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

Fig. 6.

Fig. 6.

Global loss of AR signaling protects against the reduction in adiponectin levels, adipocyte hypertrophy, and altered glucose homeostasis in the PCOS mouse model. (A) Serum levels of adiponectin, confirming DHT-induced suppression of serum adiponectin levels in WT mice and showing no significant reduction in adiponectin levels in DHT-induced PCOS ARKO female mice. Data are the mean ± SEM; n = 5 to 7 per genotype/treatment group. (B) Adipocyte size, showing no development of adipocyte hypertrophy in DHT-induced PCOS ARKO female mice. Data are the mean ± SEM; n = 3 sections per mouse, 3 mice per genotype/treatment group. (C) Histological sections of representative parametrial fat pads from each treatment group, showing no development of adipocyte hypertrophy in DHT-induced PCOS ARKO female mice. (D) Average fasting glucose levels showing no significant increase in glucose levels in DHT-induced PCOS ARKO female mice. Data are the mean ± SEM; n = 5 to 9 per genotype/treatment group. (E) Area under the curve (AUC) analysis of the oral glucose tolerance test, showing an overall effect of DHT treatment. Data are the mean ± SEM; n = 5 to 9 per genotype/treatment group. G, genotype; ns, no significant difference; T, DHT treatment; *, significant difference. (Magnification: 40×.) (*P < 0.05, two-way ANOVA.)