Epinephrine peptide or steroid hormone

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.

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If OAA is converted to PEP by mitochondrial PEPCK, it is transported to the cytosol where it is a direct substrate for gluconeogenesis and nothing further is required. Transamination of OAA to aspartate allows the aspartate to be transported to the cytosol where the reverse transamination occurs yielding cytosolic OAA. This transamination reaction requires continuous transport of glutamate into, and 2-oxoglutatrate (α-ketoglutarate) out of, the mitochondrion. Therefore, this process is limited by the availability of these other substrates. Either of these latter two reactions will predominate when the substrate for gluconeogenesis is lactate. Whether mitochondrial decarboxylation or transamination occurs is a function of the availability of PEPCK or transamination intermediates.

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]

Epinephrine peptide or steroid hormone

epinephrine peptide or steroid hormone

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]

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