The Acute Insulin Synergistic Activity of Growth Hormone - I) Inhibition by Chronic Growth Hormone Administration[*]

Abstract

Mahler, Richard J.; Szabo, Olga: The Acute Insulin Synergistic Activity of Growth Hormone - II) Reversal of Chronic Growth Hormone Effect by Actinomycin D. Horrn.Metab.Res. 2: 65-71 (1969). We have suggested that the initial reduction in blood sugar following a single injection of growth hormone to the intact animal might be due to enhancement of endogenous insulin action resulting from inhibited insulin degradation. This postulate is based upon the observation that a) liver and kidney slices prepared from G. H. injected animals demonstrate impaired degradation of ¹³¹I insulin in vitro and b) kidney slices and hemidiaphragms from G. H. injected animals reveal significant enhancement of insulin action upon carbohydrate metabolism in vitro.

Since the chronic effect of G. H. administration is to cause a reversal of its acute hypoglycemic activity the present report has considered the influence of repetitive G. H. administration upon the acute insulin synergistic activity of growth hormone.

We report that pre-treatment of the animal for 24 hours prior to G. H. injection fails to influence the ability of an acute G. H. injection to both impair the rate of insulin degradation and enhance the metabolic activity of insulin; whereas pre-treatment for 48 hours or longer results in an inability of a subsequent G. H. injection to either impair insulin degradation or enhance the metabolic activity of insulin.

We conclude that the chronic administration of G. H. results in the generation of a material capable of inhibiting the acute insulin synergistic activity of growth hormone.

Key words

GH-treatment in rats - Impairment of Insulin Degradation - Enhancement of Insulin Activity - Inhibition of GH Insulin Synergism

1 This work was supported in part by Grant No. U-1836 of the Health Research Council of the City of New York and by Grant No. GB 5251 X of the Division of Biological and Medical Sciences, National Science Foundation,Washington, D. C. Dr. Mahler is the recipient of aResearch and Development Award of the American Diabetes Association.

1 This work was supported in part by Grant No. U-1836 of the Health Research Council of the City of New York and by Grant No. GB 5251 X of the Division of Biological and Medical Sciences, National Science Foundation,Washington, D. C. Dr. Mahler is the recipient of aResearch and Development Award of the American Diabetes Association.

2 We are indebted to Dr. Rachmiel Levine for his helpful advice and encouragement.