The metabolic syndrome is characterized by the clustering of various common metabolic abnormalities in an individual and it is associated with increased risk for the development of type 2 diabetes and cardiovascular diseases. Its prevalence in the general population is approximately 25%. Central fat accumulation and insulin resistance are considered as the common denominators of the abnormalities of the metabolic syndrome. Subjects with metabolic syndrome have autonomic nervous system dysfunction characterized by predominance of the sympathetic nervous system in many organs, i.e. heart, kidneys, vasculature, adipose tissue, and muscles. Sympathetic nervous system activation in metabolic syndrome is detected as increased heart rate and blood pressure, diminished heart rate variability, baroreceptor dysfunction, enhanced lipolysis in visceral fat, increased muscle sympathetic nerve activity, and high urine or plasma catecholamine concentrations as well as turnover rates. The augmented sympathetic activity in individuals with metabolic syndrome worsens prognosis of this high-risk population. The mechanisms linking metabolic syndrome with sympathetic activation are complex and not clearly understood. Whether sympathetic overactivity is involved in the development of the metabolic syndrome or is a consequence of it remains to be elucidated since data from prospective studies are missing. Intervention studies have demonstrated that the autonomic disturbances of the metabolic syndrome may be reversible.

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Polycystic ovary syndrome (PCOS) is a complex and heterogeneous disorder characterized by hyperandrogenemia, hyperinsulinemia, insulin resistance, and chronic anovulation. It is the most common endocrine disorder in women of reproductive age with an enigmatic pathophysiologic and molecular basis. The high prevalence of affected individuals and the wide range of phenotypic expression can be explained by the interaction of a number of key genes with environmental factors. Heritability of PCOS has been inferred from studies of the syndrome in various population groups (ethnic groups, twins, and PCOS families). Although evidence of familial segregation and clustering of the disease in first-degree relatives of women diagnosed with PCOS has been presented, no particular pattern of inheritance has emerged. Some of the problems in genetic studies have been the lack of uniform criteria for diagnosis, heterogeneity of phenotypic features, and the fact that the disorder is only expressed clinically in women during their reproductive years. Even within affected families and between sisters with polycystic ovaries, there is heterogeneity in presentation. However, regardless of diagnostic criteria used to identify the propositus and to determine affected status in the kindred, the genetic studies available suggest a strong familial component. Currently, PCOS is considered a polygenic trait that might result from the interaction of susceptible and protective genomic variants and environmental factors, during either prenatal or postnatal life.

Both RYGB and SG exert comparable effects on weight loss and improvement of cardiovascular parameters. RYGB displays a more beneficial influence on epicardial fat thickness and left ventricular performance than SG.

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OBJECTIVE: To investigate liver enzymes in a cohort of women with Polycystic Ovary Syndrome (PCOS) and controls divided according to body mass index (BMI) and their association with features of the syndrome. DESIGN: Eighty-three PCOS women and 64 healthy women were studied. Patients and controls were subdivided into two groups, a lean subgroup (BMI <25kg/ m 2 ) and an overweight/obese subgroup (BMI >25kg/m 2 ). Clinical history, height and weight were obtained and metabolic and hormonal parameters were determined. RESULTS: Serum fasting insulin, fasting glucose, HOMA-IR, triglycerides and total cholesterol were significantly higher (p<0.05) in women with PCOS compared to controls. No significant difference in serum liver enzymes levels between PCOS women and controls was detected. However, serum levels of alanine aminotransferase (ALT) (17.7 vs. 14.1 U/L, p<0.05) and γ-glutamyl transpeptidase (γGT) (17.9 vs. 13.4 U/L, p<0.05) were significantly higher in overweight/obese PCOS women compared with overweight/obese controls. In overweight/obese PCOS patients and controls, ALT levels were positively correlated with free androgen index (FAI) (r=0.25 p<0.05) and total testosterone levels (r=0.33 p<0.01). CONCLUSIONS: The finding of elevated liver enzymes in overweight/obese PCOS women raises the question of screening for non-alcoholic fatty liver disease in this group.Key words: Body Mass Index, Insulin resistance, Liver enzymes, Non-alcoholic fatty liver disease, Polycystic Ovary Syndrome Research paper HORMONES 2009, 8(3):199-206 22,24 A significant elevation of aminotransferase levels (ALT and/or AST above 60 U/L) is highly likely to concur with the imaging finding of fatty infiltration in obese women with PCOS.22 Ultrasonographic evidence is more prevalent than the biochemical evidence of NAFLD in lean, overweight and obese PCOS women, 25 but the use of a lower cutoff for ALT may significantly increase the sensitivity of this marker in identifying mild NAFLD. 26Overall, existing evidence of NAFLD in PCOS women is still scarce and presents certain limitations. Of the available studies, only one included a control group. 24 Moreover, only one study included both lean and obese patients, 25 while the others either included only overweight/obese patients or did not subdivide patients according to BMI. 21,22 Additionally, serum levels of γGT were determined only in one of the available four studies. 25The aim of the present study was to investigate liver enzymes in a cohort of women with PCOS and controls divided according to BMI in order to explore a possible independent effect of PCOS and obesity on liver function and to uncover potential associations of serum liver enzymes with hormonal parameters and indices of insulin resistance.

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