Obesity and the Abdominal Phenotype in PCOS
but not the visceral fat depots. This could be due to a depot-specific inhibition of the expression of hormone-sensitive lipase (HSL) by testosterone and/or to a decrease in the amount of b2 adrenergic receptors. This could also be an important pathophysiological factor behind the insulin-resistant phenotype of the upper-body obesity in men and of the hyperandrogenic PCOS (104).
In humans, it is demonstrated that testosterone increases visceral fat in women. Female-to-male transsexuals treated with testosterone do in fact have an increase in visceral fat only when oophorec-tomized and thus eliminating the protective effects of estrogens (105). In addition, administration of androgens in postmenopausal women has been documented to increase visceral fat while reducing subcutaneous fat (106). This indicates that an increase in the testosterone to estrogen ratio in women causes accumulation of visceral adipose tissue, consistent with the important role of testosterone in determining the high prevalence of abdominal fat distribution pattern in hyperandrogenized women with PCOS.
Obesity has profound effects on the clinical and hormonal and metabolic features of PCOS, which largely depend on the degree of excess body fat and on the pattern of fat distribution. The recognition of the impact of obesity on PCOS may have some relevance in the pathophysiology of the disorder. In addition, obesity intuitively represents a target for therapeutic strategies, as weight loss produces several benefits on major complaints of women with PCOS, including hormonal and metabolic abnormalities, menses and ovulation, and therefore, fertility (107). Finally, the definition of the obesity phenotype is of great importance for prognosis, since abdominal obesity is not only associated with poorer fertility outcomes (108) but also associated with a higher probability of developing the metabolic syndrome, DM2 and, possibly, CvD.
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