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and
CAROL.M. FOSTER
Department of Physiology, The University of Michigan Medical School Ann Arbor, Michigan 48109
3T3-F442A adipocytes were used to compare the effects on glucose metabolism of pituitary human (h) GH and methionyl-hGH produced by recombinant DNA techniques (met-hGH 22K). Pituitary hGH and met-hGH 22K were similar in their ability to inhibit glucose oxidation and lipid accumulation after 48 h. After 4 h of incubation, both forms of hGH stimulated glucose oxidation transiently in 3T3 adipocytes. A bacterially produced form of the 20,000-dalton variant of hGH (met-hGH 20K) also stimulated glucose oxidation at 4 h and inhibited glucose oxidation and lipid synthesis after 48 h. All three forms of hGH had a similar ability to inhibit [(125)I]iodo-met-hGH 22K binding to 3T3-adipocytes. Thus, met-hGH 22K and 20K directly produce in 3T3 adipocytes the transient stimulation and delayed inhibition of glucose metabolism attributed to pituitary hGH, indicating that these metabolic effects are intrinsic to the hGH molecule.
* This work was supported by the American Diabetes Association, Michigan Affiliate, and NIH Grant AM-34171.
To whom all correspondence and requests for reprints should be addressed.
Present address: Department of Pediatrics, University of Michigan Medical School, Ann Arbor, Michigan 48109. Recipient of NIH Post-doctoral Traineeship AM-07245.
Received September 11, 1985.
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