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Research Article Free access | 10.1172/JCI117951

Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin-dependent diabetes mellitus.

N Cohen, M Halberstam, P Shlimovich, C J Chang, H Shamoon, and L Rossetti

Department of Medicine, Albert Einstein College of Medicine, New York 10461, USA.

Find articles by Cohen, N. in: JCI | PubMed | Google Scholar

Department of Medicine, Albert Einstein College of Medicine, New York 10461, USA.

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Department of Medicine, Albert Einstein College of Medicine, New York 10461, USA.

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Department of Medicine, Albert Einstein College of Medicine, New York 10461, USA.

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Department of Medicine, Albert Einstein College of Medicine, New York 10461, USA.

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Department of Medicine, Albert Einstein College of Medicine, New York 10461, USA.

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Published June 1, 1995 - More info

Published in Volume 95, Issue 6 on June 1, 1995
J Clin Invest. 1995;95(6):2501–2509. https://doi.org/10.1172/JCI117951.
© 1995 The American Society for Clinical Investigation
Published June 1, 1995 - Version history
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Abstract

We examined the in vivo metabolic effects of vanadyl sulfate (VS) in non-insulin-dependent diabetes mellitus (NIDDM). Six NIDDM subjects treated with diet and/or sulfonylureas were examined at the end of three consecutive periods: placebo for 2 wk, VS (100 mg/d) for 3 wk, and placebo for 2 wk. Euglycemic hyperinsulinemic (30 mU/m2.min) clamps and oral glucose tolerance tests were performed at the end of each study period. Glycemic control at baseline was poor (fasting plasma glucose 210 +/- 19 mg/dl; HbA1c 9.6 +/- 0.6%) and improved after treatment (181 +/- 14 mg/dl [P < 0.05], 8.8 +/- 0.6%, [P < 0.002]); fasting and post-glucose tolerance test plasma insulin concentrations were unchanged. After VS, the glucose infusion rate during the clamp was increased (by approximately 88%, from 1.80 to 3.38 mg/kg.min, P < 0.0001). This improvement was due to both enhanced insulin-mediated stimulation of glucose uptake (rate of glucose disposal [Rd], +0.89 mg/kg.min) and increased inhibition of HGP (-0.74 mg/kg.min) (P < 0.0001 for both). Increased insulin-stimulated glycogen synthesis (+0.74 mg/kg.min, P < 0.0003) accounted for > 80% of the increased Rd after VS, and the improvement in insulin sensitivity was maintained after the second placebo period. The Km of skeletal muscle glycogen synthase was lowered by approximately 30% after VS treatment (P < 0.05). These results indicate that 3 wk of treatment with VS improves hepatic and peripheral insulin sensitivity in insulin-resistant NIDDM humans. These effects were sustained for up to 2 wk after discontinuation of VS.

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