Steroid hormones binds to a plasma membrane receptor

Some endocrine glands are controlled by a simple negative feedback mechanism. For example, negative feedback signaling mechanisms in the parathyroid glands (located in the neck) rely on the binding activity of calcium-sensitive receptors that are located on the surface of parathyroid cells. Decreased serum calcium concentrations result in decreased calcium receptor binding activity that stimulates the secretion of parathormone from the parathyroid glands. The increased serum concentration of parathormone stimulates bone resorption (breakdown) to release calcium into the blood and reabsorption of calcium in the kidney to retain calcium in the blood, thereby restoring serum calcium concentrations to normal levels. In contrast, increased serum calcium concentrations result in increased calcium receptor-binding activity and inhibition of parathormone secretion by the parathyroid glands. This allows serum calcium concentrations to decrease to normal levels. Therefore, in people with normal parathyroid glands, serum calcium concentrations are maintained within a very narrow range even in the presence of large changes in calcium intake or excessive losses of calcium from the body.

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.

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandrosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

It turns out that vitamin D receptors are present in most if not all cells in the body. Additionally, experiments using cultured cells have demonstrated that vitamin D has potent effects on the growth and differentiation of many types of cells. These findings suggest that vitamin D has physiologic effects much broader that a role in mineral homeostasis and bone function. As one example, many immune cells not only express vitamin D receptors, but are capable of synthesizing active vitamin D, and deficiency in vitamin D has been associated with increased incidence of autoimmune disease and susceptibility to disease.

Steroid hormones binds to a plasma membrane receptor

steroid hormones binds to a plasma membrane receptor

It turns out that vitamin D receptors are present in most if not all cells in the body. Additionally, experiments using cultured cells have demonstrated that vitamin D has potent effects on the growth and differentiation of many types of cells. These findings suggest that vitamin D has physiologic effects much broader that a role in mineral homeostasis and bone function. As one example, many immune cells not only express vitamin D receptors, but are capable of synthesizing active vitamin D, and deficiency in vitamin D has been associated with increased incidence of autoimmune disease and susceptibility to disease.

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