| 總結: | Chronic anxiety, depression or physical exertion-associated stress consistently activates the hypothalamic-pituitary-adrenal (HPA) axis. Each individual component of the HPA axis, such as CRH, ACTH, β-endorphin or glucocorticoid exerts deleterious effect on the hypothalamic-pituitary-gonadal (HPG) axis and subsequently leads to reproductive failure. Gonadotropin- releasing hormone (GnRH) secretion and the response of gonadotrophs to GnRH stimulation are severely impaired. Moreover, failure of gonadal response to gonadotropin concurrently results in deficient steroidogenesis, anovulation, defective endometrial decidualization and implantation, abnormal fetal outcome and delayed parturition. In male, a consistent testosterone deficiency due to stress-linked altered functioning of the HPG axis has also been documented. Stress-associated growth hormone (GH) deficiency with a corresponding deficiency of insulin-like growth factor-1 (IGF-1) at the level of the hypothalamus, pituitary, ovary, and uterine endometrium leads to defective reproductive outcome and lactation. GH or IGF-1 deficiency also impairs testosterone biosynthesis, spermatogenesis, sperm maturation and erectile process.
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