{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T08:06:40Z","timestamp":1791274000222,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2011,10,12]],"date-time":"2011-10-12T00:00:00Z","timestamp":1318377600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2011,12]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    Aging is associated with increased adiposity in white adipose tissues and impaired thermogenesis in brown adipose tissues; both contribute to increased incidences of obesity and type 2 diabetes. Ghrelin is the only known circulating orexigenic hormone that promotes adiposity. In this study, we show that ablation of the ghrelin receptor (growth hormone secretagogue receptor, GHS\u2010R) improves insulin sensitivity during aging. Compared to wild\u2010type (WT) mice, old\n                    <jats:italic>Ghsr<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice have reduced fat and preserve a healthier lipid profile. Old\n                    <jats:italic>Ghsr<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice also exhibit elevated energy expenditure and resting metabolic rate, yet have similar food intake and locomotor activity. While GHS\u2010R expression in white and brown adipose tissues was below the detectable level in the young mice, GHS\u2010R expression was readily detectable in visceral white fat and interscapular brown fat of the old mice. Gene expression profiles reveal that\n                    <jats:italic>Ghsr<\/jats:italic>\n                    ablation reduced glucose\/lipid uptake and lipogenesis in white adipose tissues but increased thermogenic capacity in brown adipose tissues.\n                    <jats:italic>Ghsr<\/jats:italic>\n                    ablation prevents age\u2010associated decline in thermogenic gene expression of uncoupling protein 1 (UCP1). Cell culture studies in brown adipocytes further demonstrate that ghrelin suppresses the expression of adipogenic and thermogenic genes, while GHS\u2010R antagonist abolishes ghrelin\u2019s effects and increases UCP1 expression. Hence, GHS\u2010R plays an important role in thermogenic impairment during aging.\n                    <jats:italic>Ghsr<\/jats:italic>\n                    ablation improves aging\u2010associated obesity and insulin resistance by reducing adiposity and increasing thermogenesis. Growth hormone secretagogue receptor antagonists may be a new means of combating obesity by shifting the energy balance from obesogenesis to thermogenesis.\n                  <\/jats:p>","DOI":"10.1111\/j.1474-9726.2011.00740.x","type":"journal-article","created":{"date-parts":[[2011,9,5]],"date-time":"2011-09-05T13:28:33Z","timestamp":1315229313000},"page":"996-1010","source":"Crossref","is-referenced-by-count":160,"title":["Ablation of ghrelin receptor reduces adiposity and improves insulin sensitivity during aging by regulating fat metabolism in white and brown adipose tissues"],"prefix":"10.1111","volume":"10","author":[{"given":"Ligen","family":"Lin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pradip K.","family":"Saha","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaojun","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iyabo O.","family":"Henshaw","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Longjiang","family":"Shao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benny H. 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