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Sublingual GH
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diamonddiceclay
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only shots work for hgh
CYCLEON
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gh bosters are a scam - growth hormone releasing peptides are not however.
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)
--------------------------------------------------------------------------------
Abstract
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.
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)
--------------------------------------------------------------------------------
Abstract
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.
CYCLEON
New member
more goodies
New test offers advantages over insulin tolerance test for diagnosis of growth hormone deficiency
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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.
________________________________________
Authors
Frieboes RM, Murck H, Antonijevic IA, Steiger A.
Title
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
Source
Journal of Neuroendocrinology. 11(6):473-478, 1999 Jun.
Author Keywords
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.
Abstract
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]
_____________________________________
New test offers advantages over insulin tolerance test for diagnosis of growth hormone deficiency
Print Email
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.
________________________________________
Authors
Frieboes RM, Murck H, Antonijevic IA, Steiger A.
Title
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
Source
Journal of Neuroendocrinology. 11(6):473-478, 1999 Jun.
Author Keywords
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.
Abstract
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]
_____________________________________
CYCLEON
New member
an understandable write up - china mans is ghrp2 but little difference
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.
Other peptides of different size and structure are able to influence GH secretion in man and several other animal species. Amongst these, a synthetic hexapeptide (GHRP-6), derived from an enkephalin analogue, specifically stimulates GH release both after parenteral and oral administration. The oral activity of GHRP-6 has opened up new perspectives in the treatment of several conditions associated to hypothalamic growth hormone deficiency. It has also prompted the development of new synthetic peptides, possessing greater potency, a longer duration of action and an increased oral bioavailability.
Hexarelin (INN:Examorelin, MF 6003, EP 23905) is a new synthetic peptide formed by 6 aminoacids. Its chemical structure is His-DTrp(2-Me)-Ala-Trp-DPhe-Lys-NH2. Compared to GHRP-6, hexarelin is more resistant to proteolytic degradation.
An extensive package of toxicological studies has been performed. No organ specific toxicity was observed. No toxic effects were recorded on the cardiovascular system, renal function and CNS. Pharmacokinetic studies are available in rats and dogs. The drug is absorbed by the subcutaneous and oral routes. The half-life of hexarelin is 2 hours in dogs after bolus iv administration.
Hexarelin stimulates GH secretion following intravenous, subcutaneous, intranasal and oral administration. In man, a bolus intravenous dose of 1 mg/kg induces peak plasma GH concentrations of around 70 ng/mL within 15 minutes. The mechanism of action of hexarelin has still not been fully elucidated. The peptide seems to act on pituitary binding-sites and to modulate intracellular messenger pathways different from those associated with GHRH. Its low toxicity, marked and specific stimulation of GH secretion along with its rapid absorption after oral administration, strongly indicate that it could be employed as a diagnostic and therapeutic tool in GH secretory disorders.
High-affinity binding sites for hexarelin have been identified in human cardiac and vascular tissues. Various animal models have evidenced a strong protective effect of hexarelin in post-ischemic ventricular dysfunction. Hexarelin improves cardiac function in rats with experimentally induced congestive heart failure. These cardiovascular effects have also been observed in hypophysectomized animals and occur at doses far lower than those required to elicit GH secretion.
Hexarelin has been administered to about 1,000 subjects. Phase 1 studies have shown that the drug is well tolerated after i.v. administration of doses up to 2 mg/kg. Chronic intranasal administration of hexarelin has been shown to accelerate growth in short children. Endocrine effects have been demonstrated after chronic oral administration in elderly subjects.
happy now?
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.
Other peptides of different size and structure are able to influence GH secretion in man and several other animal species. Amongst these, a synthetic hexapeptide (GHRP-6), derived from an enkephalin analogue, specifically stimulates GH release both after parenteral and oral administration. The oral activity of GHRP-6 has opened up new perspectives in the treatment of several conditions associated to hypothalamic growth hormone deficiency. It has also prompted the development of new synthetic peptides, possessing greater potency, a longer duration of action and an increased oral bioavailability.
Hexarelin (INN:Examorelin, MF 6003, EP 23905) is a new synthetic peptide formed by 6 aminoacids. Its chemical structure is His-DTrp(2-Me)-Ala-Trp-DPhe-Lys-NH2. Compared to GHRP-6, hexarelin is more resistant to proteolytic degradation.
An extensive package of toxicological studies has been performed. No organ specific toxicity was observed. No toxic effects were recorded on the cardiovascular system, renal function and CNS. Pharmacokinetic studies are available in rats and dogs. The drug is absorbed by the subcutaneous and oral routes. The half-life of hexarelin is 2 hours in dogs after bolus iv administration.
Hexarelin stimulates GH secretion following intravenous, subcutaneous, intranasal and oral administration. In man, a bolus intravenous dose of 1 mg/kg induces peak plasma GH concentrations of around 70 ng/mL within 15 minutes. The mechanism of action of hexarelin has still not been fully elucidated. The peptide seems to act on pituitary binding-sites and to modulate intracellular messenger pathways different from those associated with GHRH. Its low toxicity, marked and specific stimulation of GH secretion along with its rapid absorption after oral administration, strongly indicate that it could be employed as a diagnostic and therapeutic tool in GH secretory disorders.
High-affinity binding sites for hexarelin have been identified in human cardiac and vascular tissues. Various animal models have evidenced a strong protective effect of hexarelin in post-ischemic ventricular dysfunction. Hexarelin improves cardiac function in rats with experimentally induced congestive heart failure. These cardiovascular effects have also been observed in hypophysectomized animals and occur at doses far lower than those required to elicit GH secretion.
Hexarelin has been administered to about 1,000 subjects. Phase 1 studies have shown that the drug is well tolerated after i.v. administration of doses up to 2 mg/kg. Chronic intranasal administration of hexarelin has been shown to accelerate growth in short children. Endocrine effects have been demonstrated after chronic oral administration in elderly subjects.
happy now?
ultragainz
New member
it sucks
Blindfaith
New member
think about it this way......multi BILLION dollar company's have been trying to make a GH pill and cant do it....what makes u think that some dude in an appartmant with his own lab can do it???? Make any sense???
CYCLEON
New member
well, its not GH - its a peptide that initiates GH release - of course its not as good as GH shot SC but far better than the HGH spray crap, thats what the med field thinks anyway, its a real product.
Chinaman doesnt make those, he buys his material from a pharmalab and then contracts out to a pillmaker - same way many US manufactureres do.
Chinaman doesnt make those, he buys his material from a pharmalab and then contracts out to a pillmaker - same way many US manufactureres do.
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