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Mod GRF 1-29

Sermorelin, Growth Hormone Releasing Hormone (1-29), hGRF(1-29)NH2

A synthetic peptide analog of growth hormone-releasing hormone that stimulates the pituitary gland to secrete growth hormone.

Quick Stats
Studies 227
Trials 47
Formula C149H246N44O42S
Overview Studies 227 Clinical Trials 47
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pubmed 1995

The fetal somatotropic axis during long term maternal undernutrition in sheep: evidence for nutritional regulation in utero.

Bauer. M K MK; Breier. B H BH; Harding. J E JE; Veldhuis. J D JD; Gluckman. P D PD

Nutrition is a major determinant of the somatotropic axis during postnatal life. However, little is known about the response of the fetal somatotropic axis to nutritional limitation. From day 100 of gestation (term = 147 days), singleton-bearing ewes were fed either ad libitum (control; n = 6) or 25% of the recommended energy and protein requirements (restricted; n = 7). Ewes and fetuses were chronically catheterized on day 110. On day 120, paired maternal and fetal blood samples were taken over a 6-h period at 15-min intervals. Forty-eight hours later, fetuses were given a 20-micrograms GRF bolus (i.v.), and samples were collected for 48 h. Undernourished mothers and fetuses had higher GH concentrations (P < 0.05). Although plasma GH profiles were independent in mothers and their fetuses, both maternal and fetal GH peak and nadir levels were increased (P < 0.05) by nutritional restriction, but the peak/nadir ratio and the number of pulses remained unaltered. Deconvolution analysis showed that the GH mass secreted per burst was higher in nutritionally restricted animals, whereas basal GH secretion and GH serum half-life were not influenced by undernutrition. Both maternal and fetal insulin-like growth factor-I levels were reduced (P < 0.01 and P < 0.05), whereas insulin-like growth factor-II concentrations were not influenced by the feed restriction. Fetuses from restricted mothers had higher peak GH concentrations after a GRF challenge (P < 0.001), but after correction The specific binding of [125I]ovine placental lactogen ([125I]oPL) or [125I]oGH to maternal or fetal hepatic microsomal membrane preparations was not changed by the maternal undernutrition. Maternal oPL concentrations showed considerable short term fluctuations, whereas fetal oPL levels revealed no major fluctuations. Mean maternal oPL levels tended (P < 0.06) to be elevated, whereas fetal oPL concentrations tended (P < 0.06) to be decreased in restricted animals. These results provide evidence that the somatotropic axis is functional in utero and suggest that the fetal somatotropic axis plays an active role during adaptation of the fetus to nutritional limitation.

pubmed 1994

Priming with GHRH (1-29) NH2: an aid in differential diagnosis between hypothalamic and pituitary deficiencies.

Bueno. G G; Bueno. M M; Garagorri. J M JM; Juste. G G; Rejas. J J; Alvarez. I I

The study looked at whether giving a short series of growth‑hormone‑releasing‑hormone (GHRH) shots could help doctors tell if a child's growth problem comes from the brain (hypothalamus) or the pituitary gland. They gave 16 short‑statured kids a 5 µg/kg GHRH injection for six days, then tested the GH response again. Half the kids showed a bigger GH spike after this “priming,” while the other half did not, allowing the researchers to separate the two groups.

pubmed 1994

Development of homologous radioimmunoassays for equine growth hormone and equine prolactin and their application to the detection of circulating levels of hormone in horse plasma.

Cahill. C M CM; Van der Kolk. H H; Goode. J A JA; Hayden. T J TJ

The paper describes how scientists built very sensitive lab tests to measure growth hormone and prolactin in horse blood. It shows the detection limits of the tests and reports natural hormone fluctuations in lactating mares, but it does not provide any information on using GRF‑1‑29 in humans or suggest any practical protocols.

pubmed 1993

Suppression of growth hormone (GH) secretion by a selective GH-releasing hormone (GHRH) antagonist. Direct evidence for involvement of endogenous GHRH in the generation of GH pulses.

