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Figure 2.1 The endocrine control of female reproductive function. The menstrual cycle lasts foran average of 28 days. This can be divided into a distinct follicular phase (days 1–13) duringwhich estrogen, LH, and FSH stimulate follicular development. Ovulation driven by highconcentrations of LH and estrogen occurs on day 14. The luteal phase (days 15–28) is drivenby hormone production from the corpus luteum, which produces high concentrations ofprogesterone and estrogen to prepare the uterine lining for implantation of a fertilized embryo.In the absence of fertilization, feedback inhibition of progesterone promotes the degenerationof the corpus luteum and menstrual bleeding.
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 astimulatory effect on the hypothalamic–pituitary–ovarian axis.
Figure 2.3 Leptin receptor signaling cascade. Binding of leptin to the membrane bound Ob-Rbreceptor activates multiple signaling pathways, including the phosphoinositol 3 kinase (PI3K)pathway and the RAS-MAP kinase pathway. Binding of leptin activates JAK2, whichphosphorylates STAT3. Formation of phosphorylated STAT3 complexes drives activation oftranscription of target genes including NPY and AgRP. Leptin resistance develops throughleptin up-regulation of the expression of suppressor of the cytokine signaling-3 (SOCS3), whichinhibits the JAK2-STAT3 pathway.
Table 2.1 Reactive oxygen species and antioxidants in biological systems
Research Highlight 2 Complex relationship between alcohol and fertility in women
Figure 2.4 Endocrine control of male reproductive function. In males, pulsatile hypothalamicproduction of GnRH stimulates the release of FSH and LH, which stimulate the productionof testosterone and the development of mature sperm in the testes. Testes derived inhibin-Band testosterone have negative feedback effects in the anterior pituitary and hypothalamusand thereby regulate the hypothalamic–pituitary–testicular axis.
Figure 2.5 The formation of mature sperm. Sperm production in the male reproductive tract consistsof mitotic and meiotic divisions followed by a differentiation phase in which sperm acquire theirspecialized structures.
Figure 2.6 The relationship between male obesity and subfertility. Obesity and insulin resistanceare 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 theandrogens.
Table 2.2 Environmental sources of human exposure to endocrine disrupting chemicals
Table 2.3 Organic food, pesticide exposure and semen quality
Table 2.4 Factors that impact on parental health during the peri-conceptual period
Figure 2.7 The metabolism of vitamin A. Dietary sources of vitamin A deliver preformedretinol (from animal sources) or ß-carotene. Retinol from the diet or formed within the liver isused to generate rhodopsin in the retina, is converted to retinoic acid which modulates geneexpression via the RAR/RXR receptors. Retinoic acid can be metabolized to a number ofintermediates that are known to have teratogenic properties in animals and humans.
Figure 2.8 Vitamin A supplementation and fetal malformations. The relationship between vitamin Asupplementation and fetal malformations was explored in a population of Spanish women. The datashows odds of malformations associated with vitamin A in a multivitamin supplement, higher levels ofvitamin A in a multivitamin supplement, and with megadose supplements of vitamin A alone.Data taken and redrawn from Martinez-Frias and Salvador (1990).
