Abstract

Chronic treatment of growing pigs with porcine growth hormone (pGH) markedly increases growth rate, improves feed efficiency (feed/gain), increases muscle growth and inhibits adipose tissue accretion. Growth hormone regulates a number of important metabolic and somatogenic events that include: elevation of plasma insulin-like growth factor 1 (IGF-I) concentration, stimulation of satellite cell proliferation, inhibition of glucose utilization by porcine adipocytes (due to a decrease in glucose transport, fatty acid synthesis and inhibition of several lipogenic enzymes) and antagonism of the stimulatory effects of insulin on glucose utilization in adipose tissue. These effects of GH on muscle and adipose tissue growth are coordinated in a manner that enables GH to alter the normal rate of nutrient partitioning between lipid and protein accretion to achieve the rather marked increase in protein deposition that occurs in parallel with the decrease in lipid deposition in pigs treated with exogenous pGH. In porcine adipose tissue, the metabolic effects of pGH are direct and are not mediated by IGF-I. The decrease in insulin sensitivity of porcine adipose tissue is not associated with any change in insulin binding or tyrosine kinase activity of the insulin receptor. The mechanisms by which pGH elicits its somatogenic effects in pigs are undoubtedly due in large part to the pGH-dependent elevation in serum IGF-I concentration. In association with the pGH-dependent rise in IGF-I there is a concurrent increase in a 150 kDa pGH-dependent IGF-I binding protein (IGF-BP) that acts as an inhibitor of IGF-I action. Further resolution of the mechanisms by which pGH affects pig growth and metabolism may lead to new strategies to enhance the biological potency of pGH or identify other ways of altering pig growth performance.

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