Endocrine function gonads

Endocrine function HMG-CoA reductase inhibitors interfere with cholesterol synthesis and lower cholesterol levels and, as such, might theoretically blunt adrenal or gonadal steroid hormone production. 

Though less frequently sought, endocrine disturbances form an essential part of the clinical picture in malnutrition. Their importance has been emphasized by Samuels (1948), Zubirdn (1949), and by Gillman and Gillman (1951). The similarity between the clinical manifestations of malnutrition and those of altered endocrine function are evidenced by the frequency of serious sexual disturbances, pigmentations of the skin, lowered metabolic rates, gynecomastia, asthenia, hypotension, and other symptoms which could be attributed to dysfunction of the thyroid, the adrenals, the pituitary, or the gonads in undernourished individuals. 

Such events show how the immune, endocrine and central nervous systems are integrated in their responses to any form of stress. It is well established that physical or psychosocial stress causes increased secretions of prolactin, growth hormones, thyroid, and gonadal hormones, in addition to ACTH. Endogenous opioids are secreted under such conditions and function as immunomodulators, while also elevating the pain threshold. Receptors for such hormones exist on immunocompetent cells, along with receptors for catecholamines, serotonin and acetylcholine. 

Moore KE, Lookingland KJ, Gunnet JW (1987) Effects of gonadal steroids and pituitary hormones on the activity of tuberoinfundibular dopaminergic neurons. In Genazzam AR (Ed), The Brain and Female Reproduction Function, Front. Gynecol. Endocrine Series, pp. 117-125. Parthenin Pub. Group, New Jersey. 

Figure 33.2. Endocrine feedback loops of the mammalian hypothalamic-pituitary-gonadal (HPG) axis. (Adapted from La Barbera A. R. Differentiation and function of the female reproductive system. In Boekelheide, K., Chapin, R. E., Hoyer, P. B., and Harris, C. (Eds.). Comprehensive Toxicology, Vol. 10, Reproductive and Endocrine Toxicology, Elsevier, New York, 1997, pp. 255-272 and Creasy, D. M., and Foster, P. M. D. Male reproductive system. In Haschek, W. M., Rousseaux, C. G. and Wallig, M. A. (Eds.). Handbook of Toxicologic Pathology, 2nd ed., Academic Press, San Diego, 2002,pp. 785-846. E2, estradiol T, testosterone, DHT, dihydrotestosterone, FSH, follicle stimulating hormone LH, luteinizing hormone.

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