in heart were detected among the groups. Thus, diabetes and insulin treatment regulate LPL expression pretranslationally, translationally, and post-translationally, with tissue-specific differences apparent in the mechanisms involved.

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