Jaffe. C A CA; Friberg. R D RD; Barkan. A L AL

To study the potential involvement of growth hormone-releasing hormone (GHRH) in the generation of growth hormone (GH) pulses in humans we have used a competitive antagonist to the GHRH receptor, (N-Ac-Tyr1,D-Arg2)GHRH(1-29)NH2(GHRH-Ant). Six healthy young men were given a bolus injection of GHRH-Ant 400 micrograms/kg body wt or vehicle at 2200 h and nocturnal GH concentrations were assessed by every 10-min blood sampling until 0800 h. Integrated total and pulsatile GH secretion were suppressed during GHRH-Ant treatment by 40 +/- 6 (SE) % and 75 +/- 5%, respectively. GHRH-Ant suppressed maximum (7.6 +/- 2.2 vs 1.8 +/- 0.5 micrograms/liter; P < 0.001) and mean (3.3 +/- 1.0 vs 1.1 +/- 0.2 micrograms/liter; P = 0.02) GH pulse amplitudes. There was no change in integrated nonpulsatile GH levels, pulse frequency, or interpulse GH concentration. GHRH-Ant 400 micrograms/kg also suppressed the GH responses to intravenous boluses of GHRH 0.33 micrograms/kg given 1, 6, 12, and 24 h later by 95, 81, 59, and 4%, respectively. In five healthy men, the responses to 10-fold larger GHRH boluses (3.3 micrograms/kg) were suppressed by 82 and 0%, 1 and 6 h after GHRH-Ant 400 micrograms/kg, respectively. These studies provide the first direct evidence that endogenous GHRH participates in the generation of spontaneous GH pulses in humans.

pubmed Oct 16, 1992

Enzymatic semisynthesis of a superpotent analog of human growth hormone-releasing factor.

Bongers. J J; Lambros. T T; Liu. W W; Ahmad. M M; Campbell. R M RM; Felix. A M AM; Heimer. E P EP

A superpotent analog of human growth hormone-releasing factor, [desNH2Tyr1,D-Ala2,Ala15]-GRF(1-29)-NH2 (4), was prepared from the precursor, [Ala15,29]-GRF(4-29)-OH (1), by a two-step enzymatic semisynthesis. The amidated C-terminus, essential for high biological potency, was obtained via a carboxypeptidase Y-catalyzed exchange of Ala29-OH for Arg29-NH2 to produce [Ala15]-GRF(4-29)-NH2 (2). The N-terminal desNH2Tyr-D-Ala moiety, which greatly increases in vivo duration of action, was then incorporated by V8 protease-catalyzed condensation of segment 2 with desNH2Tyr-D-Ala-Asp(OH)-OR [R = CH3CH2- (3a) or 4-NO2C6H4CH2-(3b)]. The main focus of this report was to develop conditions to use the V8 protease-catalyzed coupling while avoiding a competing cleavage of the proteolytically-sensitive Asp25-Ile26 bond in GRF. Conversion of 2 to 4 in couplings employing the alpha-ethyl ester of the acyl component 3a was limited to about 60% by competing proteolysis at Asp25-Ile26. This system was adequate for preparing, isolating, and fully characterizing the target analog 4 and identifying the side products. The 4-nitrobenzyl ester 3b proved to be a superior substrate, resulting in 90% conversion of 2 to 4 with no detectable loss to proteolysis and requiring significantly lesser amounts of catalyst. These results demonstrate that enzymatic semisynthesis of a biologically-active peptide amide which contains unnatural amino acids at the N-terminus can be achieved from a biosynthetic precursor in good yield and purity.

pubmed 1993

Growth hormone response to growth hormone-releasing hormone in early abstinent alcoholic patients.

De Marinis. L L; Mancini. A A; Fiumara. C C; Conte. G G; Iacona. T T; Ianiri. L L; Zeppetelli. E E;...

