Non-insulin-dependent diabetes and hyperglycemia impair rat intestinal flow-mediated regulation

Jong Shiaw Jin, H. Bohlen

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Release of nitric oxide from small arteries and larger arterioles of the intestine maintains their dilation and thereby supports mucosal blood flow. This flow-dependent mechanism can be studied by isosmotic replacement of sodium chloride with mannitol over the mucosa to lower mucosal metabolism and blood flow requirements. We tested the hypothesis that flow-mediated regulation is impaired in the non-insulin-dependent Zucker fatty diabetic (ZFD) male rats because of their marginally impaired endothelium-dependent dilation. Furthermore, we determined whether the depressed acetylcholine dilation associated with acute hyperglycemia in normoglycemic Zucker (NZ) rats also impairs flow-mediated regulation. When mannitol replaced sodium chloride over the villi, intestinal blood flow decreased significantly (P < 0.05) less in ZFD (80.9 ± 6.8% of control) than NZ rats (40.9 ± 6.4% of control). After 300 mg/dl hyperglycemia for 30 min, normal arterioles had impaired responses to acetylcholine and the resting blood flow and oxygen consumption were suppressed about 60%, which indicate the importance of basal nitric oxide release for intestinal vascular support of metabolism. The evidence of impaired flow-mediated dilation in ZFD and decreased resting blood flow after hyperglycemia in NZ rats demonstrated that both acute and chronic hyperglycemia disturb endothelial regulation of the intestinal vasculature.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume41
Issue number2
StatePublished - Feb 1997

Fingerprint

Hyperglycemia
Zucker Rats
Dilatation
Arterioles
Mannitol
Sodium Chloride
Acetylcholine
Nitric Oxide
Large Intestine
Oxygen Consumption
Endothelium
Blood Vessels
Mucous Membrane
Arteries

Keywords

  • Diabetes mellitus
  • Nitric oxide
  • Zucker fatty diabetic

ASJC Scopus subject areas

  • Physiology

Cite this

@article{668a01fff1a84105b3610dcb666df2a6,
title = "Non-insulin-dependent diabetes and hyperglycemia impair rat intestinal flow-mediated regulation",
abstract = "Release of nitric oxide from small arteries and larger arterioles of the intestine maintains their dilation and thereby supports mucosal blood flow. This flow-dependent mechanism can be studied by isosmotic replacement of sodium chloride with mannitol over the mucosa to lower mucosal metabolism and blood flow requirements. We tested the hypothesis that flow-mediated regulation is impaired in the non-insulin-dependent Zucker fatty diabetic (ZFD) male rats because of their marginally impaired endothelium-dependent dilation. Furthermore, we determined whether the depressed acetylcholine dilation associated with acute hyperglycemia in normoglycemic Zucker (NZ) rats also impairs flow-mediated regulation. When mannitol replaced sodium chloride over the villi, intestinal blood flow decreased significantly (P < 0.05) less in ZFD (80.9 ± 6.8{\%} of control) than NZ rats (40.9 ± 6.4{\%} of control). After 300 mg/dl hyperglycemia for 30 min, normal arterioles had impaired responses to acetylcholine and the resting blood flow and oxygen consumption were suppressed about 60{\%}, which indicate the importance of basal nitric oxide release for intestinal vascular support of metabolism. The evidence of impaired flow-mediated dilation in ZFD and decreased resting blood flow after hyperglycemia in NZ rats demonstrated that both acute and chronic hyperglycemia disturb endothelial regulation of the intestinal vasculature.",
keywords = "Diabetes mellitus, Nitric oxide, Zucker fatty diabetic",
author = "Jin, {Jong Shiaw} and H. Bohlen",
year = "1997",
month = "2",
language = "English",
volume = "41",
journal = "American Journal of Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Non-insulin-dependent diabetes and hyperglycemia impair rat intestinal flow-mediated regulation

AU - Jin, Jong Shiaw

AU - Bohlen, H.

PY - 1997/2

Y1 - 1997/2

N2 - Release of nitric oxide from small arteries and larger arterioles of the intestine maintains their dilation and thereby supports mucosal blood flow. This flow-dependent mechanism can be studied by isosmotic replacement of sodium chloride with mannitol over the mucosa to lower mucosal metabolism and blood flow requirements. We tested the hypothesis that flow-mediated regulation is impaired in the non-insulin-dependent Zucker fatty diabetic (ZFD) male rats because of their marginally impaired endothelium-dependent dilation. Furthermore, we determined whether the depressed acetylcholine dilation associated with acute hyperglycemia in normoglycemic Zucker (NZ) rats also impairs flow-mediated regulation. When mannitol replaced sodium chloride over the villi, intestinal blood flow decreased significantly (P < 0.05) less in ZFD (80.9 ± 6.8% of control) than NZ rats (40.9 ± 6.4% of control). After 300 mg/dl hyperglycemia for 30 min, normal arterioles had impaired responses to acetylcholine and the resting blood flow and oxygen consumption were suppressed about 60%, which indicate the importance of basal nitric oxide release for intestinal vascular support of metabolism. The evidence of impaired flow-mediated dilation in ZFD and decreased resting blood flow after hyperglycemia in NZ rats demonstrated that both acute and chronic hyperglycemia disturb endothelial regulation of the intestinal vasculature.

AB - Release of nitric oxide from small arteries and larger arterioles of the intestine maintains their dilation and thereby supports mucosal blood flow. This flow-dependent mechanism can be studied by isosmotic replacement of sodium chloride with mannitol over the mucosa to lower mucosal metabolism and blood flow requirements. We tested the hypothesis that flow-mediated regulation is impaired in the non-insulin-dependent Zucker fatty diabetic (ZFD) male rats because of their marginally impaired endothelium-dependent dilation. Furthermore, we determined whether the depressed acetylcholine dilation associated with acute hyperglycemia in normoglycemic Zucker (NZ) rats also impairs flow-mediated regulation. When mannitol replaced sodium chloride over the villi, intestinal blood flow decreased significantly (P < 0.05) less in ZFD (80.9 ± 6.8% of control) than NZ rats (40.9 ± 6.4% of control). After 300 mg/dl hyperglycemia for 30 min, normal arterioles had impaired responses to acetylcholine and the resting blood flow and oxygen consumption were suppressed about 60%, which indicate the importance of basal nitric oxide release for intestinal vascular support of metabolism. The evidence of impaired flow-mediated dilation in ZFD and decreased resting blood flow after hyperglycemia in NZ rats demonstrated that both acute and chronic hyperglycemia disturb endothelial regulation of the intestinal vasculature.

KW - Diabetes mellitus

KW - Nitric oxide

KW - Zucker fatty diabetic

UR - http://www.scopus.com/inward/record.url?scp=33750853805&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750853805&partnerID=8YFLogxK

M3 - Article

C2 - 9124431

AN - SCOPUS:33750853805

VL - 41

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0193-1857

IS - 2

ER -