{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T13:49:01Z","timestamp":1793627341995,"version":"4.5.1"},"reference-count":30,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T00:00:00Z","timestamp":1783468800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T00:00:00Z","timestamp":1783468800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl J Eating Disorders"],"published-print":{"date-parts":[[2026,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Glucagon\u2010like peptide\u20101 receptor (GLP\u20101R) agonists reduce food intake and body weight, suggesting they should be avoided in anorexia nervosa. However, preclinical evidence that these drugs reduce activity and reward\u2010seeking behavior raises the possibility that they might attenuate the compulsive\u2010like hyperactivity central to ABA pathology and slow weight loss. Here, we employed a widely used rodent model of AN (activity\u2010based anorexia, ABA) to determine whether a GLP\u20101R agonist would worsen or rather lessen weight loss and hyperactivity.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>\n                      Female mice that had continuous access to a running wheel and time\u2010restricted food availability received systemic administration of a GLP\u20101R agonist, a GLP\u20101R antagonist, or vehicle once daily before food presentation (\n                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u200910\/group).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>GLP\u20101R agonist treatment exacerbated ABA\u2010associated weight loss, confirming the concern that appetite suppression would worsen outcomes and failing to support the possibility that reduced compulsive\u2010like activity might provide benefit. This effect was driven by a further suppression of food intake, while wheel running remained unchanged. Pharmacological blockade of GLP\u20101R signaling had no detectable effect on any parameter monitored relative to vehicle controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These findings provide the first experimental evidence that GLP\u20101R agonism worsens outcomes in an animal model of anorexia nervosa. The lack of effect of GLP\u20101R antagonism suggests endogenous GLP\u20101 signaling does not substantially contribute to ABA pathology. Together, these data raise caution regarding the use of GLP\u20101R agonists in individuals vulnerable to restrictive eating as they are unlikely to reduce the motivation for excessive activity and can further reduce food intake.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/eat.70169","type":"journal-article","created":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T03:52:27Z","timestamp":1783569147000},"page":"2549-2554","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>GLP<\/scp>\n                    \u20101 Receptor Agonism Exacerbates Activity\u2010Based Anorexia in Mice"],"prefix":"10.1002","volume":"59","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8852-7389","authenticated-orcid":false,"given":"Amit","family":"Thakar","sequence":"first","affiliation":[{"name":"Department of Integrative Physiology and Neuroscience Washington State University  Pullman Washington 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