The alpha-2-adrenoceptor agonist clonidine is able to stimulate GHRH secretion directly or via beta-endorphin and, therefore, induces a GH release in normal subjects. This effect has been shown to be blunted in alcoholism during early abstinence, due to central alterations of adrenergic mechanisms. To evaluate pituitary responsiveness to direct stimulation with GHRH, we have studied the GH and PRL response to GHRH in 10 alcoholics during early abstinence. Our data indicate that the pituitary response to GHRH is intact in abstinent alcoholics, except in obese patients, who displayed a blunted GH response. GHRH did not increase PRL. The dissociation between clonidine and GHRH in GH stimulation could reveal a different neuroendocrine mechanism, in comparison with other psychiatric disorders (anorexia nervosa), in which such a dissociation is accompanied by a PRL response to GHRH.

pubmed 1992

Lactation performance of sows injected with growth hormone-releasing factor during gestation and(or) lactation.

Farmer. C C; Petitclerc. D D; Pelletier. G G; Brazeau. P P

Fifty-two Yorkshire x Landrace gilts were equally allotted to four treatments: 1) controls, saline injections (CTL); 2) injections of 12 mg of growth hormone-releasing factor (GRF) (1-29)NH2 thrice daily (0700, 1500, and 2300) from d 100 of gestation until parturition (GEST); 3) injections of GRF thrice daily from d 3 to 29 of lactation (LACT); and 4) injections of GRF thrice daily during gestation (d 100 to parturition) and lactation (d 3 to 29) (GEST-LACT). Within 48 h of birth, litters were standardized to 9 +/- 1 pigs. Weights of the pigs were recorded weekly from birth (less than 24 h) until weaning (d 30) and on d 42 and 56. Weights of gilts at mating, d 110 of gestation, 1 d postfarrowing, and at weaning also were recorded. On d 24 of lactation, milk yield was estimated by the weigh-suckle-weigh method, and a representative milk sample was obtained the next day. Jugular vein cannulas were inserted into six sows per treatment on d 26, and a 6-h blood profile (sampling every 20 min from 0600 to 1200) was obtained on d 29. Daily feed consumption of sows was recorded throughout the study. Weights of the pigs at any one time or survival until weaning were not affected by treatments (P greater than .1). Sows injected with GRF during GEST (P = .05) and(or) LACT (P less than .01) were lighter than CTL sows at weaning; in addition, sows treated during lactation had less backfat (P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

pubmed Mar 1, 1989

The effects of vasoactive intestinal peptide (VIP) antagonists, and VIP and peptide histidine isoleucine antisera on non-adrenergic, non-cholinergic relaxations of tracheal smooth muscle.

Ellis. J L JL; Farmer. S G SG

1. The effects of several drugs, including antagonists of vasoactive intestinal peptide (VIP), and antisera to VIP or peptide histidine isoleucine (PHI), on relaxation responses of guinea-pig isolated trachea to electrical field stimulation (EFS) have been examined. 2. beta-Adrenoceptor blockade with propranolol only partially blocked the inhibitory response to EFS, but had no effect in tissues from animals pretreated with 6-hydroxydopamine or reserpine. 3. Neither adenosine deaminase, in the presence of dipyridamole, nor the potent adenosine antagonist NPC205 (1,3-n-dipropyl-8-(4-hydroxyphenyl)-xanthine) had any effect on the inhibitory response to EFS. 4. The VIP antagonists, [Ac-Tyr1, D-Phe2]-GRF(1-29)-NH2 and [4-Cl-D-Phe6, Leu17]-VIP had no effect on the inhibitory response to EFS. Moreover, they were without effect on responses to exogenous VIP or PHI. 5. Overnight incubation with VIP antisera markedly reduced the inhibitory response to EFS. PHI antisera had a similar, but smaller effect. 6. In the presence of a concentration of VIP that is maximal for its relaxant effect, inhibitory responses to electrical stimulation were greatly inhibited. 7. Naloxone and reactive blue 2 each had no effect on inhibitory responses indicating that endogenous opioids and adenosine 5'-triphosphate (ATP) respectively are not involved. 8. The results suggest that VIP and PHI, but not adenosine, contribute to non-adrenergic, noncholinergic inhibitory nerve responses of guinea-pig trachea. Moreover, the surprising lack of effect of both VIP antagonists on these responses, and in particular, on responses to exogenous VIP, suggests that the receptors mediating VIP-induced tracheal relaxation are different from those that mediate pancreatic secretion.

