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

H. G. Bohlen, Geoffrey P. Nase

Research output: Contribution to journalArticle

35 Scopus citations

Abstract

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-ΒII (PKC-ΒII) 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-ΒII 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-ΒII mechanism and the hyperglycemic threshold for endothelial NO suppression is reduced to 200 mg/dl D-glucose.

Original languageEnglish (US)
Pages (from-to)H391-H397
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume283
Issue number1 52-1
DOIs
StatePublished - Jan 1 2002

Keywords

  • Diabetes
  • Hyperglycemia
  • LY-333531

ASJC Scopus subject areas

  • Physiology

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