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. 2017 Mar 20;114(16):E3334–E3343. doi: 10.1073/pnas.1616467114

Fig. 7.

Fig. 7.

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.)