{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,11]],"date-time":"2026-04-11T15:33:38Z","timestamp":1775921618906,"version":"3.50.1"},"reference-count":69,"publisher":"The Endocrine Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,2,1]]},"abstract":"<jats:p>Central glucagon-like-peptide-1 (GLP-1) receptor activation reduces food intake; however, brain nuclei and mechanism(s) mediating this effect remain poorly understood. Although central nervous system GLP-1 is produced almost exclusively in the nucleus of the solitary tract in the hindbrain, GLP-1 receptors (GLP-1R) are expressed throughout the brain, including nuclei in the mesolimbic reward system (MRS), e.g. the ventral tegmental area (VTA) and the nucleus accumbens (NAc). Here, we examine the MRS as a potential site of action for GLP-1-mediated control of food intake and body weight. Double immunohistochemistry for Fluorogold (monosynaptic retrograde tracer) and GLP-1 neuron immunoreactivity indicated that GLP-1-producing nucleus tractus solitarius neurons project directly to the VTA, the NAc core, and the NAc shell. Pharmacological data showed that GLP-1R activation in the VTA, NAc core, and NAc shell decreased food intake, especially of highly-palatable foods, and body weight. Moreover, blockade of endogenous GLP-1R signaling in the VTA and NAc core resulted in a significant increase in food intake, establishing a physiological relevance for GLP-1 signaling in the MRS. Current data highlight these nuclei within the MRS as novel sites for GLP-1R-mediated control of food intake and body weight.<\/jats:p>","DOI":"10.1210\/en.2011-1443","type":"journal-article","created":{"date-parts":[[2011,12,1]],"date-time":"2011-12-01T14:28:30Z","timestamp":1322749710000},"page":"647-658","source":"Crossref","is-referenced-by-count":422,"title":["GLP-1 Neurons in the Nucleus of the Solitary Tract Project Directly to the Ventral Tegmental Area and Nucleus Accumbens to Control for Food Intake"],"prefix":"10.1210","volume":"153","author":[{"given":"Amber L.","family":"Alhadeff","sequence":"first","affiliation":[{"name":"Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104"}]},{"given":"Laura E.","family":"Rupprecht","sequence":"first","affiliation":[{"name":"Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104"}]},{"given":"Matthew R.","family":"Hayes","sequence":"first","affiliation":[{"name":"Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104"}]}],"member":"80","reference":[{"key":"2020071612211041700_B1","doi-asserted-by":"crossref","first-page":"2131","DOI":"10.1053\/j.gastro.2007.03.054","article-title":"Biology of incretins: GLP-1 and GIP.","volume":"132","author":"Baggio","year":"2007","journal-title":"Gastroenterology"},{"key":"2020071612211041700_B2","doi-asserted-by":"crossref","first-page":"262","DOI":"10.1038\/nrendo.2009.48","article-title":"Incretin-based therapies for type 2 diabetes mellitus.","volume":"5","author":"Lovshin","year":"2009","journal-title":"Nat Rev Endocrinol"},{"key":"2020071612211041700_B3","doi-asserted-by":"crossref","first-page":"1409","DOI":"10.1152\/physrev.00034.2006","article-title":"The physiology of glucagon-like peptide 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