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AJP - Renal Physiology, Vol 259, Issue 2 251-F257, Copyright © 1990 by American Physiological Society
ARTICLES |
S. B. Miller, P. Rotwein, J. D. Bortz, P. J. Bechtel, V. A. Hansen, S. A. Rogers and M. R. Hammerman
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
We examined insulin-like growth factor I (IGF I) gene expression in kidney in two models of hypersomatotropism, rats implanted with GH3 pituitary tumors, and rats administered exogenous growth hormone (GH). Both GH3 tumor-bearing rats and rats administered GH gained weight more rapidly than control animals, and had kidneys that were larger than those of controls. Tumor-bearing rats had increased levels of circulating IGF I. Glomeruli from tumor-implanted rats were sclerotic. Immunostainable IGF I was increased in medullary collecting ducts from tumor-bearing and GH-injected rats compared with kidneys from control animals. Levels of IGF I mRNA in kidneys of rats implanted with GH3 tumors and GH-injected rats were elevated compared with levels in kidneys from controls. Our findings demonstrate enhanced renal IGF I gene expression in hypersomatotropism. Stimulation of renal IGF I synthesis by GH could be causative of changes in renal function and renal size that occur in states of GH excess such as acromegaly.
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