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Results: 5

1.
Figure 2

Figure 2. From: Polycystic Ovary Syndrome and its Developmental Origins.

Effect of prenatal T treatment from days 30 to 90 of gestation on the distribution of follicles (top panel) and oocyte diameter (bottom panel) in fetal ovine ovaries at 140 d of gestation. Each bar represents mean ± SEM. Asterisks indicate significant differences (P < 0.05) (Data from reference 31).

Daniel A. Dumesic, et al. Rev Endocr Metab Disord. ;8(2):127-141.
2.
Figure 1

Figure 1. From: Polycystic Ovary Syndrome and its Developmental Origins.

Mean (±SEM) serum values in early (open bars) and late (grey bars) treated prenatally T-treated and control (black bars) adult female rhesus monkeys reflecting (a) testosterone, (b) estradiol, (c) testosterone:estradiol ratio, (d) bioactive LH, (e) immunoactive LH and (f) immunoactive FSH during either the early follicular phase of the menstrual cycle or equivalent time during a 30-day anovulatory period. * p<0.05, versus controls, δ p<0.08 versus controls (Data from reference 39).

Daniel A. Dumesic, et al. Rev Endocr Metab Disord. ;8(2):127-141.
3.
Figure 3

Figure 3. From: Polycystic Ovary Syndrome and its Developmental Origins.

Ovarian follicular dynamics determined by ultrasonography in both ovaries of a representative control and prenatal T-treated sheep are shown in the left panel. Each line represents one follicle. Only follicles that reached a size of 3 mm and persisted for at least 2 days are shown. Note the increase in maximum size and duration of the larger follicles on the ovary in prenatal T-treated sheep. Mean number (bottom right) and duration (top right) of persistent follicles in ovaries of control (n=8) and prenatal T-treated (n=14) sheep. Numbers within bottom histogram indicate number of animals in each group showing persistent follicles (Data from reference 31).

Daniel A. Dumesic, et al. Rev Endocr Metab Disord. ;8(2):127-141.
4.
Figure 4

Figure 4. From: Polycystic Ovary Syndrome and its Developmental Origins.

A). Mean (upper 95% confidence limit) percentage of zygotes developing to the 5–8 cell (open bars) and blastocyst (solid bars) stages in 5 early prenatally T-treated, 5 late prenatally T-treated and 5 control adult female rhesus monkeys following ovarian hyperstimulation for IVF. a: p<0.05 versus control and late prenatally T-treated females at the same stage; b: p<0.05 versus 5–8 cell stage (Data modified from reference 20). B) Histograms on the right shows percentage of prenatal T-treated sheep (n=12) that successfully mated or conceived following estrus synchronization with two injections of PGF2α administered 11 days apart. To overcome mating preference, ram access was limited to only prenatal T-treated females. First service mating and pregnancy results for the breeding herd (n=109; hatched bar) bred during the same time are provided for comparison (Data modified from reference 112).

Daniel A. Dumesic, et al. Rev Endocr Metab Disord. ;8(2):127-141.
5.
Figure 5

Figure 5. From: Polycystic Ovary Syndrome and its Developmental Origins.

Diagrammatic representation of possible early gestation, fetal androgen excess programming of adult PCOS traits. Genetic or environmental mechanisms induce fetal hyperandrogenism causing permanent changes in reproductive and metabolic function. Reproductive consequences include: (1) altered hypothalamic-pituitary function causing LH hypersecretion, (2) ovarian hyperandrogenism with or without LH hypersecretion, (3) reduced steroid hormone negative feedback regulation of LH, (4) adrenal hyperandrogenism, and (5) ovulatory dysfunction. Metabolic consequences include: (1) increased abdominal adiposity with elevated circulating total free fatty acid levels, (2) impaired pancreatic insulin secretory response to glucose, (3) impaired insulin action and compensatory hyperinsulinemia, (4) hyperglycemia, and (5) increased incidence of type 2 diabetes. Insulin resistance and compensatory hyperinsulinemia may be functionally implicated in the anovulatory mechanism (Data from reference 39).

Daniel A. Dumesic, et al. Rev Endocr Metab Disord. ;8(2):127-141.

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