AJP - Endocrinology and Metabolism, Vol 247, Issue 2 243-E250, Copyright © 1984 by American Physiological Society
Intrahepatic glucose: a requirement for neonatal ODC induction by specific hormones
G. Evoniuk, C. Kuhn and S. Schanberg
We have shown previously that short-term nutritional deprivation causes a
tissue-specific loss of liver ornithine decarboxylase (ODC) induction after
isoproterenol, phenylephrine, or glucagon administration in rat pups. To
examine the role of nutrition in the regulation of hepatic ODC, we tested
the ability of intragastric nutrient administration to reverse
nutritionally related deficits in the ODC response to hormonal challenge.
Intragastric whole milk was effective in restoring ODC induction and
accumulation of its immediate product, putrescine, in response to
isoproterenol administration. Glucose was shown to mediate this effect by
the ability of intragastric skimmed milk, lactose, galactose, or D-glucose
to return ODC induction, and the inability of casein, sucrose, fructose,
L-glucose, or pyruvate plus lactate to do so. D-Glucose also reestablished
ODC induction by phenylephrine and glucagon. Parenteral administration of
D-glucose produced results comparable to those obtained after intragastric
administration. Isoproterenol induction of ODC was prevented when hepatic
glucose uptake was blocked by phlorizin but not by blockade of central
nervous system glucose uptake with 2-deoxyglucose. We conclude that
intrahepatic glucose is an absolute requirement for hepatic ODC induction
by isoproterenol, phenylephrine, or glucagon in preweanling rats.
