Growth hormone (GH) exerts a variety of metabolic actions in vivo. These diverse effects, which include alterations in lipid and carbohydrate metabolism as well as the stimulation of growth, are brought about through multiple mechanisms. This chapter will be focused on the interrelationship between GH and somatomedin- C/Insulin like growth factor I (SM-C/IGF-I), a mediator of the growth promoting action of GH. While not intended to be a comprehensive review of either GH or SMC/ IGF-I, we hope to provide the reader with insights into current understanding of the actions of these peptides.

Growth hormone has both direct and indirect actions

GH is secreted by the pituitary in an episodic pulsatile manner, with secretory bursts occurring several times daily (Bercu &Diamond, 1986). Despite these secretory bursts, the stimulation of SM-C/IGF-I secretion by growth hormone requires 4 or more hours to be detected in blood (Copeland et ai, 1980). In direct contrast, plasma concentrations SM-C/IGF-I are quite stable, and reflect integrated GH secretion rather than minute to minute fluctuations. Although the precise role of pulsatile GH secretion is unknown, it may be involved in the direct effects of GH on carbohydrate and lipid metabolism since these changes occur very rapidly after GH administration (Goodman & Knobil, 1961) (Figure 1). Injection of GH causes breakdown of triglycerides into free fatty acids and glycerol (Rabel & Hollenberg, 1959), and produces rapid increases in blood glucose. The net result of these direct actions of GH may be to facilitate the utilization of lipid and carbohydrate substrates to satisfy the energy requirements of growing tissues. However, the mechanisms that link these metabolic processes to long-term growth are not defined.