The GH response to a variety of provocative stimuli (insulin-hypoglycemia, arginine, opiates, glucagon, levodopa and GHRH), is diminished in obese subjects (52). One study evaluating spontaneous GH secretory dynamics in obese men (body mass index [BMI] >42) demonstrated a reduction in endogenous GH half-life relative to control subjects (BMI < 31), a daily production rate of GH 4.1-fold less compared with controls and a threefold decrease in GH secretory burst frequency despite preservation of the GH ultradian rhythm (52). This principle applies to children as well.
Cholinesterase inhibitors, including pyridostigmine, decrease somatostatin tone. Following exogenous pyridostigmine, obese subjects have an increase in the GH secretory response to provocative stimuli, supporting the SRIF hypothesis. These reports suggest the postprandial period is associated with reduced cholinergic tone and a parallel increase in somatostatin tone in normal and obese subjects (53). Sustained weight reduction in man and experimental animals leads to a partial restoration of GH release in obese subjects (52). Short-term very low-calorie diets appear to have no effect on the 24-h GH secretory profile (54).
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