Adrenocorticotropic hormone epinephrine

Otfier fiormones accelerate tfie release of free fatty acids from adipose tissue and raise tfie plasma free fatty acid concentration by increasing the rate of lipolysis of the triacylglycerol stores (Figure 25—8). These include epinephrine, norepinephrine, glucagon, adrenocorticotropic hormone (ACTH), a- and P-melanocyte-stimulat-ing hormones (MSH), thyroid-stimulating hormone (TSH), growth hormone (GH), and vasopressin. Many of these activate the hormone-sensitive hpase. For an optimal effect, most of these lipolytic processes require the presence of glucocorticoids and thyroid hormones. These hormones act in a facilitatory or permissive capacity with respect to other lipolytic endocrine factors. 

The adrenal glands are located anatomically above the kidneys. They comprise a three-layer cortex and a medulla. The medulla is the source of catecholamines such as epinephrine, the fight-or-flight hormone. The cortex is the source of aldosterone, the primary mineralocorticoid that is involved in the regulation of sodium reabsorption in the kidneys. In addition, the cortex is also the source of steroids known as glucocorticoids, of which cortisol is the principal endogenous representative. Synthesis and release of cortisol is under the control of adrenocorticotropic hormone (ACTH). 

The initial event in the utilization of fat as an energy source is the hydrolysis of triacylglycerols by lipases, an event referred to as lipolysis. The lipase of adipose tissue are activated on treatment of these cells with the hormones epinephrine, norepinephrine, glucagon, and adrenocorticotropic hormone. In adipose cells, these hormones trigger 7TM receptors that activate adenylate cyclase (Section 15,1.3 ). The increased level of cyclic AMP then stimulates protein kinase A, -which activates the lipases by phosphorylating them. Thus, epinephrine, norepinephrine, glucagon, and adrenocorticotropic hormone induce lipolysis (Figure 22.6). In contrast, insulin inhibits lipolysis. The released fatty acids are not soluble in blood plasma, and so, on release, serum albumin binds the fatty acids and serves as a carrier. By these means, free fatty acids are made accessible as a fuel in other tissues. 

The adrenal glands, which are divided into the medulla (core) and the cortex (outer layer), furnish catecholamines and steroids, respectively. The catecholamines are hormonally active, and consist of norepinephrine and epinephrine. Steroids variously affect carbohydrate, protein, and lipid metabolism, regulate the sall/water losses of the kidneys, and affect sexual development and function. Androgens and estrogens fall in the last-mentioned category. Another adrenal hormone of note is ACTH, or adrenocorticotropic hormone. Cortisol is an adrenal product, which can be converted to cortisone. 

Membrane-bound hormone receptors were detected in the late 1960s. The binding of insulin, glucagon, and epinephrine to isolated plasma membranes of the rat liver or to isolated fat cells and fat cell membranes has been reported (Tomasi et al., 1970 Rodbell et al., 1971 Cuatrecasas, 1971a,b Freychet et al., 1971 Dunnick and Marinetti, 1971). Species-specific interaction between growth hormones and erythrocyte membranes has been shown by Cambiaso et al. (1971). Lef-kowitz et al. (1971) have published a detailed description of the interaction of adrenocorticotropic hormone with its receptors in the adrenal cortex, which appears to be a membrane-associated interaction (Finn et al., 1972). The modes of action for polypeptide hormones and their receptors have been the subject of intense investigation, and a number of reviews on this subject have been published (Cuatrecasas, 1974 Kahn, 1975 Catt and Dufau, 1977). 

Bar, H. P., and Hechter, O., 1969, Adenyl cyclase and hormone action. I. Effects of adrenocorticotropic hormone, glucagon and epinephrine on the plasma membrane of rat fat cells, Proc. Natl. Acad. Sci. USA 63 350. 

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