The role of insulin and igf-i in activation of muscle protein synthesis following oral feeding. Svanberg, Elisabeth, Helen Zachrisson, Claes Ohlsson, Britt-Marie Iresj[diaeresis]o, and Kent G. Lundholm. Department of Surgery and Internal Medicine, Sahlgrenska University Hospital, University of G[diaeresis]oteborg, Sweden
APStracts 2:0247E, 1995.
The aim was to evaluate the role of insulin and insulin-like growth factor (IGF-I) in activation of muscle protein synthesis following oral feeding. Synthesis rate of globular and myofibrillar proteins in muscle tissue was quantified by a flooding dose of radioactive phenylalanine. Muscle tissue expression of IGF-I mRNA was measured. Normal (C57 Bl) and diabetic mice (type-I; type-II) were subjected to an overnight fast (18 hrs) with subsequent refeeding procedures for 3 hrs with either oral chow intake or provision of insulin, IGF-I, glucose and amino acids. Anti-insulin and anti-IGF-I were provided i.p. before oral refeeding in some experiments . An overnight fast reduced synthesis of both globular (38+/-3%) and myofibrillar proteins (54+/-3%) in skeletal muscles, which was reversed by oral refeeding. Muscle protein synthesis, following starvation/refeeding, was proportional and similar to changes in skeletal muscle IGF-I mRNA expression. Diabetic mice responded quantitatively similarly to starvation/refeeding in muscle protein synthesis compared to normal mice (C57 Bl). Both anti-insulin and anti-IGF-I attenuated significantly the stimulation of muscle protein synthesis in response to oral feeding, while exogenous provision of either insulin or IGF-I to overnight starved and freely-fed mice did not clearly stimulate protein synthesis in skeletal muscles. Our results support the suggestion that insulin and IGF-I either induce or facilitate the protein synthesis machinery in skeletal muscles rather than exerting a true stimulation of the biosynthetic process during feeding. 

Received 5 July 1995; accepted in final form 21 November 1995.
APS Manuscript Number E310-5.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95