The aim of the study were to answer the question 1.) Whether circulating pro-inflammatory markers of endothelial dysfunction and due to chronic low-grade
inflammation of
obesity, are altered in untreated lean, young relatively healthy
polycystic ovary syndrome (PCOS) patients in comparison with healthy controls; 2.) Whether postprandial plasma concentration pattern of
ghrelin and PYY can be predictable as risk factors for
atherosclerosis and depend of
obesity. Forty young women with PCOS were divided in two groups: 19 lean and 21 obese. The control group included 20 lean, healthy volunteers. Plasma total and active
ghrelin, total PYY and PYY(3-36), serum
adiponectin and
insulin were measured using RIA technique, serum sCD40L,
visfatin, sP-, sE-
selectins,
resistin by EIA. Composition of test meal was: 527 kcal total and consisted of 24.1% fat, 54.4%
carbohydrate and 21.5%
protein. Total and active
ghrelin and total PYY were significantly lower in obese PCOS women, whereas active
ghrelin was also significantly lower in lean PCOS women compared to controls. Postprandial plasma total
ghrelin levels decrease were blunted in lean and obese compared to controls (12.8 % and 18.2% vs 28.2 %). Postprandial plasma active
ghrelin decreased in lean and obese PCOS groups (49.9 % and 44.1 %) and controls (63.8 %). PCOS subjects exhibited smaller rises in postprandial levels of total PYY. Postprandial plasma PYY(3-36) levels increased in obese PCOS women (30.9 %) and controls (41%), whereas lean PCOS women exhibited blunted increase (11.5%). sCD40L levels increased, whereas
adiponectin decreased in PCOS groups independently, whereas rise in
visfatin, sE- and sP-
selectin and the fall in
adiponectin was associated with
obesity. sP- and sE -
selectins correlated positively with
obesity. In summary, our study provides the first evidence that lean untreated young PCOS women contribute to the so called "pancreatic islet adaptation to
insulin resistance" because of
ghrelin and PYY profiles. We confirmed existing of low-grade chronic
inflammation in early stage of
visceral obesity in lean PCOS patients. The lost endogenous "islet adaptation to
insulin resistance" may lead to endothelial dysfunction and promote acceleration of
atherosclerosis.