Mechanism Linking Obesity and PCOS

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The mechanisms linking obesity and PCOS are unclear but may be related to insulin resistance and hyperandrogenism, both of which are commonly documented in lean and obese women with this condition. Insulin resistance is a common but not universal feature of PCOS, although women with insulin resistance appear to be more clinically affected (2).

Insulin is a physiological hormone regulating ovarian function, specifically ovarian steroidogenesis and androgen blood transport and/or activity in the target tissues (3). The high insulin levels associated with insulin resistance stimulate the ovary to make excessive amounts of androgens. Additionally, high insulin levels decrease levels of sex hormone-binding globulin (SHBG), increasing the bioavailability of androgens. Moreover, high insulin levels may also work at the level of the brain, causing increased luteinizing hormone (LH) secretion, which in turn stimulates greater ovarian androgen production.

Because insulin resistance is strongly influenced by obesity in non-PCOS subjects, it was initially debated whether insulin resistance and hyperinsulinemia are a primary metabolic disturbance of PCOS or a symptom of the obesity commonly observed in PCOS. Hyperandrogenemia and insulin resistance appear to be independent features of PCOS, with hyperinsulinemia enhancing the expression of hyperandrogenemia by increasing bioavailability of androgens (4) (Fig. 1). Obese women with PCOS show decreased insulin sensitivity and hyperinsulinemia to an extent greater than can be explained by obesity alone (4,5). A synergistic interaction appears to exist with the degree of insulin resistance and hyperinsulinemia in lean PCOS women augmented in those who have obesity. Not all women with PCOS exhibit hyperinsulinemia and insulin resistance, and discrepant results may be explained by the heterogeneity and complex etiology of the syndrome. Silfen et al. (6) found a more pronounced alteration in the hypothalamic-pituitary-adrenal axis in non-obese adolescents with PCOS, including higher levels of LH, SHBG, androstenedione, dehydroepiandrosterone sulfate

(DHEAS), dihydrotestosterone, and free insulin-like growth factor-1, but a more marked insulin resistance in obese adolescents with PCOS.

Hyperandrogenism is postulated to result from either or both increased adrenal and ovarian androgen production. The predominance of abdominal obesity, insulin resistance, glucose intolerance, hypertension, and other conditions suggests that the metabolic syndrome may be more common in PCOS, and indeed this has been reported by a number of investigators (7). It is therefore obvious that for adequate treatment of patients with androgen excess, there needs to be a reduction in hyperinsulinemia and insulin resistance as well as in obesity per se. Both weight reduction and increases in physical activity are highly effective in increasing insulin sensitivity. These interrelated and yet separate issues are the focus of the following discussion.

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