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General Peptide Use & Information
Strung out on Ipamorelin, does it lower cortisol or worsen adrenal fatigue?
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<blockquote data-quote="BigTex" data-source="post: 249725" data-attributes="member: 43589"><p><h2>Abstract</h2><p>The development and pharmacology of a new potent growth hormone (GH) secretagogue, ipamorelin, is described. Ipamorelin is a pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2), which displays high GH releasing potency and efficacy in vitro and in vivo. As an outcome of a major chemistry programme, ipamorelin was identified within a series of compounds lacking the central dipeptide Ala-Trp of growth hormone-releasing peptide (GHRP)-1. In vitro, ipamorelin released GH from primary rat pituitary cells with a potency and efficacy similar to GHRP-6 (ECs) = 1.3+/-0.4nmol/l and Emax = 85+/-5% vs 2.2+/-0.3nmol/l and 100%). A pharmacological profiling using GHRP and growth hormone-releasing hormone (GHRH) antagonists clearly demonstrated that ipamorelin, like GHRP-6, stimulates GH release via a GHRP-like receptor. In pentobarbital anaesthetised rats, ipamorelin released GH with a potency and efficacy comparable to GHRP-6 (ED50 = 80+/-42nmol/kg and Emax = 1545+/-250ng GH/ml vs 115+/-36nmol/kg and 1167+/-120ng GH/ml). In conscious swine, ipamorelin released GH with an ED50 = 2.3+/-0.03 nmol/kg and an Emax = 65+/-0.2 ng GH/ml plasma. Again, this was very similar to GHRP-6 (ED50 = 3.9+/-1.4 nmol/kg and Emax = 74+/-7ng GH/ml plasma). GHRP-2 displayed higher potency but lower efficacy (ED50 = 0.6 nmol/kg and Emax = 56+/-6 ng GH/ml plasma). The specificity for GH release was studied in swine. None of the GH secretagogues tested affected FSH, LH, PRL or TSH plasma levels. Administration of both GHRP-6 and GHRP-2 resulted in increased plasma levels of ACTH and cortisol.<strong> Very surprisingly, ipamorelin did not release ACTH or cortisol in levels significantly different from those observed following GHRH stimulation. This lack of effect on ACTH and cortisol plasma levels was evident even at doses more than 200-fold higher than the ED50 for GH release.</strong> In conclusion, ipamorelin is the first GHRP-receptor agonist with a selectivity for GH release similar to that displayed by GHRH. The specificity of ipamorelin makes this compound a very interesting candidate for future clinical development.</p><p></p><p>[URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/9849822/[/URL]</p><p></p><p></p><p>This is why Ipamorelin has been so popular, It can be used at much higher than normal saturation levels of peptides and not increase ACTH/cortisol. <strong>Adrenocorticotropic hormone (ACTH) is a hormone your pituitary gland releases that triggers your adrenal glands to release cortisol, the “stress hormone.” </strong>With GHR-6 and 2 is is very possible at dose larger than saturation levels (or 1mcg/kg) to increase cortisol and prolactin levels. So it is important to stick close to the saturation level as possible.</p><p></p><p>Here is something on the GH effect on cortisol</p><h2>Abstract</h2><p>The adrenocortical responses to the daily administration of 10 mg human GH (hGH) for 4-6 days were compared in 12 patients with Cushing's disease, 2 patients with cortisol-secreting adrenal cortical adenoma, and 4 healthy subjects. The administration of hGH resulted in a significant mean percent decrease in urinary 17-hydroxycorticosteroids [17OHCS; 30 +/- 7.8 (SE)], cortisol secretion rate (32 +/- 5.5), plasma 17OHCS (31 +/- 5.1), and urinary 17-ketosteroids (46 +/- 6.0) in the patients with Cushing's disease. In contrast, it did not significantly decrease urinary or plasma 17OHCS or the cortisol secretion rate in the other groups of subjects similarly studied. Treatment with hGH did not impair the adrenocortical response to exogenous ACTH, but it decreased the response to metyrapone in all subjects tested. In one of the healthy subjects who had exhibited diminished response to metyrapone on hGH, measurement of plasma ACTH levels demonstrated a lower rise after the administration of the drug. Treatment with hGH did not alter the peripheral metabolism of cortisol, as measured by cortisol turnover rates. <strong>We conclude that hGH inhibits ACTH release</strong> and that this effect is maximally demonstrated in patients with increased hypothalamic-pituitary-adrenal function.</p><p></p><p><span style="font-size: 14px"><span style="font-family: 'Verdana'">[URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/7364929/[/URL]</span></span></p><p></p><p><strong>question</strong> - "I also wonder if Ipamorelin or other GH secreting peptides will raise GH or IGF-1" Absolutely it does both</p></blockquote><p></p>
