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Am J Physiol Heart Circ Physiol 283: H391-H397, 2002; doi:10.1152/ajpheart.00019.2002
0363-6135/02 $5.00
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Vol. 283, Issue 1, H391-H397, July 2002

Obesity lowers hyperglycemic threshold for impaired in vivo endothelial nitric oxide function

H. G. Bohlen and Geoffrey P. Nase

Department of Cellular and Integrative Physiology, Indiana University Medical School, Indianapolis, Indiana 46202

Obesity is a risk for type II diabetes mellitus and increased vascular resistance. Disturbances of nitric oxide (NO) physiology occur in both obese animals and humans. In obese Zucker rats, we determined whether a protein kinase C-beta II (PKC-beta II) mechanism may lower the resting NO concentration ([NO]) and predispose endothelial NO abnormalities at lower glucose concentrations than occur in lean rats. NO was measured with microelectrodes touching in vivo intestinal arterioles. At rest, the [NO] in obese Zucker rats was 60 nm less than normal or about a 15% decline. After local blockade of PKC-beta II with LY-333531, the [NO] increased ~90 nm in obese rats but did not change in lean rats. In lean rats, administration of 300 mg/dl D-glucose for 45 min depressed endothelium-dependent dilation; only 200 mg/dl was required in obese animals. These various observations indicate that resting [NO] is depressed in obese rats by a PKC-beta II mechanism and the hyperglycemic threshold for endothelial NO suppression is reduced to 200 mg/dl D-glucose.

diabetes; hyperglycemia; LY-333531


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