1. Learning objectives

2. Figure 2. 1 The endocrine control of female reproductive function
Figure 2.1 The endocrine control of female reproductive function. The menstrual cycle lasts for an average of 28 days. This can be divided into a distinct follicular phase (days 1–13) during which estrogen, LH, and FSH stimulate follicular development. Ovulation driven by high concentrations of LH and estrogen occurs on day 14. The luteal phase (days 15–28) is driven by hormone production from the corpus luteum, which produces high concentrations of progesterone and estrogen to prepare the uterine lining for implantation of a fertilized embryo. In the absence of fertilization, feedback inhibition of progesterone promotes the degeneration of the corpus luteum and menstrual bleeding.

3. Figure 2.2 Adipose tissue derived leptin and the hypothalamic–pituitary–ovarian axis. Leptin from adipose tissue promotes production of GnRH, FSH, and LH and therefore has a stimulatory effect on the hypothalamic–pituitary–ovarian axis.

4. Figure 2. 3 Leptin receptor signaling cascade
Figure 2.3 Leptin receptor signaling cascade. Binding of leptin to the membrane bound Ob-Rb receptor activates multiple signaling pathways, including the phosphoinositol 3 kinase (PI3K) pathway and the RAS-MAP kinase pathway. Binding of leptin activates JAK2, which phosphorylates STAT3. Formation of phosphorylated STAT3 complexes drives activation of transcription of target genes including NPY and AgRP. Leptin resistance develops through leptin up-regulation of the expression of suppressor of the cytokine signaling-3 (SOCS3), which inhibits the JAK2-STAT3 pathway.

5. Table 2.1 Reactive oxygen species and antioxidants in biological systems

6. Research Highlight 2 Complex relationship between alcohol and fertility in women

7. Figure 2. 4 Endocrine control of male reproductive function
Figure 2.4 Endocrine control of male reproductive function. In males, pulsatile hypothalamic production of GnRH stimulates the release of FSH and LH, which stimulate the production of testosterone and the development of mature sperm in the testes. Testes derived inhibin-B and testosterone have negative feedback effects in the anterior pituitary and hypothalamus and thereby regulate the hypothalamic–pituitary–testicular axis.

8. Figure 2. 5 The formation of mature sperm
Figure 2.5 The formation of mature sperm. Sperm production in the male reproductive tract consists of mitotic and meiotic divisions followed by a differentiation phase in which sperm acquire their specialized structures.

9. Figure 2. 6 The relationship between male obesity and subfertility
Figure 2.6 The relationship between male obesity and subfertility. Obesity and insulin resistance are a cause of infertility as they interfere with the normals secretion and transport of androgens. As androgens are activators of lipolysis, further adiposity is stimulated by impaired action of the androgens.

10. Table 2.2 Environmental sources of human exposure to endocrine disrupting chemicals

11. Table 2.3 Organic food, pesticide exposure and semen quality

12. Table 2.4 Factors that impact on parental health during the peri-conceptual period

13. Figure 2. 7 The metabolism of vitamin A
Figure 2.7 The metabolism of vitamin A. Dietary sources of vitamin A deliver preformed retinol (from animal sources) or ß-carotene. Retinol from the diet or formed within the liver is used to generate rhodopsin in the retina, is converted to retinoic acid which modulates gene expression via the RAR/RXR receptors. Retinoic acid can be metabolized to a number of intermediates that are known to have teratogenic properties in animals and humans.

14. Figure 2. 8 Vitamin A supplementation and fetal malformations
Figure 2.8 Vitamin A supplementation and fetal malformations. The relationship between vitamin A supplementation and fetal malformations was explored in a population of Spanish women. The data shows odds of malformations associated with vitamin A in a multivitamin supplement, higher levels of vitamin A in a multivitamin supplement, and with megadose supplements of vitamin A alone. Data taken and redrawn from Martinez-Frias and Salvador (1990).

15. Summary Box 2

16. Self-Assessment Questions