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Ghsr  -  growth hormone secretagogue receptor

Mus musculus

Synonyms: C530020I22Rik, GH-releasing peptide receptor, GHRP, GHS-R, Ghrelin receptor, ...
 
 
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Disease relevance of Ghsr

  • However, recent studies by Wortley et al. and Zigman et al. demonstrate that Ghrl-/- and Ghsr-/- mice are resistant to diet-induced obesity when fed a high-fat diet during the early post-weaning period [1].
  • Serum insulin-like growth factor 1 levels and body weights of mature Ghsr-null mice are modestly reduced compared to wild-type littermates, which is consistent with ghrelin's property as an amplifier of GH pulsatility and its speculated role in establishing an insulin-like growth factor 1 set-point for maintaining anabolic metabolism [2].
  • Ghrelin receptor agonists offer a treatment option for syndromes like anorexia nervosa, cancer cachexia, or AIDS wasting [3].
  • We devised a method to selectively ablate these neurons in neonatal mice and then tested adult mice for their feeding responses to fasting, mild hypoglycemia, 2-deoxy-d-glucose and a ghrelin receptor agonist [4].
 

Psychiatry related information on Ghsr

 

High impact information on Ghsr

 

Biological context of Ghsr

  • These metabolic effects are unlikely to be mediated by the GHS receptor [8].
  • Our results indicate that MCG 101-bearing mice became ghrelin resistant despite upregulation of hypothalamic GHS-R expression, which confirms similar indirect observations in cancer patients [9].
  • We found that [Trp3, Arg5]-ghrelin(1-5) (GSWFR), a novel pentapeptide composed of all L-amino acids, had affinity for the GHS receptor (IC50 = 10 microM) [10].
  • Our results demonstrate that ghrelin inhibits adipogenesis by stimulation of cell proliferation via the mediation of a ghrelin receptor, likely a novel unidentified subtype [11].
  • Peptide and non-peptide GHS-R agonists accelerate gastric emptying of solids in an equipotent manner through activation of GHS receptors, possibly located on local cholinergic enteric nerves [12].
 

Anatomical context of Ghsr

 

Associations of Ghsr with chemical compounds

 

Physical interactions of Ghsr

 

Regulatory relationships of Ghsr

 

Other interactions of Ghsr

  • In addition, treating primary pituitary cell cultures from lean mice with insulin reduced GH release as well as GH, GHRH receptor, and ghrelin receptor mRNA levels compared with vehicle-treated controls, where the magnitude of suppression of pituitary mRNA levels was similar to that observed in the DIO mouse [20].
  • Repeated administration of GHS-R antagonist was continued for six days in ob/ob obese mice [19].
  • These observations demonstrate that NPY is not required for basal regulation of the GH axis, but is required for fasting-induced suppression of GHRH and SRIH expression, as well as fasting-induced augmentation of pituitary GHS-R mRNA [21].
  • These changes were associated with increases in pituitary expression of GHRH-R and GHS-R and a concomitant suppression of sst2 [21].
  • The results showed that ArKO/OVX mice have a low expression of pituitary GH, GHRH-R, GHS-R and Pit-1, and significantly reduced GH levels [22].
 

Analytical, diagnostic and therapeutic context of Ghsr

  • To identify neurons that express the ghrelin receptor [GH secretagogue receptor (GHS-R)], we generated GHS-R-IRES-tauGFP mice by gene targeting [7].
  • Immunohistochemical staining and Western blot analyses were used to identify GHS-R expression in the brain as well as its relationship to NPY expression in hypothalamic neurons [9].

