Biosynthesis of adrenal steroids

Epinephrine acts by binding to a variety of adrenergic receptors . Epinephrine is a nonselective agonist of all adrenergic receptors, including the major subtypes α 1 , α 2 , β 1 , β 2 , and β 3 . [59] Epinephrine's binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas , stimulates glycogenolysis in the liver and muscle , [60] and stimulates glycolysis and inhibits insulin-mediated glycogenesis in muscle. [61] [62] β adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland , and increased lipolysis by adipose tissue . Together, these effects lead to increased blood glucose and fatty acids , providing substrates for energy production within cells throughout the body. [62]

The function of serotonin is exerted upon its interaction with specific receptors. Several serotonin receptors have been cloned and are identified as 5HT 1 , 5HT 2 , 5HT 3 , 5HT 4 , 5HT 5 , 5HT 6 , and 5HT 7 . Within the 5HT 1 group there are subtypes 5HT 1A , 5HT 1B , 5HT 1D , 5HT 1E , and 5HT 1F . There are three 5HT 2 subtypes, 5HT 2A , 5HT 2B , and 5HT 2C as well as two 5HT 5 subtypes, 5HT 5a and 5HT 5B . Most of these receptors are coupled to G-proteins that affect the activities of either adenylate cyclase or phospholipase Cβ (PLCβ). The 5HT 3 class of receptors are ion channels, referred to as ionotropic receptors.

Hepatic and adrenal cholesterol biosynthesis were investigated in the human fetus in vitro by measuring the incorporation of acetate-2- 14 C into cholesterol by slices of liver and adrenals from the same fetus. To differentiate neutral lipids from cholesterol biosynthesis, the radioactivity was measured in the nonsaponifiable neutral lipid fraction and in cholesterol isolated and purified as its crystalline 5,6-dibromo-derivative. Expressed in mμmoles acetate incorporated/hr/g tissue into neutral lipids (.) and cholesterol, the values were: fetus I (11 wk. old), liver (), ; adrenals (), ; fetus II (14 wk. old), liver (), ; adrenals (), , respectively. Liver and adrenal cholesterogenesis was inhibited by a specific inhibitor [ trans -1,4- bis (2-chlorobenzylaminomethyl)cyclohexane dihydrochloride = AY-9944] of 7-dehydrocholesterol Δ 7 -reductase. This finding provided (indirect) evidence that 7-dehydrocholesterol is an obligatory intermediate in the biosynthesis of cholesterol in both of these organs. The percent incorporation of acetate into cholesterol in the human fetal liver was greater than that in any other tissue previously reported.

The possibility exists that in the isolation of the subcellular particles the cholesterol hydroxylating enzyme is altered in some manner or a compartment is destroyed that permits it to interact with its substrate, a process normally mediated by ACTH. In this case, the primary action of ACTH would be either on the activation or synthesis of a “permease” or a specific synthetase. However, ability of NADPH-generator systems to bypass the stimulatory effect of ACTH on corticoid secretion in certain in vitro studies () argues against this possibility and further supports the hypothesis that places the control of corticosteroidogenesis on a regulation of energy metabolism.

Biosynthesis of adrenal steroids

biosynthesis of adrenal steroids

The possibility exists that in the isolation of the subcellular particles the cholesterol hydroxylating enzyme is altered in some manner or a compartment is destroyed that permits it to interact with its substrate, a process normally mediated by ACTH. In this case, the primary action of ACTH would be either on the activation or synthesis of a “permease” or a specific synthetase. However, ability of NADPH-generator systems to bypass the stimulatory effect of ACTH on corticoid secretion in certain in vitro studies () argues against this possibility and further supports the hypothesis that places the control of corticosteroidogenesis on a regulation of energy metabolism.

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