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We hypothesized that if ghrelin acts as a survival signal, enhancing the responsivity of the\n                    <jats:italic>GH secretagogue receptor<\/jats:italic>\n                    (GHSR) should favor GHSR protective responses. To test this, we used rats with genetically enhanced GHSR sensitivity (\n                    <jats:italic>Ghsr<\/jats:italic>\n                    <jats:sup>Q343X<\/jats:sup>\n                    ) and wild\u2010type littermate controls and examined their acute responses to pharmacological challenges. Consistent with our hypothesis,\n                    <jats:italic>Ghsr<\/jats:italic>\n                    <jats:sup>Q343X<\/jats:sup>\n                    rats, despite normal glucose and insulin tolerance, exhibited a significant increase in blood glucose in response to GHSR agonism, accompanied by elevated counter\u2010regulatory hormones including corticosterone. Concurrently, these rats displayed a notable decrease in locomotor activity and delayed feeding response. Also, GHSR agonism partially altered the cocaine\u2010induced hyperlocomotion of\n                    <jats:italic>Ghsr<\/jats:italic>\n                    <jats:sup>Q343X<\/jats:sup>\n                    rats while they showed unaltered locomotor sensitization to cocaine. At the cellular level, functional studies indicated that the\n                    <jats:italic>Ghsr<\/jats:italic>\n                    <jats:sup>Q343X<\/jats:sup>\n                    mutation prolongs ghrelin\u2010induced GHSR\u2010G protein canonical signaling. Altogether, in a model of increased GHSR sensitivity, GHSR agonist stimulation was sufficient to promote a robust blood glucose increase, while the acute feeding response was delayed in a context of unexpected hypolocomotor response. This mechanism may have implications for severe states of undernutrition such as restrictive anorexia nervosa.\n                  <\/jats:p>","DOI":"10.1111\/jne.70143","type":"journal-article","created":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T07:10:46Z","timestamp":1771053046000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>GHSR<\/scp>\n                    agonism increases blood glucose but delays food intake in\n                    <scp>GHSR<\/scp>\n                    hyperresponsive rats"],"prefix":"10.1111","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8838-0762","authenticated-orcid":false,"given":"Philippe","family":"Zizzari","sequence":"first","affiliation":[{"name":"Universit\u00e9 de Bordeaux, INSERM, Neurocentre Magendie  Bordeaux 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