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- W970567985 abstract "Catecholamines activate β-adrenergic receptors (β-ARs) in the liver and stimulate hepatic glucose production by multiple mechanisms. Glycogenolysis and gluconeogenesis are enhanced, whereas glycogen synthesis is inhibited. In addition to stimulating the entry of glucose into the bloodstream, catecholamines decrease plasma glucose clearance by both direct (β)- and indirect (α)-adrenergic mechanisms. These multiple catecholamine effects are synergistic as they all serve to increase plasma glucose concentrations. These mechanisms become physiologically important in the setting of hypoglycemia, the classical stimulus to epinephrine (EPI) secretion by the adrenal medulla. Thus, the autonomic activation associated with hypoglycemia serves the ultimate purpose of mobilizing endogenous substrates for glucose production and increasing glucose concentrations in the bloodstream so that the central nervous system's demand for its obligatory fuel can be met. Catecholamines also act directly on adipose tissue to stimulate fat breakdown. This is a β 1 -adrenergic effect involving adenyl cyclase-mediated activation of hormone-sensitive triacylglycerol lipase, the enzyme that cleaves triglyceride in the adipose tissue into fatty acids and glycerol. Insulin inhibits catecholamine-induced lipolysis; thus, catecholamine-mediated suppression of insulin secretion is synergistic with the direct catecholamine effects on adipose tissue." @default.
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- W970567985 date "2004-01-01" @default.
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- W970567985 title "Regulation of Metabolism" @default.
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- W970567985 doi "https://doi.org/10.1016/b978-012589762-4/50031-1" @default.
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