Moreno-Reyes. R R; Kerkhofs. M M; L'Hermite-Balériaux. M M; Thorner. M O MO; Van Cauter. E E; C...
In a small study of healthy young men, a single late‑night dose of GHRP‑2 raised growth hormone levels but did not increase deep (slow‑wave) sleep. The peptide caused a brief rise in prolactin and a normal GH pulse, but sleep patterns stayed the same, with a slight, non‑significant trend toward more wakefulness right after the injection.
In male rats, a new six‑amino‑acid peptide called KP‑102 can trigger a big release of growth hormone, especially when it’s given together with a growth‑hormone‑releasing factor (GRF) or after a drug called cysteamine. The effect depends a lot on the timing of the body’s natural hormone cycles.
Sawada. H H; Sugihara. H H; Onose. H H; Minami. S S; Shibasaki. T T; Wakabayashi. I I
In rats, a new six‑amino‑acid peptide called KP-102 can boost growth hormone (GH) release, but only when it’s used together with a GH‑releasing factor (GRF) or when the body’s natural GH‑blocking hormone (somatostatin) is blocked. On its own, KP-102 has only a tiny effect.
Adams. E F EF; Huang. B B; Buchfelder. M M; Howard. A A; Smith. R G RG; Feighner. S D SD; van der Pl...
The study examined pituitary tumor cells and found that they all carry the gene for the growth hormone secretagogue receptor (GHS‑R) that GHRP‑2 binds to. Some GH‑producing tumors responded to GHRP‑2 with increased hormone release, while others did not, showing that the response can vary. Prolactin‑producing tumors also responded, but non‑functioning tumors lacked the receptor.
Ferro. P P; Ventura. R R; Pérez-Mañá. C C; Farré. M M; Segura. J J
The study looked at ways to spot illegal growth hormone use by checking blood for certain genes and proteins, not by testing the hormone itself. It found that changes in the FN1 gene and protein, and the RAB31 gene, could signal recent growth hormone intake, and that a common growth‑hormone‑releasing peptide (GHRP‑2) doesn’t mess up these signals. This is mainly useful for anti‑doping labs, not for people who take GHRP‑2 to boost performance.
A 28‑year‑old man with Hashimoto's thyroiditis had repeated severe low‑blood‑sugar episodes caused by a sudden loss of ACTH, the hormone that tells the adrenal glands to make cortisol. Tests showed his pituitary was otherwise normal, and imaging showed small adrenal glands. He was treated with hydrocortisone and stopped having hypoglycemia. The case suggests that isolated ACTH deficiency, though rare, can cause dangerous low blood sugar and should be considered in similar situations.
Moskaleva. Natalia E NE; Markin. Pavel A PA; Kuznetsov. Roman M RM; Andronova. Tatiana M TM; Appolon...
Researchers created a sensitive lab test to measure the drug GMDP (an immune‑boosting compound) in human blood and used it to see how the drug behaves after a person swallows it. The test works well, but the study doesn’t give dosing advice or clear benefits for everyday use.
Kamoi. Kyuzi K; Shimatsu. Akira A; Kobayashi. Mai M
A single healthy young man showed unusually low growth hormone (GH) responses to standard stimulation tests (insulin tolerance test and GHRP‑2) even though his overall hormone system looked normal. The researchers think he might have an unknown brain circuit that controls GH and other hormones, but the study doesn’t reveal how to change or use this information.
A 46‑year‑old woman with a stomach tumour (GIST) had dangerous low blood sugar that didn't improve with glucose. Doctors measured her growth hormone response using a GHRP‑2 test, found it was high, and treated her with steroids, which fixed the hypoglycaemia. The tumour likely released a big form of IGF‑II that caused the problem.
Esposito. Simone S; Deventer. Koen K; Geldof. Lore L; Van Eenoo. Peter P
The study shows that lab tests using human liver microsomes and S9 fractions can mimic how peptide drugs like GHRP‑2 break down in the body, helping scientists spot their use in sports doping. It doesn’t give any tips on how to use the peptide for health or performance.
Lange. Tobias T; Thomas. Andreas A; Walpurgis. Katja K; Thevis. Mario M
Scientists created a fully automated way to prepare tiny drops of blood on filter paper so they can spot low‑weight peptides like GHRP‑2 using a high‑tech lab test. The method can find these substances at very low levels (0.5‑20 ng/mL) and works even with new blood‑collection devices that use microneedles.
Weekers. Frank F; Van Herck. Erik E; Coopmans. Willy W; Michalaki. Marina M; Bowers. Cyril Y CY; Vel...
In a rabbit study of severe burns and prolonged critical illness, researchers used GHRP‑2 to test how the pituitary hormones GH, TSH and prolactin respond. They found that sick rabbits showed a temporary spike in GH release and an even bigger response to GHRP‑2 over time, while thyroid and prolactin hormones behaved differently. The work mainly shows how the body’s hormone system reacts to extreme stress, not how healthy people might use GHRP‑2.
Saito. Ei-suke ES; Kaiya. Hiroyuki H; Takagi. Tomo T; Yamasaki. Izumi I; Denbow. D Michael DM; Kanga...
In baby chickens, injecting GHRP‑2 (a synthetic ghrelin‑like peptide) into the brain reduced how much they ate. The same effect was seen with natural ghrelin from chickens, rats, and even bullfrogs. This shows that the chick’s appetite‑control system responds to several ghrelin‑type molecules.
Van den Berghe. G G; Wouters. P P; Weekers. F F; Mohan. S S; Baxter. R C RC; Veldhuis. J D JD; Bower...
