This finding contradicts our initial hypothesis that dietary inta

This finding contradicts our initial hypothesis that dietary intake would be associated with insulin resistance, lipid profile, and hormone abnormalities in PCOS. Although the high prevalence of obese women in both groups might have resulted in a lower discriminative effect, which would preclude detection of differences, previous studies [14] have reported similar results in US PCOS patients and controls with BMI values similar to those of our subjects. In addition,

a study comparing Italian and US women with PCOS found no statistical differences in energy and nutrient intake between the 2 groups, whereas saturated fat intake was almost twice as high in US as compared with Italian women [44]. However, the fact that US participants had higher BMIs than those in DAPT mw the Italian group may have affected this result. Some investigators have suggested that women with PCOS have a tendency to overeat, either for emotional [45] or for biological reasons. Holte et al [46] postulated that insulin-resistant PCOS patients experience recurrent hypoglycemia. These hypoglycemic episodes could cause carbohydrate cravings and decreased postprandial satiety, leading to overeating and

obesity. Other studies on disordered metabolism and PCOS have produced contradictory findings [47] and [48]. Robinson et al [48] found that obese and lean women with PCOS exhibited reduced postprandial thermogenesis AZD8055 (a measure of metabolic efficiency) for compared with obese and lean women without PCOS; the reduction in postprandial thermogenesis

in women with PCOS was correlated with reduced insulin sensitivity. In contrast, other studies [49] found no difference in resting metabolic rate or postprandial thermogenesis between obese women with and without PCOS. The present study shows that, despite being younger than controls, participants with PCOS had more central obesity as measured by the sum of trunk skinfolds, waist circumference, and waist-to-hip ratio. Central obesity, defined as increased abdominal fat, is a marker of insulin resistance and a risk factor for cardiovascular disease [50] and [51]. In fact, PCOS patients have been considered a high-risk subgroup for diabetes and cardiovascular disease. In our study, women with PCOS also had lower SHBG and higher androgen levels and a more adverse metabolic profile than the control group, confirming previous observations made by our group [6] and [23] and by others [52] and [53]. In PCOS patients, the compensatory hyperinsulinemia that follows insulin resistance leads to both an increase in ovarian androgen secretion and a reduction in SHBG levels. Hence, obese women with PCOS are frequently more hyperandrogenic that nonobese ones [54], [55], [56] and [57]. A complex interrelationship between different nutritional factors and endocrine status is recognized.

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