AJP - Gastrointestinal and Liver Physiology, Vol 255, Issue 5 542-G546, Copyright © 1988 by American Physiological Society
Role of glucagon in intestinal hyperemia associated with early experimental diabetes mellitus
L. F. Yrle, J. K. Smith, J. N. Benoit, D. N. Granger and R. J. Korthuis
Department of Physiology and Biophysics, Louisiana State University Medical Center, School of Medicine, Shreveport 71130.
The role of glucagon as a blood-borne mediator of the intestinal hyperemia
associated with experimental diabetes mellitus was assessed in anesthetized
fasted (18-24 h) rats 4 wk after the administration of streptozotocin (65
mg/kg body wt) or its vehicle. Selective removal of pancreatic glucagon
from the circulation was accomplished by the intravenous administration of
a highly specific glucagon antiserum. Blood flow to the gastrointestinal
tract and kidneys was measured with radioactive microspheres using the
reference sample technique. Blood flows were increased by at least 60% in
each segment of the gastrointestinal tract of diabetic animals compared
with control rats. Glucagon antiserum had no effect on blood flows in the
gastrointestinal tract of control animals. However, the antiserum produced
a significant reduction in blood flow to the stomach (26%), duodenum (25%),
jejunum (12%), and kidneys (16%) in diabetic rats. There was no change in
blood flow to the ileum or colon of diabetic animals with antiserum
administration. The results of this study support the hypothesis that
glucagon mediates a portion of the hyperemia noted in the stomach,
duodenum, and jejunum. However, glucagon does not appear to play a role in
the genesis of the hyperemia noted in more distal segments of the
gastrointestinal tract (ileum and colon). A possible role for glucagon in
the maintenance of renal blood flow in diabetic rats is suggested.
