Polycystic ovary syndrome (PCOS) is a heterogeneous syndrome characterized by hyperandrogenism and insulin resistance. The mechanism that is responsible for insulin resistance is unclear and several hypotheses have been suggested. Resistin, and visfatin, a new protein with potential insulin-mimetic action are adipokines which are suggested to play a role in the pathogenesis of insulin resistance. The aim of the study is to assess the relationship between both serum resistin and plasma visfatin

more »

... nd insulin resistance and hyperandrogenism in PCOS patients. The present study included 60 women with polycystic ovary syndrome (PCOS) (group II: 30 with BMI < 25 kg/m 2 and group IV: 30 with BMI > 25 kg/m 2 ) and 20 healthy women (group I: 10 with BMI < 25 kg/m 2 and group III: 10 with BMI > 25 kg/m 2 ) served as controls. Fasting blood samples were withdrawn between the 3 rd and the 6 th day of the menstrual cycle of the ovulating women and between the 3 rd and the 6 th day of a spontaneous bleeding of the anovulatory women. Serum LH, FSH free testosterone, resistin, plasma glucose, insulin and visfatin were estimated in all patients and controls. Insulin resistance was assessed using the homeostatic assessment model (HOMA). Resistin and visfatin levels were significantly higher in women with PCOS (13.26±7.58 ng/ml and 35.82±8.94 ng/ml) than normal controls (7.95± 2.17 ng/ml and 11.88±1.84 ng/ml) (p=0.003, p<0.0001), respectively. Serum resistin levels in groups III and IV were significantly higher compared to groups I and II (p< 0.001, p< 0.001) being higher in group IV, whereas no significant difference existed between groups I and II. Resistin correlated positively with BMI, fasting plasma glucose, fasting plasma insulin and HOMA index in women with BMI > 25 kg/ m 2 (groups III and IV).In other words, resistin was found to correlate significantly with all obesityassociated parameters. Plasma visfatin levels were significantly higher in groups II and IV being higher in group IV when compared to the control groups I and III, whereas no significant difference existed between control groups I and III. Visfatin also positively correlated with, fasting plasma insulin (r = 0.882, p< 0.01 and r = 0.952, p< 0.01) and HOMA (r = 0.908, p< 0.01 and r = 0.942, p< 0.01) in women with PCOS (groups II and IV), respectively. In women with PCOS (groups II and IV), both resistin and visfatin positively correlated with free testosterone (r =0.6, p = 0.003 and r = 0.973, p< 0.01) and (r = 0.969, p<0.01 and r = 0.922, p<0.01), respectively. In women with PCOS (groups II and IV), resistin correlated positively with visfatin (r = 0.784, p< 0.01, r =0.954, p< 0.01), respectively. From the current Bull. Egypt. Soc. Physiol. Sci. 27 (2) 2007 Ahmed & Ghamry 158 data, it could be suggested that resistin levels correlate with insulin resistance as a consequence of obesity itself, rather than a, causative factor. Also the possibility that resistin may play a role in augmenting androgen biosynthesis in women with PCOS could arise. We presume that, in PCOS the increase in plasma visfatin is a secondary event in order to prevent further development of insulin resistance. Finally, the insulin-like visfatin action might stimulate ovarian androgen synthesis and secretion and thus contribute to the pathogenesis of PCOS.