Luft et al. (26) clearly demonstrated the glycaemic control to deteriorate following exposure to a single supraphysiological dose of human GH in hypophysectomised adults with type 1 diabetes mellitus. Somewhat surprisingly, only modest effects of GH on glucose metabolism were recorded in the first metabolic balance studies involving adult hypopituitary patients (27, 28). More recent studies on glucose homeostasis in GH deficient adults have generated results, which at first glance may appear contradictory. Insulin resistance may be more prevalent in untreated GH deficient adults (29, 30), whereas the impact of GH replacement on this feature seems to depend on the duration and the dose. Below, some of the metabolic effects of GH in human subjects, with special reference to the interaction between glucose and lipid metabolism, will be reviewed. Studies In Normal Adults Almost forty years ago it was shown that infusion of high dose GH into the brachial artery of healthy adults reduced forearm glucose uptake in both muscle and adipose tissue (31). This was parallelled by a drop in RQ and an increase in muscle uptake of FFA, both of which suggest oxidation of FFA by the muscle. This pattern was opposite that of insulin, and co-administration of insulin and GH resulted in only minimal changes in net fluxes of glucose and FFA across the forearm bed. These studies clearly indicated direct insulin antagonistic effects of GH on muscle and adipose tissue. The introduction of reliable radioimmunoassays for GH revealed the pulsatile and episodic nature of GH release (32) now known to be generated by alternating secretion of GHRH and SST. A GH pulse is released roughly every second hour with a mean daily secretion of 0.5 mg (33). Apart from a circadian variation in terms of elevated nocturnal GH levelsduring the early hours of sleep, GH secretion is amplified during fasting and stress, whereas meals suppress GH release. We studied the metabolic effect of a
Luft et al. (26) clearly demonstrated the glycaemic control to deteriorate following exposure to a single supraphysiological dose of human GH in hypophysectomised adults with type 1 diabetes mellitus. Somewhat surprisingly, only modest effects of GH on glucose metabolism were recorded in the first metabolic balance studies involving adult hypopituitary patients (27, 28). More recent studies on glucose homeostasis in GH deficient adults have generated results, which at first glance may appear contradictory. Insulin resistance may be more prevalent in untreated GH deficient adults (29, 30), whereas the impact of GH replacement on this feature seems to depend on the duration and the dose. Below, some of the metabolic effects of GH in human subjects, with special reference to the interaction between glucose and lipid metabolism, will be reviewed. Studies In Normal Adults Almost forty years ago it was shown that infusion of high dose GH into the brachial artery of healthy adults reduced forearm glucose uptake in both muscle and adipose tissue (31). This was parallelled by a drop in RQ and an increase in muscle uptake of FFA, both of which suggest oxidation of FFA by the muscle. This pattern was opposite that of insulin, and co-administration of insulin and GH resulted in only minimal changes in net fluxes of glucose and FFA across the forearm bed. These studies clearly indicated direct insulin antagonistic effects of GH on muscle and adipose tissue. The introduction of reliable radioimmunoassays for GH revealed the pulsatile and episodic nature of GH release (32) now known to be generated by alternating secretion of GHRH and SST. A GH pulse is released roughly every second hour with a mean daily secretion of 0.5 mg (33). Apart from a circadian variation in terms of elevated nocturnal GH levelsduring the early hours of sleep, GH secretion is amplified during fasting and stress, whereas meals suppress GH release. We studied the metabolic effect of a
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