{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tahiri A"],"funding":["National Institute of Neurological Disorders and Stroke","Japan IDDM Network","National Institute of Diabetes and Digestive and Kidney Diseases","NIMH NIH HHS","National Center for Complementary and Integrative Health","Ministry of Education, Culture, Sports, Science and Technology","National Institute of Diabetes and Digestive and Kidney Diseases Division of Diabetes Endocrinology and Metabolic Diseases","NCCIH NIH HHS","NIDDK NIH HHS","NINDS NIH HHS","National Institute of Mental Health","New York Medical College","Human Islet Research Network","Japan Science and Technology Agency","New Jersey Council on Developmental Disabilities","Robert Wood Johnson Foundation"],"pagination":["51-61.e4"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11706709"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["60(1)"],"pubmed_abstract":["Vagal nerve stimulation has emerged as a promising modality for treating a wide range of chronic conditions, including metabolic disorders. However, the cellular and molecular pathways driving these clinical benefits remain largely obscure. Here, we demonstrate that fibroblast growth factor 3 (Fgf3) mRNA is upregulated in the mouse vagal ganglia under acute metabolic stress. Systemic and vagal sensory overexpression of Fgf3 enhanced glucose-stimulated insulin secretion (GSIS), improved glucose excursion, and increased energy expenditure and physical activity. Fgf3-elicited insulinotropic and glucose-lowering responses were recapitulated when overexpression of Fgf3 was restricted to the pancreas-projecting vagal sensory neurons. Genetic ablation of Fgf3 in pancreatic vagal afferents exacerbated high-fat diet-induced glucose intolerance and blunted GSIS. Finally, electrostimulation of the vagal afferents enhanced GSIS and glucose clearance independently of efferent outputs. Collectively, we demonstrate a direct role for the vagal afferent signaling in GSIS and identify Fgf3 as a vagal sensory-derived metabolic factor that controls pancreatic β-cell activity."],"journal":["Developmental cell"],"pubmed_title":["Vagal sensory neuron-derived FGF3 controls insulin secretion."],"pmcid":["PMC11706709"],"funding_grant_id":["R01DK122167","R15 NS130456","R01 DK122167","74260","UC4 DK104162","U24 DK104162","CAUT24DFP","23H03324","R21 AT011387","R15NS130456","RF1 MH120144","R01 DK131452","U01 DK104162"],"pubmed_authors":["Moon S","Zhao JY","Inoue R","Youssef A","Wang L","Kwon H","El Ouaamari A","Ulloa L","Tahiri A","Berroug L","Nguyen XTA","Shirakawa J","Alsarkhi L","Pang ZP"],"additional_accession":[]},"is_claimable":false,"name":"Vagal sensory neuron-derived FGF3 controls insulin secretion.","description":"Vagal nerve stimulation has emerged as a promising modality for treating a wide range of chronic conditions, including metabolic disorders. However, the cellular and molecular pathways driving these clinical benefits remain largely obscure. Here, we demonstrate that fibroblast growth factor 3 (Fgf3) mRNA is upregulated in the mouse vagal ganglia under acute metabolic stress. Systemic and vagal sensory overexpression of Fgf3 enhanced glucose-stimulated insulin secretion (GSIS), improved glucose excursion, and increased energy expenditure and physical activity. Fgf3-elicited insulinotropic and glucose-lowering responses were recapitulated when overexpression of Fgf3 was restricted to the pancreas-projecting vagal sensory neurons. Genetic ablation of Fgf3 in pancreatic vagal afferents exacerbated high-fat diet-induced glucose intolerance and blunted GSIS. Finally, electrostimulation of the vagal afferents enhanced GSIS and glucose clearance independently of efferent outputs. Collectively, we demonstrate a direct role for the vagal afferent signaling in GSIS and identify Fgf3 as a vagal sensory-derived metabolic factor that controls pancreatic β-cell activity.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2026-06-06T20:04:11.161Z","creation":"2026-06-04T03:14:56.009Z"},"accession":"S-EPMC11706709","cross_references":{"pubmed":["39413782"],"doi":["10.1016/j.devcel.2024.09.016"]}}