gh bosters are a scam - growth hormone releasing peptides are not however. I dont know how well they work in the field and im sure a few vets will come spit on my post but the real scientific studies do show that the substance does work. Thats also why you dont see Muscletek selling any either.
The effects of GH-releasing peptide-6 (GHRP-6) and GHRP-2 on intracellular adenosine 3',5'-monophosphate (cAMP) levels and GH secretion in ovine and rat somatotrophs
D Wu, C Chen, J Zhang, C Y Bowers(1) and I J Clarke
Prince Henry's Institute of Medical Research, PO Box 5152, Clayton, Victoria 3168, Australia and (1) Department of Medicine, Tulane University Medical Center, New Orleans, Louisiana 70112, USA
(Requests for offprints should be addressed to C Chen)
The mechanism of action of GH-releasing peptide-6 (GHRP-6) and GHRP-2 on GH release was investigated in ovine and rat pituitary cells in vitro. In partially purified sheep somatotrophs, GHRP-2 and GH-releasing factor (GRF) increased intracellular cyclic AMP (cAMP) concentrations and caused GH release in a dose- dependent manner; GHRP-6 did not increase cAMP levels. An additive effect of maximal doses of GRF and GHRP-2 was observed in both cAMP and GH levels whereas combined GHRP-6 and GHRP-2 at maximal doses produced an additive effect on GH release only. Pretreatment of the cells with MDL 12,330A, an adenylyl cyclase inhibitor, prevented cAMP accumulation and the subsequent release of GH that was caused by either GHRP-2 or GRF. The cAMP antagonist, Rp-cAMP also blocked GH release in response to GHRP-2 and GRF. The cAMP antagonist did not prevent the effect of GHRP-6 on GH secretion whereas MDL 12,330A partially reduced the effect. An antagonist for the GRF receptor, [Ac- Tyr(1) ,d- rg(2) ]-GRF 1-29, significantly diminished the effect of GHRP-2 and GRF on cAMP accumulation and GH release, but did not affect GH release induced by GHRP-6. Somatostatin prevented cAMP accumulation and GH release responses to GHRP-2, GRF and GHRP-6. Ca(2+) channel blockade did not affect the cAMP increase in response to GHRP-2 or GRF but totally prevented GH release in response to GHRP-2, GRF and GHRP-6. These results indicated that GHRP-2 acts on ovine pituitary somatotrophs to increase cAMP concentration in a manner similar to that of GRF; this occurs even during the blockade of Ca(2+) influx. GHRP-6 caused GH release without an increase in intracellular cAMP levels. GHrelease in response to all three secretagogues was reduced by somatostatin and was dependent upon the influx of extracellular Ca(2+) . The additive effect of GHRP-2 and GRF or GHRP-6 suggested that the three peptides may act on different receptors. In rat pituitary cell cultures, GHRP-6 had no effect on cAMP levels, but potentiated the effect of GRF on cAMP accumulation. The synergistic effect of GRF and GHRP-6 on cAMP accumulation did not occur in sheep somatotrophs. Whereas GHRP-2 caused cAMP accumulation in sheep somatotrophs, it did not do so in rat pituitary cells. These data indicate species differences in the response of pituitary somatotrophs to the GHRPs and this is probably due to different subtypes of GHRP receptor in rat or sheep.
New test offers advantages over insulin tolerance test for diagnosis of growth hormone deficiency
NEW YORK, Oct 2 (Praxis Press) The insulin tolerance test (ITT) used to diagnose growth hormone (GH) deficiency in adults has several drawbacks, including limited reproducibility, absence of a normal range, and contraindication in certain clinical situations. Popovic and colleagues studied the safety, convenience, and reliability of a new provocative test in 125 adult patients with known organic pituitary disease and severe GH deficiency (GH peak after ITT of !U?3 micrograms/L) and 125 healthy adult controls. The test entailed intravenous administration of GH-releasing hormone (GHRH, 1 micrograms/kg) plus GH-releasing peptide-6 (GHRP-6, 1 micrograms/kg) followed by tracking of GH levels for 120 minutes. The GH peaks triggered by the GHRH/GHRP-6 test did not produce any side effects, differ between men and women, correlate with age or body mass index, or vary with the use of different GH assays. Mean GH peaks after the GHRH/GHRP-6 test were 59.2 !A` 2.2 micrograms/L in controls and 4.1 !A` 0.3 micrograms/L in patients; corresponding mean GH peaks after the ITT were 14.3 !A` 1.7 micrograms/L and 0.5 !A` 0.06 micrograms/L. The difference between patient and control GH peaks was greater when using the GHRH/GHRP-6 test than when using the ITT (P < 0.001). Although GH peaks using the GHRH/GHRP-6 test spanned a continuum for both patients and controls, a cut-off value of 15 micrograms/L largely differentiated between the two groups. For the GHRH/GHRP-6 test, the authors propose that GH peak values of 20.00 micrograms/L and greater be considered normal and values of 10.00 micrograms/L and less be considered an indication of GH deficiency. The accompanying commentary notes that the GHRH/GHRP-6 test may be better for patients with pituitary disease, whereas the ITT may be better for patients with hypothalamic disease; it also argues for continued efforts toward global standardization of GH immunoassays.
Frieboes RM, Murck H, Antonijevic IA, Steiger A.
Effects of growth hormone-releasing peptide-6 on the nocturnal secretion of GH, ACTH and cortisol and on the sleep EEG in man: Role of routes of administration
Journal of Neuroendocrinology. 11(6):473-478, 1999 Jun.
Growth hormone, Growth hormone-releasing peptides, Corticotropins, Clinical neuroendocrinology, Sleep.
KeyWords Plus® by ISI®
Normal men, Factor-i, Secretagogue, Receptor, Hexarelin, Pituitary, Insulin, Intranasal, Prolactin, Efficacy.
After repeated intravenous (i.v.) boluses of growth hormone-releasing peptide-6 (GHRP-6) we found recently increases of growth hormone (GH), corticotropin (ACTH) and cortisol levels and of the amount of stage 2 sleep, In clinical use, oral (p.o.), intranasal (i.n.) and sublingual (s.l.) routes of administration have advantages over i.v. administration, We compared the sleep-endocrine effects of 300 mu g/kg of body weight (b.w.) GHRP-6 in enteric-coated capsules given p.o. at 21.00 h and of 30 mu g/kg GHRP-6 i.n. or 30 mu g/kg GHRP-6 st. given at 22.45 h in normal young male controls with placebo conditions. After GHRP-6 p.o. secretion of GH, ACTH and cortisol remained unchanged. The only effect of GHRP-6 s.l. was a trend toward an increase in GH in the first half of the night. GHRP-6 i.n. prompted a significant increase in GH concentration during the total night and a trend toward an increase in ACTH secretion during the first half of the night, whereas cortisol secretion remained unchanged. Furthermore, after GHRP-6 i.n., sleep stage 2 increased in the second half of the night by trend, and spectral analysis of total night non-rapid eye movement (REM) sleep revealed a decrease of delta power by trend. In contrast sleep stage 2 decreased during the second half of the night after GHRP-6 p.o. Our data demonstrate that GHRP-6 is capable of modulating GH and ACTH secretion as well as sleep. However, the effects depend upon dosage, duration and route of administration. [References: 41]
The secretion of growth hormone (GH) from the pituitary gland is regulated by the central nervous system. At the hypothalamic level, two peptides, growth hormone releasing hormone (GHRH) and somatostatin modulate the secretion of GH. GHRH stimulates GH secretion while somatostatin exhibits an inhibitory influence.
Thread: gh(GHRP-2) bosters are a scam