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Department of Physiology, University of Michigan Medical Schoo Ann Arbor, Michigan 48109;
nd the Hormone Research Laboratory, University of California (H.P) San Francisco, California 94143
Address requests for reprints to: Dr. Jack L. Kostyo, Department of Physiology, The University of Michigan Medical School, Ann Arbor, Michigan 48109.
Abstract
Purified GHs isolated from ostrich, sea turtle, snapping turtle, bullfrog, Tilapia, and sturgeon were tested for in vivo diabetogenic activity in the hereditarily obese ob/ob mouse and for in vitro insulin-like activity in isolated adipose tissue from hypophysectomized rats. GHs from all species exhibited significant diabetogenic activity, causing fasting hyperglycemia and decreased glucose tolerance when administered at doses of 100 µg/day (ostrich, bullfrog, and sturgeon) or 200 µg/ day (sea turtle, snapping turtle, and Tilapia) for 3 days. Similar responses were obtained when purified human GH was administered at a dose of 10 /gday for 3 days. GHs from most species also exhibited significant insulin-like activity, stimulating increased [14C]glucose oxidation to 14CO2 by isolated adipose tissue from hypophysectomized rats when employed at concentrations of 50 nM (bullfrog), 250 nM (sturgeon), 500 nM (ostrich), or 2500 nM (sea turtle and Tilapia). Purified human GH gave similar responses at concentrations of 2.5–5 nM in this assay. These results support the hypothesis that diabetogenic and insulin-like activities are intrinsic properties of GH and provide strong evidence that the structural determinants for diabetogenic and insulin-like activities arose early in the evolution of the GH molecule. (Endocrinology 116: 1501–1505,1985)
Footnotes
* Presented in part of the Seventh International Congress of Endocrinology, July 1984, Quebec City, Canada. This work was supported in part by The University of Michigan Biomedical Research Council and NSF Grant PCM-81-09846 (to H.P.).
Recipient of National Research Service Award Fellowship F32-AM-07268-02.
Received July 27, 1984.
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