ArticleThe journal of physiological sciences : JPS2023
Sugar signals from oral glucose transporters elicit cephalic-phase insulin release in mice.
Article in The journal of physiological sciences : JPS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The substitute ENSO 16 has low impact on glucose metabolism in healthy humans: a randomized, double-blind, active-controlled, cross-over trial.Scientific reports · 2024Trial
- Pharmaceutical agents targeting KThe journal of physiological sciences : JPS · 2026Article
- Cellular coding of ingestion in the caudal brainstem.bioRxiv : the preprint server for biology · 2026Article
- Sugar type and route of delivery influence insulin and glucose-dependent insulinotropic polypeptide responses in rats.American journal of physiology. Endocrinology and metabolism · 2025Article
- Mice Condition Cephalic-Phase Insulin Release to Flavors Associated with Postoral Actions of Concentrated Glucose.Nutrients · 2024Article
- Mechanisms and Functions of Sweet Reception in Oral and Extraoral Organs.International journal of molecular sciences · 2024Review
- Addition of low sodium does not increase sensitivity to glucose in wild-type mice, or lead to partial glucose taste detection in T1R3 knock-out mice.Physiology & behavior · 2024Article
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6 authors.
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Abstract
Cephalic-phase insulin release (CPIR) occurs before blood glucose increases after a meal. Although glucose is the most plausible cue to induce CPIR, peripheral sensory systems involved are not fully elucidated. We therefore examined roles of sweet sensing by a T1R3-dependent taste receptor and sugar sensing by oral glucose transporters in the oropharyngeal region in inducing CPIR. Spontaneous oral ingestion of glucose significantly increased plasma insulin 5 min later in wild-type (C57BL/6) and T1R3-knockout mice, but intragastric infusion did not. Oral treatment of glucose transporter inhibitors phlorizin and phloretin significantly reduced CPIR after spontaneous oral ingestion. In addition, a rapid increase in plasma insulin was significantly smaller in WT mice with spontaneous oral ingestion of nonmetabolizable glucose analog than in WT mice with spontaneous oral ingestion of glucose. Taken together, the T1R3-dependent receptor is not required for CPIR, but oral glucose transporters greatly contribute to induction of CPIR by sugars.
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