Extended Data Fig. 7: Diet-induced maternal obesity and prenatal androgen exposure alters mitochondrial morphology in MII oocytes of F1, F2 and F3.
From: Prenatal androgen exposure and transgenerational susceptibility to polycystic ovary syndrome

a, e, and i Representative transmission electron microscopy (TEM) images of F1–F3 MII oocytes (n = 5 MII oocytes per mice per group from three adult offspring). Blue arrows denote abnormal mitochondria shape and vacuoles. Yellow arrow denotes normal mitochondrial shape. b, f, and j, Average number of mitochondria per MII oocytes (n = number of animals per group). For average mitochondrial number, there was a main effect in the obese lineage in F1 female offspring (two-way ANOVA) [F 1, 210 = 12.10, P = 0.0006] and in in F3 offspring (one-way ANOVA) [F2, 115 = 3.746; P = 0.026]. c, g, and k, Mitochondrial DNA content per MII oocytes, expressed in 2-ΔCT value (n = number of animals per group). For mitochondrial DNA content, there was a main effect in the androgenized lineage in F1 female offspring (two-way ANOVA) [F 1, 52 = 8.335, P = 0.0057]. d, h, and l, Quantitative analysis of lipid droplets in MII oocytes in the four different groups (n = number of animals per group). For average lipid droplets, there was a main effect in the androgenized lineage in F1 female offspring (two-way ANOVA) [F 1, 16 = 19.98, P = 0.0004]. Comparisons between groups F1 and 2 generations were performed using two-way ANOVA followed by Tukey’s post hoc analysis and F3 generation one-way ANOVA followed by Dunnett’s post hoc analysis. Data are presented as mean ± s.e.m. Veh = vehicle; DHT = dihydrotestosterone; CD = control diet; HFHS = high-fat high-sucrose; Mat = maternal; GMat = grand-maternal; GGMat = great-grand maternal.