Steroid hormone principal pathways

Hypercalcemia may develop both spontaneously and as a result of androgen therapy in women with disseminated breast carcinoma.  If it develops while on this agent, the drug should be discontinued. Caution is required in administering these agents to patients with cardiac, renal or hepatic disease.  Cholestatic jaundice is associated with therapeutic use of anabolic and androgenic steroids.  Edema may occur occasionally with or without congestive heart failure.  Concomitant administration of adrenal steroids or ACTH may add to the edema.  In children, anabolic steroid treatment may accelerate bone maturation without producing compensatory gain in linear growth.  This adverse effect may result in compromised adult stature.  The younger the child the greater the risk of compromising final mature height.   The effect on bone maturation should be monitored by assessing bone age of the wrist and hand every six months.  This drug has not been shown to be safe and effective for the enhancement of athletic performance. Because of the potential risk of serious adverse health effects, this drug should not be used for such purpose.

• Enhanced weight loss. There is evidence that DHEA helps promote weight loss in laboratory animals, and perhaps in humans as well, although the results are inconsistent, and it is unclear what the operative mechanism is. It may involve appetite suppression or thermogenesis (fat burning) or both. A curious observation is that, in men who lose weight without DHEA supplementation, the natural levels of this hormone tend to rise. This is not true of women, however - still more evidence of the different ways in which this remarkable hormone is metabolized by the two sexes.

The secretion of hypothalamic, pituitary, and target tissue hormones is under tight regulatory control by a series of feedback and feed- forward loops. This complexity can be demonstrated using the growth hormone (GH) regulatory system as an example. The stimulatory substance growth hormone releasing hormone (GHRH) and the inhibitory substance somatostatin (SS) both products of the hypothalamus, control pituitary GH secretion. Somatostatin is also called growth hormone-inhibiting hormone (GHIH). Under the influence of GHRH, growth hormone is released into the systemic circulation, causing the target tissue to secrete insulin-like growth factor-1, IGF-1. Growth hormone also has other more direct metabolic effects; it is both hyperglycemic and lipolytic. The principal source of systemic IGF-1 is the liver, although most other tissues secrete and contribute to systemic IGF-1. Liver IGF-1 is considered to be the principal regulator of tissue growth. In particular, the IGF-1 secreted by the liver is believed to synchronize growth throughout the body, resulting in a homeostatic balance of tissue size and mass. IGF-1 secreted by peripheral tissues is generally considered to be autocrine or paracrine in its biological action.

Steroid hormone principal pathways

steroid hormone principal pathways

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