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Endocrinology Vol. 140, No. 10 4850-4860
Copyright © 1999 by The Endocrine Society


ARTICLES

Investigation of Insulin-Like Growth Factor (IGF)-I and Insulin Receptor Binding and Expression in Jejunum of Parenterally Fed Rats Treated with IGF-I or Growth Hormone1

Denise M. Ney, David J. Huss, Melanie B. Gillingham, Karen R. Kritsch, Elizabeth M. Dahly, Jose L. Talamantez and Martin L. Adamo

Department of Nutritional Sciences (D.M.N., D.J.H., M.B.G., K.R.K., E.M.D.), University of Wisconsin-Madison, Madison, Wisconsin 53706; and Department of Biochemistry (J.L.T., M.L.A.), University of Texas Health Science Center at San Antonio, San Antonio, Texas 78284

Address all correspondence and requests for reprints to: Denise M. Ney, Ph.D., Department of Nutritional Sciences, University of Wisconsin-Madison, 1415 Linden Drive, Madison, Wisconsin 53706. E-mail: ney{at}nutrisci.wisc.edu

To investigate the ability of insulin-like growth factor-I (IGF-I), but not GH, to stimulate jejunal growth, we compared indices of IGF-I and insulin receptor expression in jejunal membranes from rats maintained with total parenteral nutrition (TPN) and treated with rhIGF-I and/or rhGH. TPN without growth factor treatment (TPN control) induced jejunal atrophy, reduced serum IGF-I, increased serum insulin concentrations, and increased IGF-I receptor number, IGF-I receptor messenger RNA, and insulin-specific binding to 133% to 170% of the orally fed reference values, P < 0.01. Compared with TPN control, IGF-I or IGF-I + GH stimulated jejunal mucosal hyperplasia; IGF-I treatment increased serum IGF-I by 2- to 3-fold and decreased serum insulin concentrations by 60%, decreased IGF-I receptor number by 50% (P < 0.001), and increased insulin receptor affinity and insulin receptor protein content. Treatment with GH alone increased serum IGF-I concentration, did not alter TPN-induced jejunal atrophy, and decreased insulin-specific binding and insulin receptor protein content (39% and 59%, respectively, of the TPN control values, P < 0.01). We conclude that: 1) jejunal IGF-I receptor content reflects circulating concentration of ligand and is not limiting for jejunal growth; and 2) increased circulating concentration of IGF-I may promote jejunal growth via interaction with jejunal insulin or IGF-I receptors.




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