Polycystic ovary syndrome and nonalcoholic fatty liver in obese adolescents: association with metabolic risk profile

Abstract

To investigate the relationship between liver fat and in vivo insulin sensitivity, body composition, abdominal adiposity, and lipid metabolism in obese adolescent girls with polycystic ovary syndrome (PCOS). Cross-sectional case-control study. Research center. Thirty Tanner stage V obese girls with PCOS. None. Liver fat, abdominal adiposity, in vivo insulin-stimulated glucose disposal, whole-body lipolysis, fat oxidation, lipoprotein particle size and concentration, and liver enzymes (alanine aminotransferase and aspartate aminotransferase). Fatty liver index <1 is indicative of fatty liver. Fatty liver was present in 6.7% of the individuals (6.7%). Levels of alanine aminotransferase and aspartate aminotransferase were not different between those with fatty liver vs. without. Fatty liver index was associated with age (r = -0.53), body mass index (r = -0.41), total (r = -0.43) and subcutaneous (r = -0.41) abdominal adiposity, insulin-stimulated glucose disposal (r = 0.36), and small, medium small, and very small low-density lipoprotein concentrations (r ≥ -0.43). In a multiple regression analysis, age, total T, race, and insulin-stimulated glucose disposal explained 43% of the variance (R(2) = 0.43) in fatty liver index, with age (R(2) = 0.28) and total T (R(2) = 0.11) being independent contributors. Liver fat is associated with increasing age, even in the narrow adolescent age range, increasing abdominal adiposity, worsening insulin sensitivity, and dyslipoproteinemia in obese adolescent girls with PCOS. Targeting these abnormalities early in the course of PCOS may halt future nonalcoholic fatty liver disease in adulthood.