Obese adolescent girls with PCOS have increased cardiometabolic disease including insulin resistance (IR) and hepatic steatosis. Excess pancreatic fat (PF) is hypothesized to disturb pancreatic hormone secretion and relate to excess hepatic fat (HF). Associations between PF and IR or HF have not been measured in youth with PCOS.


Secondary analysis from 65 sedentary, non-diabetic (HbA1c<6.5%) adolescent girls (age 15.3±1.9 years) with or without PCOS and BMI≥90th percentile, who were enrolled in 3 cross-sectional studies. Participants underwent fasting laboratory tests, a 2-hour 75-gram oral glucose tolerance test (OGTT), and an abdominal MRI to quantify PF and HF via proton density fat fraction six-echo Dixon methodology. Participants were categorized by PF, either above or below the median PF of 3.1% [High PF, n=32, 4.4(3.9,5.1)% and Low PF, n=33, 2.2(1.7,2.7)%]. Insulin sensitivity (Si) was calculated using the oral minimal model. Group differences and correlations between PF and metabolic variables were performed.


PF did not differ by PCOS diagnosis (p=0.36) nor correlate with serum androgens (r=0.13, p=0.29). Whereas the High PF group had significantly more HF [6.1(3.5,10)% High vs 3.9(2.6,4.9)% Low, p<0.01], individual PF and HF did not correlate (r=0.23, p=0.07). There was no difference in insulin sensitivity (Si, p=0.59; insulinogenic index, p=0.54) or β-cell function (disposition index, p=0.27). High PF had higher insulin concentrations during the OGTT (p=0.02).


Neither PCOS status nor androgens relate to PF. PF is not associated with pancreatic function, which is likely a reflection of early disease state in these adolescents. However, late postprandial hyperinsulinemia is seen in those with high PF, which could be related to elevated HF and, therefore, hepatic steatosis. Future studies should be directed toward identifying methods to reduce visceral fat in this at-risk population to prevent the progression of metabolic disease.