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Enterotrophic Effect of Insulin-Like Growth Factor-I but not Growth Hormone and Localized Expression of Insulin-Like Growth Factor-I, Insulin-Like Growth Factor Binding Protein-3 and -5 mRNAs in Jejunum of Parenterally Fed Rats
Catherine A. Peterson, PhD, RD
Department of Nutritional Sciences, University of Missouri-Columbia, Missouri
Melanie B. Gillingham, PhD
Departments of Nutritional Sciences and Comparative Biosciences, University of Wisconsin-Madison, Wisconsin
Niru K. Mohapatra, PhD
Department of Cell and Molecular Physiology and Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, North Carolina
Elizabeth M. Dahly, BS
Departments of Nutritional Sciences and Comparative Biosciences, University of Wisconsin-Madison, Wisconsin
Martin L. Adamo, PhD
Department of Biochemistry, University of Texas Health Science Center at San Antonio, Texas
Hannah V. Carey, PhD
Departments of Nutritional Sciences and Comparative Biosciences, University of Wisconsin-Madison, Wisconsin
Pauline Kay Lund, PhD
Department of Cell and Molecular Physiology and Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, North Carolina
Denise M. Ney, PhD
Departments of Nutritional Sciences and Comparative Biosciences, University of Wisconsin-Madison, Wisconsin, ney{at}nutrisci.wisc.edu
Background: Administration of insulin-like growth factor (IGF)-I, but not growth hormone (GH), stimulates mucosal hyperplasia in surgically stressed rats with intestinal atrophy induced by hypocaloric total parenteral nutrition (TPN). Our aim was to characterize the basis for this disparity in enterotrophic action by assessing the relationships between stimulation of intestinal growth, nutritional adequacy, and localization of expression of IGF-I, insulin-like growth factor binding protein (IGFBP)-3 and IGFBP-5 mRNAs in jejunum. Methods: Rats were maintained with TPN for 8 days and treated with IGF-I or GH and adequate nutrition for 5 days after recovery from surgery. Jejunal mass, morphology, and sucrase activity were assessed. Localization of expression of IGF-I, IGFBP-3, and IGFBP-5 mRNAs in jejunum was accomplished by in situ hybridization. Results: Serum IGF-I and body weight gain were significantly increased by IGF-I or GH. Jejunal mucosal dry mass, morphology, and sucrase activity were improved with IGF-I but not GH. There were no differences in IGF-I mRNA. IGFBP-3 mRNA was localized in the lamina propria of the villi. IGF-I or GH stimulated IGFBP-3 expression. IGF-I strongly stimulated IGFBP-5 expression in the lamina propria and the muscularis and induced a twofold increase in IGFBP-5 mRNA based on RNase protection assay of intact jejunum total RNA. GH induced a modest increase in IGFBP-5 expression in the muscularis with no effect on intact jejunum total RNA. Conclusions: The GH resistance observed in the jejunal mucosa of TPN rats cannot be fully explained by inadequate nutrition. The expression of IGFBP-5 in the lamina propria suggests it may modulate the enterotrophic action of exogeneous IGF-I. (Journal of Parenteral and Enteral Nutrition 24:288-295, 2000)
Journal of Parenteral and Enteral Nutrition, Vol. 24, No. 5,
288-295 (2000)
DOI: 10.1177/0148607100024005288
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