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DEVELOPMENT AND TISSUE PLASTICITY

IGF-I augments resection-induced mucosal hyperplasia by altering enterocyte kinetics

¹Department of Nutritional Sciences, University of Wisconsin-Madison, Madison 53706; and ²Department of Pathology and Laboratory Medicine, University of Wisconsin Hospitals and Clinics, Madison, Wisconsin 53792

Submitted 10 January 2003 ; accepted in final form 19 May 2003

Our objective was to determine if exogenous insulin-like growth factor-I (IGF-I) augments the adaptive growth response to mid small bowel resection in association with changes in enterocyte kinetics. We determined structural adaptation and concomitant changes in enterocyte proliferation, apoptosis, and migration of the jejunum in growing, parenterally fed rats after mid small bowel resection or small bowel transection, and treatment with IGF-I or vehicle. IGF-I treatment in resected rats significantly increased jejunal mucosal mass by 20% and mucosal concentrations of protein and DNA by 36 and 33%, respectively, above the response to resection alone. The enhancement of resection-induced adaptive growth and cellularity by IGF-I reflected an increase in enterocyte proliferation, an expansion of the proliferative compartment in the crypt, and no further decrease in enterocyte apoptosis or increase in enterocyte migration beyond the effects of resection. The ability of IGF-I to augment the mucosal hyperplasia stimulated by the endogenous response to resection substantiates the role of IGF-I as an intestinal mitogen that promotes tissue regeneration.

enterocyte proliferation and apoptosis; insulin-like growth factor-I; intestinal adaptation; bowel resection; total parenteral nutrition

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