pubmed 1990

Insulin-like growth factor-I concentration in Holstein female cattle: variations with age, stage of lactation and growth hormone-releasing factor administration.

Abribat. T T; Lapierre. H H; Dubreuil. P P; Pelletier. G G; Gaudreau. P P; Brazeau. P P; Petitclerc....

Plasma insulin-like growth factor-I (IGF-I) concentrations were monitored in Holstein females through different periods of their growth, lactation and after acute or chronic growth hormone-releasing factor (GRF) administration. Plasma samples were radioimmunoassayed using a human IGF-I antibody after a 24 hr incubation in a HCl(.1N)-glycine(.2M) buffer (pH 2). In a first study, IGF-I concentrations were measured in Holstein females of different ages and(or) stages of lactation (n = 6 per group). The IGF-I concentrations in newborn calves (102.0 +/- 11.3 ng/ml) markedly decreased (P less than .01) in 1 mo old animals (50.2 +/- 7.1 ng/ml), then increased (P less than .01) to 137.0 +/- 5.1 and 137.4 +/- 11.0 ng/ml in 6 and 10 mo old heifers, respectively. In dairy cows, IGF-I concentrations were low 24 hr post-partum (44.7 +/- 7.6 ng/ml) and then increased (P less than .05) to remain stable throughout lactation (91.3 +/- 4.9, 92.8 +/- 12.9, 96.1 +/- 7.6, 90.7 +/- 8.8 ng/ml at 2, 3, 6 and 9 mo of lactation, respectively). There was a further increase (P less than .05) to 113.7 +/- 3.1 ng/ml during the dry period. In a second trial, blood samples were collected from lactating dairy cows every 2 hr for 24 hr following a sc injection of saline (n = 4) or human (h) GRF (1-29)NH2 (10 micrograms/kg BW, n = 4). The IGF-I peak concentration was reached on average 10 hr after the GRF injection and was higher (P less than .01) in treated cows than in control cows (135.4 vs 86.9 +/- 16.2 ng/ml). In the last trial, daily sc injections of 10 micrograms of hGRF(1-29)NH2 per kg BW to dairy cows (252 days of lactation) for 57 days, which increased milk production by 14% (2 kg/day), also increased (P less than .01) IGF-I concentration: 127.1 +/- 5.3 and 118.0 +/- 1.6 vs 90.7 +/- 4.7 and 96.0 +/- 5.0 ng/ml on days 29 and 57 of treatment for treated (n = 9) and control (n = 8) cows, respectively. Thus, the IGF-I concentration in dairy cattle varies with age and stage of lactation, and is increased by GRF administration in lactating dairy cows.

pubmed Mar 1, 1988

The effects of antagonists of vasoactive intestinal peptide on nonadrenergic noncholinergic inhibitory responses in feline airways.

Thompson. D C DC; Altiere. R J RJ; Diamond. L L

In a cat lung study, the peptide GRF‑1‑29 (used as a VIP blocker) didn’t stop the airway‑relaxing effects of VIP, and another VIP blocker only worked at very high doses. This means these compounds aren’t reliable tools for influencing VIP‑driven airway responses.

pubmed Dec 1, 1991

Effects of vasoactive intestinal polypeptide antagonists on cholinergic neurotransmission in dog and cat trachea.

