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Plasma adrenocorticotropic hormone

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. [Pg.215]

However, nicotine also has been shown to stimulate the hypothalamic-pituitary-adrenal axis in rodents, leading to elevated plasma levels of adrenocorticotropic hormone and corticosterone (Andersson et al. 1983 Cam et al. 1979), which are known to exert a wake-promoting effect. However, studies in humans have shown that only intense smoking is able to activate the hypothalamic-pituitary-adrenal axis (Gilbert et al. 1992 Kirschbaum et al. 1992). Nicotine patches, in addition to their use in nicotine suppression and craving, have been used to explore the relationship between sleep and nicotine in human... [Pg.448]

A counterpart of evidence that CCK agonists are anxiogenic is to answer the question of whether the CCK system is functionally implicated in non-provoked symptoms of panic or anxiety. It is conceivable that endogenous variations of central and/or peripheral CCK activity may be a neurochemical concomitant of anxiety. It is interesting to mention that serum concentrations of gastrin, a CCK-B agonist, fluctuate in correlation with self-reported tension, conflict, and anxiety in psychiatrically healthy men (M. Feldman et al. 1992). Plasma CCK levels were markedly elevated in sportsmen before a competitive marathon run, as compared with CCK levels under control conditions (Phillip et al. 1992). Plasma concentrations of adrenocorticotropic hormone (ACTH), cortisol, and noradrenaline were also elevated and increased extensively after the running performance. However, CCK levels re-... [Pg.422]

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. [Pg.903]

The response during any major surgical procedure is maximal because the administration of adrenocorticotropic hormone (ACTH) during major surgery produces no further increase in the plasma cortisol level, but within 24 hours there is an immediate response to a further ACTH stimulus. [Pg.258]

In the horse, U2 agonists are associated with a decrease in levels of catecholamines (Raekallio et al 1991). This is attributed to decreased sympathetic outflow from the CNS as well as decreased stress response owing to the sedative effects of these drugs (Raekallio et al 1991, 1992). Cortisol levels do not decrease following the administration of U2 agonists even though the release of adrenocorticotropic hormone from the pituitary is depressed (Alexander Irvine 2000, Raekallio et al 1991). However, plasma total cortisol levels may not be an accurate indicator of stress levels in the horse (Alexander Irvine 1998). [Pg.270]

Adrenocorticotropic hormone (ACTH), insulin, and parathyroid hormone (PTH) are examples of polypeptide or protein hormones. They are generally water soluble and circulate freely in plasma as the whole molecule or as active or inactive fragments. The half-life of these hormones in plasma is quite short (10 to 30 minutes or less), and wide... [Pg.1019]

Lefkowitz P, Roth J, Paston I. Radioreceptor assay of adrenocorticotropic hormone New approach to assay of polypeptide hormones in plasma. Science 1970 170 633-5. [Pg.1999]

Figure 54-1 Schematic representation of steroid and protein hormone production by the placenta. DHEA-S, Dehydro-epiandrosterone sulfate CG, chorionic gonadotropin PL, placental lactogen ACTH, adrenocorticotropic hormone TRH, thyroid-stimulating hormone CT, chorionic thyrotropin GnRH, gonadotropin-releasing hormone CRH, corticotropin-releasing hormone PAPP-A, pregnancy associated plasma protein-A. Figure 54-1 Schematic representation of steroid and protein hormone production by the placenta. DHEA-S, Dehydro-epiandrosterone sulfate CG, chorionic gonadotropin PL, placental lactogen ACTH, adrenocorticotropic hormone TRH, thyroid-stimulating hormone CT, chorionic thyrotropin GnRH, gonadotropin-releasing hormone CRH, corticotropin-releasing hormone PAPP-A, pregnancy associated plasma protein-A.
Nicotine binds selectively to the nicotinic receptors that are present in the adrenal medulla, brain, autonomic ganglia, and neuromuscular junctions. It causes the release of several neurotransmitters and hormones such as acetylcholine, norepinephrine, dopamine, serotonin, arginine vasopressin, j3-endorphin, adrenocorticotropic hormone, and cortisol (187). This neuro-regulatory effect of nicotine is dose-dependent and occurs as plasma nicotine level rises when tobacco is smoked. The neurotransmitters released in the brain medi-... [Pg.454]

Challis J, Richardson B, Rurak D, Wlodek M, Patrick J. Plasma adrenocorticotropic hormone and cortisol and adrenal hlood flow during sustained hypoxemia in fetal sheep. Am J Ohstet Gynecol 1986 155(6) 1332-1336. [Pg.228]

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). [Pg.379]


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See also in sourсe #XX -- [ Pg.1983 ]




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