With increased adiposity, GH secretion is blunted with a decrease in the mass of GH secreted per burst but without any major impact on GH secretory burst frequency (46). Moreover, the metabolic clearance rate of GH is accelerated (32). The serum insulin-like growth factor (IGF)-1 concentration is primarily GH dependent and influences GH secretion though a negative feed-back system (47). The serum levels of IGF-1 are inversely related to the percentage of body fat (46). In addition, the low serum IGF-1 concentration in obesity is predominantly related to the amount of visceral adipose tissue and not to the amount of subcutaneous fat mass (48). The relationship between regional fat distribution and GH secretion has only recently been considered. No significant correlation was found between the waist-to-hip ratio and 24-h GH secretion rates in a study of 21 healthy men (49). However, measured by computed tomography, the amount of visceral adiposity was a major determinant of stimulated (arginine and clonidine) GH secretion in non-obese healthy adults (50). Also the integrated 24-h GH concentration was found to be negatively associated with visceral fat mass in both young and old men and women (51). These findings, together with other endocrine disturbances in central obesity, suggest that the low GH secretion and serum IGF-1 is secondary to a central disturbance of the neuroendocrine regulation.
Low levels of GH may be of importance for the metabolic consequences and the maintenance of the obese condition. One trial has, however, demonstrated near normalization of the 24-h GH secretion and serum IGF-1 in nine obese subjects after massive weight loss (52) whereas others have not found a normalization of the GH response to provocative testing in response to weight loss (53,54). Thus, whether the multiple endocrine aberrations including low GH secretion in abdominal obesity is primarily responsible or the consequence of the obese condition remains to be elucidated.
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