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RESEARCH PRODUCT

Insulin resistance and hyperandrogenism drive steatosis and fibrosis risk in young females with PCOS

Salvatore PettaL. GalvanoAlessandro CiresiG. MerlinoCarla GiordanoAntonio CraxìRoberta BoemiJessica BiancoF. MagliozzoVincenzo Geraci

subject

0301 basic medicineSteatosisendocrine system diseasesPhysiologylcsh:MedicinePathology and Laboratory MedicineBiochemistryBody Mass IndexCytopathology0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseMedicine and Health SciencesInsulinlcsh:ScienceMultidisciplinaryLiver DiseasesFatty liverMiddle AgedPolycystic ovaryLipidsCholesterolOncologyPhysiological Parameters030211 gastroenterology & hepatologyFemalePolycystic Ovary SyndromeResearch ArticleAdultmedicine.medical_specialtyGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicinemedicineHumansObesityRisk factorTriglyceridesDiabetic Endocrinologybusiness.industryFree androgen indexHyperandrogenismCholesterol HDLBody Weightlcsh:RCancers and NeoplasmsBiology and Life Sciencesmedicine.diseaseFibrosisHormonesFatty Liver030104 developmental biologyEndocrinologyAnatomical Pathologylcsh:QSteatosisInsulin ResistancebusinessHyperandrogenismGynecological TumorsDevelopmental Biologyinsulin resistance PCOS

description

Background and aims Nonalcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) recognize obesity and insulin resistance (IR) as common pathogenic background. We assessed 1) whether PCOS is a risk factor for steatosis, and 2) the impact, in PCOS patients, of IR and hyperandrogenism on steatosis and fibrosis. Methods We considered 202 consecutive Italian PCOS nondiabetic patients and 101 age-matched controls. PCOS was diagnosed applying the Rotterdam diagnostic criteria. Steatosis was diagnosed if hepatic steatosis index (HSI) >36, while fibrosis by using the FIB-4 score. As surrogate estimate of insulin sensitivity we considered the insulin sensitivity index (ISI). Free androgen index (FAI) was calculated as estimate of biochemical hyperandrogenism. Results In the entire population, steatosis was observed in 68.8% of patients with PCOS, compared to 33.3 of controls (p<0.001), this association being maintained after adjusting for metabolic confounders (OR 3.73, 95% CI 1.74–8.02; P = 0.001). In PCOS patients, steatosis was independently linked to WC (OR 1.04, 95% CI 1.01–1.08; P = 0.006) and ISI Matsuda (OR 0.69, 95% CI 0.53–0.88; P = 0.004), not to free androgen index (OR 1.10, 95% CI 0.96–1.26; P = 0.14). Notably, ISI Matsuda was confirmed as independently associated with steatosis in both obese (OR 0.42, 95% CI 0.23–0.77, P = 0.005) and nonobese (OR 0.69, 95% CI 0.53–0.91, P = 0.009), patients, while FAI (OR 1.45, 95% CI 1.12–1.87; P = 0.004) emerged as an independent risk factor only in nonobese PCOS. Similarly, higher FIB-4 was independently associated with higher FAI (p = 0.02) in nonobese and with lower ISI Matsuda (p = 0.04) in obese patients. Conclusions We found that PCOS is an independent risk factor for steatosis, and that, IR and hyperandrogenism, this last especially in nonobese patients, are the key players of liver damage in PCOS.

yearjournalcountryeditionlanguage
2017-04-15
10.1371/journal.pone.0186136http://hdl.handle.net/10447/247182