During recent years of investigation abdominal/visceral distribution of adipose tissue has been found to be associated with endocrine disturbances, confirming the original observation by Vague (6). These disturbances include an increased cortisol activity and a blunted secretion of growth hormone (GH) and sex steroids in both men and women (29-34). These endocrine perturbations can theoretically be a consequence of the obese condition but it has also been suggested that the endocrine aberrations can have causal effects (33,35).
Recent results from testosterone intervention studies in men with abdominal/visceral obesity (33,36) may support this hypothesis. A physiological amount of testosterone in middle-aged men with abdominal/visceral adiposity induced improved insulin sensitivity, plasma lipid levels, and diastolic blood pressure, as well as a specific decrease in visceral adipose tissue mass. This might theoretically be explained by direct effects of testosterone on adipose tissue. However, as testosterone treatment in men with hypogonadotrophic hypogonadism increases GH secretion (37), the observed effects could be explained by increased GH levels or by additional or synergistic effects by GH and testosterone on adipose tissue metabolism (38).
Cortisol is of interest as it causes accumulation of abdominal/visceral adipose tissue (39) and an increased release of FFA. The latter will, in turn, cause reduced insulin binding in the liver and thereby higher circulating levels of insulin, glucose, and blood lipids by the mechanisms discussed above. The role of cortisol in obesity has been controversial during many years. Several authors have found decreased plasma cortisol levels in obese subjects while other have reported an increased cortisol secretion. We have recently found that these illusory contradictory findings can be explained by a disturbed diurnal secretion of cortisol, characterized by low morning plasma cortisol levels and increased 24-h free urinary cortisol values (30). Furthermore, previous studies on abdominally obese subjects have shown increased cortisol secretion after corticotro-phin releasing hormone (CRH) or ACTH challenge as well as after mental and physical laboratory stress tests (30,31,40). In addition, dexamethasone inhibition of cortisol secretion is blunted in abdominally obese men, suggesting a down-regulation of glucocorticoid receptors in the brain controlling CRH secretion (41).
There is considerable evidence that elevated secretion of CRH might attenuate other hypothalamic/pituitary hormonal axes including GH and gonadal steroids (42). A plausible explanation of an increased activity of the hypothalamic-pituitary-adrenal (HPA) axis in Syndrome X could be chronic or intermittent stress challenges, or an impaired ability of the individual to cope with stress (43). Furthermore, the neuro-endocrine findings discussed here show several similarities with conditions of oversecretion of cortisol such as Cushing's syndrome and depression, both of which have an increased activity of the HPA axis (45).
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