AJP - Regulatory, Integrative and Comparative Physiology, Vol 250, Issue 4 682-R690, Copyright © 1986 by American Physiological Society
Glucagon-induced inhibition of feeding is impaired by hepatic portal alloxan injection
S. Ritter, S. C. Weatherford and S. L. Stone
Subdiabetogenic doses of alloxan injected into the hepatic portal vein of
rats abolished glucagon-induced inhibition of feeding (glucagon satiety)
both in daytime tests using a palatable food and in nighttime tests using
their standard pelleted diet. In contrast, inhibition of food intake by
cholecystokinin and epinephrine and stimulation of feeding by
2-deoxy-D-glucose were not impaired by alloxan. Alloxan-induced deficits in
glucagon satiety did not appear to result from generalized hepatocellular
necrosis, because satiety deficits outlasted histological signs of toxicity
and because furosemide, which produced a similar degree of hepatotoxicity,
did not impair glucagon satiety. In addition, alloxan's effects were not
associated with impaired glycogen storage or mobilization. Recovery of
glucagon satiety occurred in some animals but not until 3-6 mo after
alloxan. The degree of recovery was inversely related to alloxan dose. Our
results indicate that, when administered into the hepatic portal vein,
alloxan may be a relatively specific toxin for cells involved in the
mediation of glucagon satiety. The specificity of the deficit and the time
course of recovery suggest that the alloxan-sensitive cells may be hepatic
vagal neurons.
