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Insulin sensitivity is preserved despite disrupted endothelial function.

Sudha S Shankar¹, Robert V Considine, J Christopher Gorski

¹Division of Endocrinology, Department of Medicine, Indiana University School of Medicine, 975 W. Walnut, IB 424 D, Indianapolis, IN 46202, USA.

American Journal of Physiology. Endocrinology and Metabolism

|May 18, 2006

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Endothelial dysfunction alone does not impair insulin-mediated glucose disposal. The human immunodeficiency virus (HIV)-1 protease inhibitor indinavir causes endothelial dysfunction but not insulin resistance in healthy individuals.

Area of Science:

Metabolism
Vascular Biology
Pharmacology

Background:

Endothelial dysfunction and insulin resistance are often linked.
The direct role of endothelial dysfunction in impairing insulin sensitivity remains unclear.

Purpose of the Study:

To investigate if endothelial dysfunction induced by the HIV-1 protease inhibitor indinavir impairs insulin-mediated glucose disposal.
To determine if indinavir-induced endothelial dysfunction is associated with insulin resistance.

Main Methods:

Hyperinsulinemic euglycemic clamp studies to measure whole-body and skeletal muscle glucose disposal.
Vascular function studies to assess endothelium-dependent and insulin-mediated vasodilation.
Administration of indinavir for 4 weeks in healthy, HIV-negative subjects.

Related Experiment Videos

Main Results:

Indinavir significantly reduced endothelium-dependent vasodilation, confirming endothelial dysfunction.
Insulin-mediated vasodilation was significantly impaired after indinavir treatment.
No significant changes were observed in whole-body or skeletal muscle insulin-mediated glucose disposal.
Indinavir did not affect insulin-stimulated glucose uptake in adipose tissue.

Conclusions:

Endothelial dysfunction alone is insufficient to cause insulin resistance.
Indinavir-induced endothelial dysfunction appears to be a direct drug effect on the endothelium, uncoupled from insulin resistance.