Xie. Z Q ZQ; Hirose. T T; Hakoda. H H; Ito. Y Y

This study looked at how two VIP‑blocking peptides change nerve‑to‑muscle signaling in the airways of dogs and cats. The peptides made the nerve signals stronger in cat trachea but had little effect in dog trachea. The work is purely basic science on animal tissue and does not suggest any human health or performance benefits.

pubmed Nov 13, 1991

Vasoactive intestinal peptide receptor antagonists in rat seminal vesicle membranes.

Rodríguez-Pena. M S MS; Guijarro. L G LG; Prieto. J C JC

Vasoactive intestinal peptide (VIP) receptors coupled to activation of adenylate cyclase have been previously identified in seminal vesicle membranes of rat. In the present study we demonstrate that the synthetic peptides [4-Cl-D-Phe6,Leu17]VIP and the growth hormone releasing factor (GRF) analog [Ac-Tyr1,D-Phe2]GRF1-29-NH2 inhibit in a competitive manner the specific 125I-VIP binding to the same membrane preparation. The order of potency of the two peptides compared to VIP was: VIP (IC50 = 1.3 +/- 0.5 nM) greater than [4-Cl-D-Phe6,Leu17]VIP(IC50 = 1600 +/- 45.0 nM) greater than [Ac-Tyr1,D-Phe2]GRF1-29-NH2(IC50 = 290.0 +/- 59.4 nM). Whereas VIP showed a stimulatory activity upon adenylate cyclase with a potency (ED50 = 7.0 +/- 0.7 nM) compatible with the affinity of the VIP binding sites previously described, the other two peptides tested showed no effect at that level. The behavior as antagonists of both [4-Cl-D-Phe6,Leu17]VIP and [Ac-Tyr1,D-Phe2]GRF1-29-NH2 was confirmed by: (a) the parallel shifts of the VIP dose-response curves for stimulation of adenylate cyclase activity in the presence of the antagonists; (b) the close agreement between the binding affinity and the inhibition of adenylate cyclase activity for the two peptides; and (c) the lack of effect of the two antagonists upon the adenylate cyclase activity stimulated by the beta-adrenoceptor agonist isoproterenol which indicates the specificity of the interaction.(ABSTRACT TRUNCATED AT 250 WORDS)

pubmed 1992

Time-dependent reduction and potentiation of growth hormone (GH) responsiveness to GH-releasing factor induced by exogenous GH: role for somatostatin.

Lanzi. R R; Tannenbaum. G S GS

Exogenous GH is known to exert a negative feedback effect on its own responsiveness to GH-releasing factor (GRF); however, the mechanism is not known. In the present study we examined the time course of effects of a single sc administration of recombinant human (rh) GH on GH responsiveness to GRF and investigated the possible involvement of somatostatin (SRIF) in this response. Free-moving adult male rats were administered 200 micrograms rhGH, sc, at 0800 h and subsequently challenged with 1 microgram GRF-(1-29)NH2, iv, at times of spontaneous peaks (1100 and 1500 h) and troughs (1300 h) in GH secretion during a 6-h (1000-1600 h) sampling period. H2O-injected control rats exhibited the typical cyclic responsiveness to GRF stimulation, with GRF-induced GH release significantly greater during peak compared to trough periods of the GH rhythm. Pretreatment with rhGH 3 h before GRF injection markedly inhibited the GH response to GRF at a peak time [integrated GH release over 30 min, 1135 +/- 271 vs. 6372 +/- 1185 ng/ml.30 min in H2O-injected controls (mean +/- SE); P less than 0.01]. In striking contrast, 5 h after rhGH administration, there was a 6-fold augmentation of GH responsiveness to GRF compared to that in H2O-injected controls at a trough time (7032 +/- 1622 vs. 1128 +/- 216 ng/ml.30 min; P less than 0.01). High GH responsiveness to GRF was preserved 7 h after rhGH injection. Passive immunization of rhGH-treated rats with SRIF antiserum reversed the rhGH-induced blunted GH response at 3 h (7985 +/- 366 vs. 1705 +/- 431 ng/ml.30 min in rhGH-treated control rats given normal sheep serum; P less than 0.01) and completely restored GH responsiveness to levels as high as those in H2O-injected controls. These results demonstrate that 1) a single sc injection of rhGH markedly attenuates GH responsiveness to GRF acutely for about 3 h, but subsequently enhances somatotroph sensitivity to the stimulatory actions of GRF; and 2) the short term blunting of GRF-induced GH release by rhGH is due at least in part to increased release of endogenous SRIF. The subsequent potentiation of GH responsiveness to GRF is probably due to a SRIF-mediated build-up of pituitary GH stores in a readily releasable pool. Such a mechanism of GH autofeedback may play a physiological role in the genesis of pulsatile GH secretion.