In a small study of very sick, older patients who had been in the ICU for weeks, a 5‑day IV infusion of the peptide GHRP‑2 together with TRH re‑started the body’s natural growth‑hormone and thyroid‑hormone pulses. This led to modest rises in bone‑building and fat‑storage signals and a drop in markers of protein breakdown, without changing cortisol levels.
In very sick patients who stay in intensive care for a long time, their natural growth hormone (GH) rhythm gets messed up. Giving a drug called GHRP (or GHRP together with GHRH) can jump‑start the normal pulsing of GH, which then raises IGF‑1 and related proteins. This effect is seen in the chronic phase of critical illness, not the early stress phase.
A cancer patient treated with the immune drug nivolumab developed a rare form of adrenal failure because the pituitary gland stopped making ACTH. The problem was spotted using a hormone test that includes GHRP-2, and the brain scan looked normal, which can make diagnosis tricky.
Sheriff. Sulaiman S; Kadeer. Nijiati N; Joshi. Rashika R; Friend. Lou Ann LA; James. J Howard JH; Ba...
Although ghrelin and GHRP-2 have been shown to inhibit skeletal muscle proteolysis in rats with burn injury, the effects of des-acyl ghrelin (DAG) have not been reported. In this paper, we demonstrate that continuous 24h administration of DAG attenuated burn-induced EDL muscle proteolysis, and normalized elevated TNFα mRNA. Combined treatment of cultured C2C12 myotubes with TNFα and IFN-γ (TNF+IFN) inhibited protein synthesis and increased protein breakdown; DAG abolished both effects. PI3 kinase inhibition by LY294002 and mTOR inhibition by rapamycin blocked the reversal of the anti-anabolic effects of TNF+IFN-treated myotubes by DAG. DAG also reversed or attenuated the TNF+IFN-induced reduction in phosphorylation of Akt, FOXO1, 4E-BP-1, and GSK-3β in myotubes. Furthermore, DAG attenuated the atrophy signal, phospho-NF-κB, and the mRNA expression of MAFbx and MuRF1, upregulated by TNF+IFN in C2C12 myotubes. We conclude that DAG reduces muscle cachexia produced by injury and proinflammatory cytokines, and that DAG or DAG-based compounds may be useful in treating wasting disorders.
Ghrelin, an acylated 28-amino peptide secreted in the gastric endocrine cells, has been demonstrated to stimulate the release of growth hormone, increase food intake, and inhibit pro-inflammatory cascade, etc. Ghrelin mainly combines with its receptor (GHS-R1α) to play the role in physiological and pathological functions. It has been reported that ghrelin plays important roles in the control of pain through interaction with the opioid system in inflammatory pain and acute pain. However, very few studies show the effect of supraspinal ghrelin system on antinociception induced by intraperitoneal (i.p.) administration of morphine. In the present study, intracerebroventricular (i.c.v.) injection of ghrelin (0.1, 1, 10 and 100 nmol/L) produced inhibition of systemic morphine (6 mg/kg, i.p.) analgesia in the tail withdrawal test. Similarly, i.c.v. injection GHRP-6 and GHRP-2 which are the agonists of GHS-R1α, also decreased analgesia effect induced by morphine injected intraperitoneally in mice. Furthermore, these anti-opioid activities of ghrelin and related peptides were not blocked by pretreatment with the GHS-R1α selective antagonist [d-Lys(3)]-GHRP-6 (100 nmol/L, i.c.v.). These results demonstrated that central ghrelin and related peptides could inhibit the analgesia effect induced by intraperitoneal (i.p.) administration of morphine. The anti-opioid effects of ghrelin and related peptides do not interact with GHS-R1a. These findings may pave the way for a new strategy on investigating the interaction between ghrelin system and opioids on pain modulation.
Mechanisms by which GHRP stimulates ACTH release in corticotrope cells were investigated using mouse corticotrope AtT20 cells by focusing on the biological activity of BMP-4. GHRP-2 increased ACTH and cAMP secretion by AtT20 cells; however, its effects were less potent than the effects of CRH. BMP-4 suppressed basal ACTH production and POMC transcription, and the inhibition of endogenous BMP receptor signaling led to an increase in ACTH production. Of note, BMP-4 suppressed ACTH production and POMC-promoter activity induced by CRH more efficaciously than that induced by GHRP-2. BMP-4 had no significant effect on cAMP synthesis induced by CRH or GHRP-2. Stimulation with CRH, but not GHRP-2, activated ERK1/2, p38, SAPK/JNK and Akt phosphorylation, in which CRH-induced phosphorylation of ERK and p38 was suppressed by BMP-4. GHRP-2-induced ACTH secretion was not affected by inhibitors of ERK, p38 and Akt pathways, which effectively suppressed CRH-induced ACTH release. Blockage of the cAMP-PKA pathway reversed CRH- as well as GHRP-2-induced ACTH secretion. Furthermore, the inhibition of ERK and p38 significantly reduced cAMP synthesis induced by CRH but not by GHRP-2. Thus, CRH activates ACTH production through ERK and p38 pathways in addition to the cAMP-PKA pathway, which is also activated downstream of MAPK. On the other hand, GHRP-2-induced ACTH production was predominantly linked to the cAMP-PKA pathway. Moreover, CRH and GHRP-2 upregulated BMP receptor signaling, while BMP-4, CRH and GHRP-2 had no significant effect on the expression level of GHSR. In addition, GHRP-2 suppressed the expression of Smad7, which is an inhibitor of the BMP-Smad1/5/8 pathway. Collectively, the results revealed a functional interaction between GHRP-2 and BMP signaling, in which endogenous BMP may act as an autoregulatory system in controlling ACTH production.