ArticleThe Journal of clinical investigation2014
Nervous glucose sensing regulates postnatal β cell proliferation and glucose homeostasis.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Brain Nutrient Sensing: A Unifying Framework.Annual review of physiology · 2026Review
- Review
- Autophagy regulator ATG5 preserves cerebellar function by safeguarding its glycolytic activity.Nature metabolism · 2025Article
- Metabolic basis of solute carrier transporters in treatment of type 2 diabetes mellitus.Acta pharmaceutica Sinica. B · 2024Review
- The role of GLUT2 in glucose metabolism in multiple organs and tissues.Molecular biology reports · 2023Review
- GLUT2 expression by glial fibrillary acidic protein-positive tanycytes is required for promoting feeding-response to fasting.Scientific reports · 2022Article
- Lipid biosynthesis enzyme Agpat5 in AgRP-neurons is required for insulin-induced hypoglycemia sensing and glucagon secretion.Nature communications · 2022Article
- Targeting Ceramides and Adiponectin Receptors in the Islet of Langerhans for Treating Diabetes.Molecules (Basel, Switzerland) · 2022Review
- MicroRNA-21 promotes pancreatic β cell function through modulating glucose uptake.Nature communications · 2022Article
- Article
- Neuronal regulation of glucagon secretion and gluconeogenesis.Journal of diabetes investigation · 2022Review
- Central Nervous System Control of Glucose Homeostasis: A Therapeutic Target for Type 2 Diabetes?Annual review of pharmacology and toxicology · 2022Review
- Fgf15 Neurons of the Dorsomedial Hypothalamus Control Glucagon Secretion and Hepatic Gluconeogenesis.Diabetes · 2021Article
- A Review of Current Trends with Type 2 Diabetes Epidemiology, Aetiology, Pathogenesis, Treatments and Future Perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Article
- EphrinB1 modulates glutamatergic inputs into POMC-expressing progenitors and controls glucose homeostasis.PLoS biology · 2020Article
- CNS control of the endocrine pancreas.Diabetologia · 2020Review
- Fanconi-Bickel Syndrome: A Review of the Mechanisms That Lead to Dysglycaemia.International journal of molecular sciences · 2020Review
- Brain substrate metabolism and ß-cell function in humans: A positron emission tomography study.Endocrinology, diabetes & metabolism · 2020Article
- Klf6 protects β-cells against insulin resistance-induced dedifferentiation.Molecular metabolism · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
How glucose sensing by the nervous system impacts the regulation of β cell mass and function during postnatal development and throughout adulthood is incompletely understood. Here, we studied mice with inactivation of glucose transporter 2 (Glut2) in the nervous system (NG2KO mice). These mice displayed normal energy homeostasis but developed late-onset glucose intolerance due to reduced insulin secretion, which was precipitated by high-fat diet feeding. The β cell mass of adult NG2KO mice was reduced compared with that of WT mice due to lower β cell proliferation rates in NG2KO mice during the early postnatal period. The difference in proliferation between NG2KO and control islets was abolished by ganglionic blockade or by weaning the mice on a carbohydrate-free diet. In adult NG2KO mice, first-phase insulin secretion was lost, and these glucose-intolerant mice developed impaired glucagon secretion when fed a high-fat diet. Electrophysiological recordings showed reduced parasympathetic nerve activity in the basal state and no stimulation by glucose. Furthermore, sympathetic activity was also insensitive to glucose. Collectively, our data show that GLUT2-dependent control of parasympathetic activity defines a nervous system/endocrine pancreas axis that is critical for β cell mass establishment in the postnatal period and for long-term maintenance of β cell function.
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