References

  1. Is ghrelin a signal for the development of metabolic systems? Grove, K.L., Cowley, M.A. J. Clin. Invest. (2005) [Pubmed]
  2. Ghrelin stimulation of growth hormone release and appetite is mediated through the growth hormone secretagogue receptor. Sun, Y., Wang, P., Zheng, H., Smith, R.G. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  3. GH-releasing peptide-2 increases fat mass in mice lacking NPY: indication for a crucial mediating role of hypothalamic agouti-related protein. Tschöp, M., Statnick, M.A., Suter, T.M., Heiman, M.L. Endocrinology (2002) [Pubmed]
  4. NPY/AgRP neurons are not essential for feeding responses to glucoprivation. Luquet, S., Phillips, C.T., Palmiter, R.D. Peptides (2007) [Pubmed]
  5. Mice lacking ghrelin receptors resist the development of diet-induced obesity. Zigman, J.M., Nakano, Y., Coppari, R., Balthasar, N., Marcus, J.N., Lee, C.E., Jones, J.E., Deysher, A.E., Waxman, A.R., White, R.D., Williams, T.D., Lachey, J.L., Seeley, R.J., Lowell, B.B., Elmquist, J.K. J. Clin. Invest. (2005) [Pubmed]
  6. Estradiol-dependent decrease in the orexigenic potency of ghrelin in female rats. Clegg, D.J., Brown, L.M., Zigman, J.M., Kemp, C.J., Strader, A.D., Benoit, S.C., Woods, S.C., Mangiaracina, M., Geary, N. Diabetes (2007) [Pubmed]
  7. Ghrelin amplifies dopamine signaling by cross talk involving formation of growth hormone secretagogue receptor/dopamine receptor subtype 1 heterodimers. Jiang, H., Betancourt, L., Smith, R.G. Mol. Endocrinol. (2006) [Pubmed]
  8. Ghrelin differentially affects hepatic and peripheral insulin sensitivity in mice. Heijboer, A.C., van den Hoek, A.M., Parlevliet, E.T., Havekes, L.M., Romijn, J.A., Pijl, H., Corssmit, E.P. Diabetologia (2006) [Pubmed]
  9. Effects of ghrelin on anorexia in tumor-bearing mice with eicosanoid-related cachexia. Wang, W., Andersson, M., Iresjö, B.M., Lönnroth, C., Lundholm, K. Int. J. Oncol. (2006) [Pubmed]
  10. [Trp3, Arg5]-ghrelin(1-5) stimulates growth hormone secretion and food intake via growth hormone secretagogue (GHS) receptor. Ohinata, K., Kobayashi, K., Yoshikawa, M. Peptides (2006) [Pubmed]
  11. Inhibition of adipogenesis by ghrelin. Zhang, W., Zhao, L., Lin, T.R., Chai, B., Fan, Y., Gantz, I., Mulholland, M.W. Mol. Biol. Cell (2004) [Pubmed]
  12. Gastric motor effects of peptide and non-peptide ghrelin agonists in mice in vivo and in vitro. Kitazawa, T., De Smet, B., Verbeke, K., Depoortere, I., Peeters, T.L. Gut (2005) [Pubmed]
  13. Peripheral ghrelin deepens torpor bouts in mice through the arcuate nucleus neuropeptide Y signaling pathway. Gluck, E.F., Stephens, N., Swoap, S.J. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2006) [Pubmed]
  14. IA-2beta, but not IA-2, is induced by ghrelin and inhibits glucose-stimulated insulin secretion. Doi, A., Shono, T., Nishi, M., Furuta, H., Sasaki, H., Nanjo, K. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  15. The mitogenic and antiapoptotic actions of ghrelin in 3T3-L1 adipocytes. Kim, M.S., Yoon, C.Y., Jang, P.G., Park, Y.J., Shin, C.S., Park, H.S., Ryu, J.W., Pak, Y.K., Park, J.Y., Lee, K.U., Kim, S.Y., Lee, H.K., Kim, Y.B., Park, K.S. Mol. Endocrinol. (2004) [Pubmed]
  16. Ghrelin inhibits the development of mouse preimplantation embryos in vitro. Kawamura, K., Sato, N., Fukuda, J., Kodama, H., Kumagai, J., Tanikawa, H., Nakamura, A., Honda, Y., Sato, T., Tanaka, T. Endocrinology (2003) [Pubmed]
  17. Discovery and pharmacological evaluation of growth hormone secretagogue receptor antagonists. Xin, Z., Serby, M.D., Zhao, H., Kosogof, C., Szczepankiewicz, B.G., Liu, M., Liu, B., Hutchins, C.W., Sarris, K.A., Hoff, E.D., Falls, H.D., Lin, C.W., Ogiela, C.A., Collins, C.A., Brune, M.E., Bush, E.N., Droz, B.A., Fey, T.A., Knourek-Segel, V.E., Shapiro, R., Jacobson, P.B., Beno, D.W., Turner, T.M., Sham, H.L., Liu, G. J. Med. Chem. (2006) [Pubmed]
  18. Upregulation of Ghrelin expression in the stomach upon fasting, insulin-induced hypoglycemia, and leptin administration. Toshinai, K., Mondal, M.S., Nakazato, M., Date, Y., Murakami, N., Kojima, M., Kangawa, K., Matsukura, S. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
  19. Antagonism of ghrelin receptor reduces food intake and body weight gain in mice. Asakawa, A., Inui, A., Kaga, T., Katsuura, G., Fujimiya, M., Fujino, M.A., Kasuga, M. Gut (2003) [Pubmed]
  20. Impact of obesity on the growth hormone axis: evidence for a direct inhibitory effect of hyperinsulinemia on pituitary function. Luque, R.M., Kineman, R.D. Endocrinology (2006) [Pubmed]
  21. Expression analysis of hypothalamic and pituitary components of the growth hormone axis in fasted and streptozotocin-treated neuropeptide Y (NPY)-intact (NPY+/+) and NPY-knockout (NPY-/-) mice. Park, S., Peng, X.D., Frohman, L.A., Kineman, R.D. Neuroendocrinology (2005) [Pubmed]
  22. Oestrogen replacement in vivo rescues the dysfunction of pituitary somatotropes in ovariectomised aromatase knockout mice. Yan, M., Jones, M.E., Hernandez, M., Liu, D., Simpson, E.R., Chen, C. Neuroendocrinology (2005) [Pubmed]
 
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