Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2013) 32 P576 | DOI: 10.1530/endoabs.32.P576

1Clinic for Endocrinology, Diabetes and Metabolic Diseases, Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade; Serbia, 2Division of Endocrinology and Human Reproduction, 2nd Department of Obstetrics and Gynecology, Aristotle University of Thessaloniki, Thessaloniki, Greece; 3Clinical-Hospital Center ‘Bežanijska kosa’, Belgrade, Serbia; 4Institute for Biologic Investigations ‘Siniša Stanković’, Belgrade, Serbia; 5Institute for Physiology, Medical Faculty, University of Belgrade, Belgrade; Serbia, 6Clinic for Obstetrics and Gynecology, Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.


Introduction: Insulin resistance is a common discriminator for a variety of chronic disorders including polycystic ovary syndrome (PCOS) and non-alcoholic fatty liver disease (NAFLD). It has recently been hypothesized that PCOS itself might be a risk for developing NAFLD.

Methods: We analyzed 560 women with PCOS (BMI: 31.19±6.75 kg/m2, age: 25.62±6.05 years) diagnosed on the basis of ESHRE/ASRM criteria. The subjects were divided and compared according to the clinical phenotype: phenotype A: anovulation + hyperandrogenism + polycystic ovaries (n=324), phenotype B: anovulation + hyperandrogenism (n=144), phenotype C: hyperandrogenism + polycystic ovaries (n=45), phenotype D: anovulation + polycystic ovaries (n=47). Subgroups did not differ in BMI (P=0.085) but there was significant difference in age (P=0.011) so all statistical analyses were done with adjustment for age. During follicular phase of menstrual cycle fasting blood samples were collected for determination of glucose, insulin, bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), testosterone and SHBG. FAI and HOMA-IR were calculated using standard formula.

Results: There was no significant difference in levels of liver enzymes between different PCOS phenotypes (AST: P=0.72; ALT: P=0.34). Significant correlations existed in phenotypes A, B, and C between ALT and insulin (r=0.35, P<0.001; r=0.32, P<0.001; r=0.34, P=0.02 respectively) and ALT and HOMA-IR (r=0.34, P<0.001; r=0.32, P<0.001; r=0.35, P=0.02 respectively), but there was no correlation between these parameters in phenotype D. There were no significant correlations between liver enzymes, testosterone and SHBG. When analyzed according to FAI, in PCOS subgroup with FAI≧6 significant correlations were found between ALT and insulin (r=0.39, P<0.001) and ALT and HOMA-IR (r=0.38, P<0.001), while there were no significant correlations between those parameters in subgroup with FAI<6.

Conclusion: PCOS phenotypes had different influence towards development of NAFLD. Besides insulin resistance, it seems that androgens may additionally influence development of liver disease.

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