Disease relevance of Pyr-his-gly

• Action of anorexigenic peptide injected into the brain: dissociation of effect on body weight and feeding in the rat [1].
• A newly described tripeptide, pyro-Glu-His-Gly-OH, which was reported to produce profound and long-term anorexia and weight loss in female mice, was initially tested in female rats [2].
• The effects of tripeptide colon mitosis inhibitor (CMI, pGlu-His-Gly-OH) on the proliferation of tumoral cells of dimethylhydrazine (DMH)-induced colonic cancers in rats were studied [3].

Psychiatry related information on Pyr-his-gly

• Thyrotropin releasing hormone (TRH), distributed throughout the gastrointestinal tract, and anorexigenic peptide (AP), isolated recently from the urine of females with "hypothalamic" anorexia nervosa, have been shown to affect food intake but no study has been performed to compare their action on gastrointestinal secretions [4].

High impact information on Pyr-his-gly

• Cocaine- and amphetamine-regulated transcript (CART) is an anorexigenic peptide widely expressed in the central, peripheral, and enteric nervous systems [5].
• However, when phosphohistidines of the phosphorylated synthetic peptide pGlu-His-Gly were taken as references, the NDP kinase and the N delta peptide phosphohistidine signals were shown to be identical, providing evidence that phosphorylation occurs on the N delta of the active site histidine residue [6].
• In the present study, it was demonstrated in two different experiments that i.p. injections of CMI, daily or 3 times a week, could inhibit the long-term s.c. growth of HT-29 cells in athymic mice [7].
• Neuromedin U (NMU), an anorexigenic peptide, was originally isolated from porcine spinal cord in 1985 [8].
• The cocaine and amphetamine regulated transcript (CART), an anorexigenic peptide responding to leptin, is expressed in various areas of the hypothalamus [9].

Biological context of Pyr-his-gly

• Previous reports on the effect of anorexigenic peptide (AXP) administered systemically in the rodent are inconsistent in terms of the effect of the tri-peptide on food intake and body weight [1].
• The aim of this study was to investigate the effect of TRH and its analogues (pGlu-HIs-Gly, pGlu-His-Gly-NH2) on cell proliferation in the intermediate pituitary lobe [10].
• The aim of this study was to investigate the relationship between the anorexigenic action of PACAP and that of corticotropin-releasing hormone (CRH), which is implicated in the regulation of energy homeostasis as a powerful anorexigenic peptide in the goldfish brain [11].
• Early oncogene mRNA expression in HT-29 cells treated with the endogenous colon mitosis inhibitor pyroglutamyl-histidyl-glycine [12].
• BACKGROUND: The colon mitosis inhibiting peptide pyroglutamyl-histidyl-glycine (pEHG) increases the expression of c-fos, fosB and egr-1 genes in the colon carcinoma cell line HT-29 [13].

Anatomical context of Pyr-his-gly

• OBJECTIVE: Leptin, the ob gene product, is an anorexigenic peptide secreted from adipose tissue [14].
• Cocaine- and amphetamine regulated transcript (CART) is a recently discovered anorexigenic peptide, widely expressed in the central nervous system [15].
• The CART-IR innervation of TRH neurons originates from at least two major sources: CART neurons in the arcuate nucleus that co-express the anorexigenic peptide, alpha-melanocyte-stimulating hormone (alpha-MSH), and adrenergic CART neurons in the medulla [15].
• The colon mitosis inhibitor pyroglutamyl-histidyl-glycine inhibits growth of non-tumorigenic colonic epithelial cells [13].
• An essentially similar pattern of results was obtained with chronic infusion into the third ventricle of the anorexigenic peptide alpha-melanocyte-stimulating hormone (alpha-MSH, 1 microg/h), in nonlactating and lactating rats [16].

Associations of Pyr-his-gly with other chemical compounds

• The effects of thyrotropin releasing hormone (TRH) and of TRH-like tripeptide pGlu-His-Gly-OH (colon mitosis inhibitor, CMI) on spontaneous proliferation of murine splenocytes were investigated in vitro [17].
• An endogenous colon mitosis inhibitor and dietary calcium inhibit the increased colonic cell proliferation induced by cholic acid [18].
• Pyroglutamyl-histidyl-glycine, the endogenous colon mitosis inhibitor, regulates cyclic AMP level in non-tumorigenic colonic epithelial cells [19].
• In vivo growth inhibition of human colon carcinoma cells (HT-29) by all-trans-retinoic acid, difluoromethylornithine, and colon mitosis inhibitor, individually and in combination [20].
• The effects of colon mitosis inhibitor (CMI), thyroliberin (TRH), and the somatostatin analogue octreotide (SMS 201-995) on rat colonic mucosal epithelial cell proliferation were studied [21].

Gene context of Pyr-his-gly

• In conclusion, the anorexigenic peptide PYY(3-36) may participate in the control of PRL secretion in the prepubertal rat, acting at pituitary (stimulatory effect) and extra-pituitary (likely inhibitory action at the hypothalamus) sites of the lactotrope axis [22].
• These findings support the hypothesized role of NmU as an endogenous anorexigenic peptide [23].
• Concomitantly, the expression of genes encoding the anorexigenic peptide, alpha-melanocyte stimulating hormone and cocaine-and-amphetamine regulatory transcript, was augmented with the latter gene displaying a dose-dependant response [24].
• These results indicated that SP may function as an endogenous anorexigenic peptide [25].
• These results indicate that NPFF may function as an endogenous anorexigenic peptide with anitiopioid function [26].

Analytical, diagnostic and therapeutic context of Pyr-his-gly

• CONCLUSIONS: The great postoperative increase in the levels of the anorexigenic peptide PYY following BPD-RYGBP may contribute to the reduced appetite observed after this type of bariatric surgery [27].
• We have previously reported that a single intraperitoneal injection of the tripeptide pGlu-His-GlyOH (colon mitosis inhibitor (CMI] is followed by a transient reduction of cell proliferation in the colonic epithelium in mice [18].
• 1. Single subcutaneous injections (0.5-10 mg/kg) or repeated oral administration (5 mg/kg, twice daily for 3 or 5 days) of the proposed anorexigenic peptide pyro-GLU-HIS-GLY-OH did not affect food intake in the mouse [28].
• Enterostatin (VPDPR), an anorexigenic peptide derived from the amino terminus of procolipase, significantly inhibited analgesia induced by the mu-opioid agonist morphine (5 mg/kg, s.c.) after i.c.v. administration to mice at a dose of 100 nmol [29].
• 2. Single intravenous injections (0.05-1 mg/kg) or daily intravenous injections (0.3-10 mg/kg, for 5 days) of pyro-GLU-HIS-GLY-OH did not affect food intake in the rat [28].

References