{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:21:16Z","timestamp":1784557276728,"version":"3.55.0"},"reference-count":97,"publisher":"Bioscientifica","issue":"3","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2023,6,21]]},"abstract":"<jats:p>The brain is tuned to integrate food-derived signals from the gut, allowing it to accurately adjust behavioral and physiological responses in accordance with nutrient availability. A key element of gut-to-brain communication is the relay of neural cues via peripheral sensory neurons (PSN) which harbor functionally specialized peripheral endings innervating the muscular and mucosal layers of gastrointestinal (GI) tract organs. In this review, we detail the properties of GI tract innervating PSN and describe their roles in regulating satiation and glucose metabolism in response to food consumption. We discuss the complex anatomical organization of vagal and spinal PSN subtypes, their peripheral and central projection patterns, and describe the limitations of unselective lesion and ablation approaches to investigate them. We then highlight the recent identification of molecular markers that allow selective targeting of PSN subtypes that innervate GI tract organs. This has facilitated accurately determining their projections, monitoring their responses to gut stimuli, and manipulating their activity. We contend that these recent developments have significantly improved our understanding of PSN-mediated gut-to-brain communication, which may open new therapeutic windows for the treatment of metabolic disorders, such as obesity and type 2 diabetes.<\/jats:p>","DOI":"10.1530\/joe-22-0320","type":"journal-article","created":{"date-parts":[[2023,6,22]],"date-time":"2023-06-22T01:35:49Z","timestamp":1687397749000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":7,"title":["Neural gut-to-brain communication for postprandial control of satiation and glucose metabolism"],"prefix":"10.1530","volume":"258","author":[{"given":"Leonie","family":"Cabot","sequence":"first","affiliation":[{"name":"Synaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Stra\u00dfe, Cologne, Germany"},{"name":"Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Stra\u00dfe, Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juliet","family":"Erlenbeck-Dinkelmann","sequence":"additional","affiliation":[{"name":"Synaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Stra\u00dfe, Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7136-9751","authenticated-orcid":true,"given":"Henning","family":"Fenselau","sequence":"additional","affiliation":[{"name":"Synaptic Transmission in Energy Homeostasis Group, Max Planck Institute for Metabolism Research, Gleueler Stra\u00dfe, Cologne, Germany"},{"name":"Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), University of Cologne, Joseph-Stelzmann-Stra\u00dfe, Cologne, Germany"},{"name":"Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital Cologne, Kerpener Stra\u00dfe, Cologne, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Cell Metabolism","article-title":"NTS catecholamine neurons mediate hypoglycemic hunger via medial hypothalamic feeding pathways","volume":"31","author":"Aklan","year":"2020","unstructured":"Aklan ISayar Atasoy NYavuz YAtes TCoban IKoksalar FFiliz GTopcu ICOncul MDilsiz P, 2020NTS catecholamine neurons mediate hypoglycemic hunger via medial hypothalamic feeding pathways. 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