Enhanced growth hormone (GH) responsiveness to GH-releasing hormone after dietary manipulation in obese and nonobese subjects

Abstract

Changes in plasma GH responses to GHRH (1 microgram/kg, iv) were assessed after dietary manipulations in obese and nonobese subjects to determine whether the impaired GH responsiveness to GHRH in obesity is the consequence of obesity per se or of altered food intake. The mean plasma GH response to GHRH in 10 obese subjects was significantly (P less than 0.05) higher after a 72-h fast than when they were eating their usual diet. Comparable increases were found when 6 of the subjects were studied after eating an 800 Cal/day diet for 6 weeks (P less than 0.05). Plasma glucose and insulin levels were lower and FFA levels higher after fasting, but not after the diet, compared to values on the usual diet. The mean plasma somatomedin-C (Sm-C) level was similar to that in nonobese subjects and was unaffected by dietary changes. The peak GH responses to GHRH before fasting were inversely correlated with plasma Sm-C levels (r = 0.64; P less than 0.05). Plasma GH responses to GHRH in normal weight subjects were also higher after fasting for 24 h (P less than 0.05) and 72 h (P less than 0.01) than after an overnight fast. Plasma glucose, insulin, and FFA changes were similar in the obese and normal weight subjects. Plasma Sm-C levels in the nonobese subjects were slightly lower after 72 h of fasting. We conclude that the increased plasma GH responsiveness to GHRH after fasting is not unique to obesity and is unlikely to reflect a reversal of the obesity-associated impairment of GH secretion. The increased plasma GH responsiveness to GHRH after as little as 24 h of fasting suggests that it is a consequence of acute nutrient deprivation rather than weight loss. The enhanced responses in obese subjects after 6 weeks of food restriction, in contrast, are probably a consequence of weight reduction.