pubmed 1992

Substance P is diminished and vasoactive intestinal peptide is augmented in psoriatic lesions and these peptides exert disparate effects on the proliferation of cultured human keratinocytes.

Pincelli. C C; Fantini. F F; Romualdi. P P; Sevignani. C C; Lesa. G G; Benassi. L L; Giannetti. A A

The study looked at two brain‑derived peptides, VIP and substance P, in psoriasis‑affected skin. VIP was higher and substance P lower in lesions, and VIP made skin cells grow while substance P stopped that growth. A short version of the peptide GRF‑1‑29 acted as a blocker of VIP’s effect on the cells.

pubmed 1992

Short-term adult exposure to estradiol feminizes the male pattern of spontaneous and growth hormone-releasing factor-stimulated growth hormone secretion in the rat.

Painson. J C JC; Thorner. M O MO; Krieg. R J RJ; Tannenbaum. G S GS

Experimental evidence indicates that the neonatal gonadal steroid environment is an important determinant of the sexual dimorphism of GH secretion and body growth. However, the influence of the sex steroids in GH control during adult life and their mechanism/site of action are largely unknown. In the present study we examined the effects of adult gonadectomy (GNX) and short term adult exposure to 17 beta-estradiol (E2) on both spontaneous and GRF-stimulated GH release in free-moving adult male rats. The rate of body weight gain was also monitored. GNX (3 weeks postoperatively) resulted in a 2-fold reduction in GH pulse amplitude compared to that in sham-operated control rats, but did not significantly alter the GH nadir or the interpeak interval. Exposure to E2 (sc implants) for 4 days markedly disrupted the spontaneous GH secretory profile of both sham-operated and GNX rats; E2-treated animals exhibited a striking elevation (4- to 20-fold) of GH trough levels and a significant decrease in GH interpeak interval, remarkably similar to the typical female rat GH secretory profile. The augmentation in both GH nadir and GH pulse frequency was evident as early as 12 h after a single sc injection of E2 valerate. In sham and GNX rats bearing control implants, the GH response to 1 micrograms rat GRF-(1-29)NH2, iv, was significantly greater when GRF was administered at peak (1100 h) than at trough (1300 h) times of GH secretion; the latter is known to be due to antagonism by the cyclical increased release of endogenous somatostatin (SRIF) in the male rat. Treatment with E2 abolished this time-dependent difference in both groups and produced a regular pattern of GH responsiveness to GRF similar to that typically observed in the female rat, thus suggesting that E2 has altered the pattern of hypothalamic SRIF secretion from a cyclic to a more continuous mode of release. Chronic exposure to E2 for 2 weeks resulted in an almost 6-fold inhibition of the rate of body weight gain in sham-operated male rats to levels comparable to those in normal adult female rats. Taken together, these results demonstrate that short term exposure to E2 during adult life can profoundly feminize the male pattern of spontaneous and GRF-stimulated GH secretion, as well as rate of somatic growth.(ABSTRACT TRUNCATED AT 400 WORDS)