help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Silverman, M. S.
Right arrow Articles by Sonenberg, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Silverman, M. S.
Right arrow Articles by Sonenberg, M.

Endocrinology, Vol 125, 2600-2604, Copyright © 1989 by Endocrine Society

ARTICLES

Antagonism by growth hormone of insulin-sensitive hexose transport in 3T3-F442A adipocytes

MS Silverman, DC Mynarcik, RE Corin, HC Haspel and M Sonenberg
Memorial Sloan-Kettering Cancer Center, Cornell University Medical College, New York, New York 10021.

We have studied the effects of GH on basal and insulin-stimulated hexose transport by 3T3-F442A adipocytes in a hormonally defined serum- free medium. Adipocytes preincubated in defined medium exhibit a low level of hexose transport which is acutely (15 min) stimulated (greater than 5-fold) by insulin (EC50, 0.1-0.2 nM). GH has acute (15-45 min) insulin-mimetic (greater than 2-fold) and chronic (4-48 h) diabetogenic (50-80%) effects on basal and insulin-stimulated hexose transport. The insulin-mimetic effect of GH has a higher EC50 (2 nM) than its diabetogenic effect (EC50, 0.2 nM). Chronic GH exposure decreases the maximal responsiveness (50-80%) and the acute sensitivity (approximately 2-fold) of hexose transport to insulin. Insulin- stimulated transport is more (approximately 5-fold) sensitive to the diabetogenic effect of GH than is basal transport. Insulin binding and degradation were not altered by chronic exposure to GH. The diabetogenic effect of GH may occur at a postinsulin binding level.


This article has been cited by other articles:


Home page
 EndocrinologyHome page
Y. Cho, M. Ariga, Y. Uchijima, K. Kimura, J.-Y. Rho, Y. Furuhata, F. Hakuno, K. Yamanouchi, M. Nishihara, and S.-I. Takahashi
The Novel Roles of Liver for Compensation of Insulin Resistance in Human Growth Hormone Transgenic Rats
Endocrinology, November 1, 2006; 147(11): 5374 - 5384.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
L. Liang, T. Zhou, J. Jiang, J. H. Pierce, T. A. Gustafson, and S. J. Frank
Insulin Receptor Substrate-1 Enhances Growth Hormone-Induced Proliferation
Endocrinology, May 1, 1999; 140(5): 1972 - 1983.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
M. Christopher, F. L. Hew, M. Oakley, C. Rantzau, and F. Alford
Defects of Insulin Action and Skeletal Muscle Glucose Metabolism in Growth Hormone-Deficient Adults Persist after 24 Months of Recombinant Human Growth Hormone Therapy
J. Clin. Endocrinol. Metab., May 1, 1998; 83(5): 1668 - 1681.
[Abstract] [Full Text]

Home page
 EndocrinologyHome page
T.-W. L. Gong, D. J. Meyer, J. Liao, C. L. Hodge, G. S. Campbell, X. Wang, N. Billestrup, C. Carter-Su, and J. Schwartz
Regulation of Glucose Transport and c-fos and egr-1 Expression in Cells with Mutated or Endogenous Growth Hormone Receptors
Endocrinology, April 1, 1998; 139(4): 1863 - 1871.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1989 by The Endocrine Society