Global and neuron but not granulosa cell loss of AR signaling ameliorates the development of dyslipidemia in the PCOS mouse model. (A) Serum cholesterol levels, confirming DHT-induced increased serum cholesterol in WT mice and showing no significant increase in cholesterol levels in DHT-induced PCOS ARKO or NeurARKO female mice. Data are the mean ± SEM; n = 5 to 7 per genotype/treatment group. (B) Serum triglyceride levels, showing an overall effect of DHT treatment and a nonsignificant trend to increased triglyceride levels in all DHT-treated groups, apart from DHT-induced PCOS ARKO and NeurARKO female mice. Data are the mean ± SEM; n = 5 to 7 per genotype/treatment group. (C) Systolic blood pressure, displaying no significant difference between control and DHT-treated PCOS mice of any genotype. Data are the mean ± SEM; n = 5 to 9 per genotype/treatment group. (D) Analysis of liver steatosis by oil red O staining, showing no significant increase in the presence of steatosis in DHT-induced PCOS ARKO female mice. Data are the mean ± SEM; n = 3 sections per mouse, 3 mice per genotype/treatment group. (D) Histological sections of representative liver sections stained with oil red O, showing reduced lipid staining in DHT-induced PCOS ARKO livers. G, genotype; ns, no significant difference; T, DHT treatment; *, significant difference. (Magnification: 40×.) (*P < 0.05, two-way ANOVA.)