[QUOTE="BigTex, post: 249725, member: 43589"] [HEADING=1]Abstract[/HEADING] The development and pharmacology of a new potent growth hormone (GH) secretagogue, ipamorelin, is described. Ipamorelin is a pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2), which displays high GH releasing potency and efficacy in vitro and in vivo. As an outcome of a major chemistry programme, ipamorelin was identified within a series of compounds lacking the central dipeptide Ala-Trp of growth hormone-releasing peptide (GHRP)-1. In vitro, ipamorelin released GH from primary rat pituitary cells with a potency and efficacy similar to GHRP-6 (ECs) = 1.3+/-0.4nmol/l and Emax = 85+/-5% vs 2.2+/-0.3nmol/l and 100%). A pharmacological profiling using GHRP and growth hormone-releasing hormone (GHRH) antagonists clearly demonstrated that ipamorelin, like GHRP-6, stimulates GH release via a GHRP-like receptor. In pentobarbital anaesthetised rats, ipamorelin released GH with a potency and efficacy comparable to GHRP-6 (ED50 = 80+/-42nmol/kg and Emax = 1545+/-250ng GH/ml vs 115+/-36nmol/kg and 1167+/-120ng GH/ml). In conscious swine, ipamorelin released GH with an ED50 = 2.3+/-0.03 nmol/kg and an Emax = 65+/-0.2 ng GH/ml plasma. Again, this was very similar to GHRP-6 (ED50 = 3.9+/-1.4 nmol/kg and Emax = 74+/-7ng GH/ml plasma). GHRP-2 displayed higher potency but lower efficacy (ED50 = 0.6 nmol/kg and Emax = 56+/-6 ng GH/ml plasma). The specificity for GH release was studied in swine. None of the GH secretagogues tested affected FSH, LH, PRL or TSH plasma levels. Administration of both GHRP-6 and GHRP-2 resulted in increased plasma levels of ACTH and cortisol.[B] Very surprisingly, ipamorelin did not release ACTH or cortisol in levels significantly different from those observed following GHRH stimulation. This lack of effect on ACTH and cortisol plasma levels was evident even at doses more than 200-fold higher than the ED50 for GH release.[/B] In conclusion, ipamorelin is the first GHRP-receptor agonist with a selectivity for GH release similar to that displayed by GHRH. The specificity of ipamorelin makes this compound a very interesting candidate for future clinical development. [URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/9849822/[/URL] This is why Ipamorelin has been so popular, It can be used at much higher than normal saturation levels of peptides and not increase ACTH/cortisol. [B]Adrenocorticotropic hormone (ACTH) is a hormone your pituitary gland releases that triggers your adrenal glands to release cortisol, the “stress hormone.” [/B]With GHR-6 and 2 is is very possible at dose larger than saturation levels (or 1mcg/kg) to increase cortisol and prolactin levels. So it is important to stick close to the saturation level as possible. Here is something on the GH effect on cortisol [HEADING=1]Abstract[/HEADING] The adrenocortical responses to the daily administration of 10 mg human GH (hGH) for 4-6 days were compared in 12 patients with Cushing's disease, 2 patients with cortisol-secreting adrenal cortical adenoma, and 4 healthy subjects. The administration of hGH resulted in a significant mean percent decrease in urinary 17-hydroxycorticosteroids [17OHCS; 30 +/- 7.8 (SE)], cortisol secretion rate (32 +/- 5.5), plasma 17OHCS (31 +/- 5.1), and urinary 17-ketosteroids (46 +/- 6.0) in the patients with Cushing's disease. In contrast, it did not significantly decrease urinary or plasma 17OHCS or the cortisol secretion rate in the other groups of subjects similarly studied. Treatment with hGH did not impair the adrenocortical response to exogenous ACTH, but it decreased the response to metyrapone in all subjects tested. In one of the healthy subjects who had exhibited diminished response to metyrapone on hGH, measurement of plasma ACTH levels demonstrated a lower rise after the administration of the drug. Treatment with hGH did not alter the peripheral metabolism of cortisol, as measured by cortisol turnover rates. [B]We conclude that hGH inhibits ACTH release[/B] and that this effect is maximally demonstrated in patients with increased hypothalamic-pituitary-adrenal function. [SIZE=14px][FONT=Verdana][URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/7364929/[/URL][/FONT][/SIZE] [B]question[/B] - "I also wonder if Ipamorelin or other GH secreting peptides will raise GH or IGF-1" Absolutely it does both [/QUOTE]
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Peptide Forums (GHRH, Sermorelin, etc)
General Peptide Use & Information
Strung out on Ipamorelin, does it lower cortisol or worsen adrenal fatigue?
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