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

H G Bohlen1, Geoffrey P Nase

  • 1Department of Cellular and Integrative Physiology, Indiana University Medical School, Indianapolis, Indiana 46202, USA. gbohlen@iupui.edu

American Journal of Physiology. Heart and Circulatory Physiology
|June 14, 2002
PubMed

Insights

Obesity lowers resting nitric oxide (NO) levels in rats via a protein kinase C-beta II (PKC-beta II) mechanism. This also reduces the glucose threshold for endothelial dysfunction, increasing type II diabetes risk.

Area of Science:

  • Physiology
  • Endocrinology
  • Vascular Biology

Background:

  • Obesity is a significant risk factor for type II diabetes mellitus and increased vascular resistance.
  • Dysregulation of nitric oxide (NO) physiology is observed in both obese animals and humans.
  • Protein kinase C-beta II (PKC-beta II) is implicated in NO pathway disturbances.

Purpose of the Study:

  • To investigate if a PKC-beta II mechanism contributes to reduced resting NO concentrations in obese Zucker rats.
  • To determine if this mechanism predisposes obese rats to endothelial NO abnormalities at lower glucose levels compared to lean rats.

Main Methods:

  • Measurement of NO concentration ([NO]) in vivo using microelectrodes in intestinal arterioles of obese and lean Zucker rats.
  • Administration of a PKC-beta II inhibitor (LY-333531) to assess its effect on [NO].
  • Assessment of endothelium-dependent dilation in response to varying D-glucose concentrations.

Main Results:

  • Resting [NO] was approximately 15% lower in obese Zucker rats compared to lean rats.
  • Blockade of PKC-beta II with LY-333531 increased [NO] in obese rats but not in lean rats.
  • The glucose concentration required to impair endothelium-dependent dilation was 200 mg/dl in obese rats versus 300 mg/dl in lean rats.

Conclusions:

  • Resting [NO] is depressed in obese rats due to a PKC-beta II mechanism.
  • The hyperglycemic threshold for endothelial NO suppression is significantly reduced in obese rats, indicating increased susceptibility to glucose-induced vascular dysfunction.

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