Growth hormone secretagogue: difference between revisions
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| 11 | GHRH analogues — [[Sermorelin|sermorelin]], [[CJC-1295|CJC-1295]], [[Tesamorelin|tesamorelin]] — mimic the hypothalamic releasing hormone. Ghrelin-receptor agonists such as [[Ipamorelin|ipamorelin]] act at a separate receptor and by a partly complementary mechanism.{{r|sigalos2018}} | 11 | GHRH analogues — [[Sermorelin|sermorelin]], [[CJC-1295|CJC-1295]], [[Tesamorelin|tesamorelin]] — mimic the hypothalamic releasing hormone. Ghrelin-receptor agonists such as [[Ipamorelin|ipamorelin]] act at a separate receptor and by a partly complementary mechanism.{{r|sigalos2018}} |
| 12 | 12 | ||
| + | 13 | Because they act through the pituitary rather than replacing the hormone, the resulting secretion retains its pulsatile pattern and remains subject to negative feedback — which limits the achievable exposure and is the main pharmacological argument for the approach.{{r|sigalos2018}} | |
| + | 14 | ||
| 13 | == Mechanisms == | 15 | == Mechanisms == |
| 14 | GHRH-receptor agonism at somatotroph cells raises cAMP and promotes synthesis and release of growth hormone. Native GHRH has a very short half-life; the analogues are modified to extend it, and [[CJC-1295|CJC-1295]] uses a linker permitting covalent binding to albumin for a much longer duration.{{r|sigalos2018}} | 16 | GHRH-receptor agonism at somatotroph cells raises cAMP and promotes synthesis and release of growth hormone. Native GHRH has a very short half-life; the analogues are modified to extend it, and [[CJC-1295|CJC-1295]] uses a linker permitting covalent binding to albumin for a much longer duration.{{r|sigalos2018}} |
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| 16 | Ghrelin-receptor agonism acts through a different pathway and also suppresses somatostatin tone, so the two mechanisms combine more than additively in some experimental settings — the rationale for combining them that appears in community discussion.{{r|sigalos2018}} | 18 | Ghrelin-receptor agonism acts through a different pathway and also suppresses somatostatin tone, so the two mechanisms combine more than additively in some experimental settings — the rationale for combining them that appears in community discussion.{{r|sigalos2018}} |
| 17 | 19 | ||
| + | 20 | Feedback remains intact in both cases: rising growth hormone and insulin-like growth factor 1 suppress further release. This is the mechanistic reason a secretagogue cannot produce the exposures achievable with exogenous growth hormone.{{r|molitch2011}} | |
| + | 21 | ||
| 18 | == References == | 22 | == References == |
| 19 | {{reflist}} | 23 | {{reflist}} |
| 20 | <ref name="sigalos2018">Sigalos JT, Pastuszak AW. "The safety and efficacy of growth hormone secretagogues." ''Sexual Medicine Reviews'' 6(1):45–53 (2018). PMID 28526632.</ref> | 24 | <ref name="sigalos2018">Sigalos JT, Pastuszak AW. "The safety and efficacy of growth hormone secretagogues." ''Sexual Medicine Reviews'' 6(1):45–53 (2018). PMID 28526632.</ref> |
| + | 25 | <ref name="molitch2011">Molitch ME, Clemmons DR, Malozowski S, et al. "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline." ''Journal of Clinical Endocrinology and Metabolism'' 96(6):1587–1609 (2011). PMID 21602453.</ref> | |
| 21 | 26 | ||
| 22 | {{DEFAULTSORT:Growth hormone secretagogue}} | 27 | {{DEFAULTSORT:Growth hormone secretagogue}} |