Androgens glands

A better link between endocrinological and pheromone research may lead to new insight about the mechanisms of chemical communication. Barki and coworkers showed that implantation of the androgenic gland into a juvenile female induced male characteristics in the female once it was fully matured (Barki et al. 2003). Normal females accepted these implanted females as males, since they allowed them to mate and deposit spermatophores. This discovery suggests that implanted... 

Barki A, Karplus I, Khalaila I, Manor R, Sagi A (2003) Male-like behavioral patterns and physiological alterations induced by androgenic gland implantation in female crayfish. J Exp Biol 206 1791-1797... 

Manor R, Weil S, Oren S, Glazer L, Aflalo ED, Ventura T, Chalifa-Caspi V, Lapidot M, Sagi A (2007) Insulin and gender an insulin-like gene expressed exclusively in the androgenic gland of the male crayfish. Gen Comp Endocrinol 150 326-336... 

The zona reticularis produces the androgens androstene-dione, dehydroepiandrosterone (DHEA), and the sulfated form of dehydroepiandrosterone (DHEA-S). Only small amounts of testosterone and estrogen are produced in the adrenal glands. Androstenedione and DHEA are converted in the periphery, largely to testosterone and estrogen. 

Adrenal hormone production is controlled by the hypothalamus and pituitary gland. Corticotropin-releasing hormone (CRH) is secreted by the hypothalamus and stimulates secretion of adrenocorticotropic hormone (ACTH), also known as corticotropin from the anterior pituitary. ACTH, in turn, stimulates the adrenal cortex to produce cortisol. When sufficient or excessive cortisol levels are reached, a negative feedback is exerted on the secretion of CRH and ACTH, thereby decreasing overall cortisol production. The control of adrenal androgen synthesis also follows a similar negative-feedback mechanism. 

In an enlarged gland, the epithelial/stromal tissue ratio is 1 5.3 Androgens stimulate epithelial, but not stromal tissue hyperplasia. Hence, androgen antagonism does not induce a complete reduction in prostate size to normal. This explains one of the limitations of the clinical effect of 5a-reductase inhibitors. 

Sebum is released by the sebaceous glands and naturally maintains hair and skin hydration. An increase in androgen levels, especially during puberty, can cause an increase in the size of the sebaceous gland and the production of abnormally high levels of sebum within those glands. This excess sebum can result in plugged follicles and acne formation. 

Androgenic deficiency in male rats given a single oral dose of 15 pg 2,3,7,8-TCDD/kg BW was evident as early as 2 days posttreatment, with persistence up to 12 days. These deficiencies may account for male reproductive pathology and dysfunction in rats treated with overtly toxic doses of TCDD. Findings included depression in plasma testosterone concentrations, as well as decreased weight of seminal vesicles (by 68%), ventral prostate gland (by 48%), testes, and epididymis (Moore et al. 1985). 

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