| http://purl.uniprot.org/citations/15070777 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15070777 | http://www.w3.org/2000/01/rdf-schema#comment | "Synthetic agonists of the growth hormone secretagogue receptor (GHSR) rejuvenate the pulsatile pattern of GH-release in the elderly, and increase lean but not fat mass in obese subjects. Screening of tissue extracts in a cell line engineered to overexpress the GHSR led to the identification of a natural agonist called ghrelin. Paradoxically, this hormone was linked to obesity. However, it had not been directly shown that the GHSR is a physiologically relevant ghrelin receptor. Furthermore, ghrelin's structure is significantly different from the synthetic agonist (MK-0677) used to expression-clone the GHSR. To address whether the GHSR mediates ghrelin's stimulatory effects on GH release and appetite, we generated Ghsr-null mice. In contrast to wild-type mice, acute treatment of Ghsr-null mice with ghrelin stimulated neither GH release nor food intake, showing that the GHSR is a biologically relevant ghrelin receptor. Nevertheless, Ghsr-null mice are not dwarfs; their appetite and body composition are comparable to that of wild-type littermates. Furthermore, in contrast to suggestions that ghrelin regulates leptin and insulin secretion, fasting-induced changes in serum levels of leptin and insulin are identical in wild-type and null mice. 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. Our results suggest that chronic treatment with ghrelin antagonists will have little effect on growth or appetite."xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.org/dc/terms/identifier | "doi:10.1073/pnas.0305930101"xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/author | "Sun Y."xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/author | "Wang P."xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/author | "Zheng H."xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/author | "Smith R.G."xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/name | "Proc Natl Acad Sci U S A"xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/pages | "4679-4684"xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/title | "Ghrelin stimulation of growth hormone release and appetite is mediated through the growth hormone secretagogue receptor."xsd:string |
| http://purl.uniprot.org/citations/15070777 | http://purl.uniprot.org/core/volume | "101"xsd:string |
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