ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017
Glucose elicits cephalic-phase insulin release in mice by activating K
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 66 citations in OpenAlex.
- Sweetness Perception is not Involved in the Regulation of Blood Glucose after Oral Application of Sucrose and Glucose Solutions in Healthy Male Subjects.Molecular nutrition & food research · 2021Trial
- Non-nutritive sweeteners attenuate reinforced cephalic phase insulin release and impair glucose tolerance in mice.The journal of physiological sciences : JPS · 2026Article
- 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
- Noncanonical Taste Transduction of Sugars Elicits Responses in a Dedicated Subset of Gustatory Afferent Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Sweet stimuli induce cephalic phase insulin release to varying degrees in humans.Physiology & behavior · 2026Article
- Mice Condition Cephalic Insulin Responses to the Flavor of Different Laboratory Chows.Nutrients · 2025Article
- Insular cortex predictions regulate glucose homeostasis.bioRxiv : the preprint server for biology · 2025Article
- Sugar type and route of delivery influence insulin and glucose-dependent insulinotropic polypeptide responses in rats.American journal of physiology. Endocrinology and metabolism · 2025Article
- Gustatory and olfactory-guided responsiveness to maltodextrin solutions in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
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- The peri-ovulatory time period in humans is associated with increased taste sensitivity to glucose but not calorie-free sweeteners.Chemical senses · 2025Article
- Article
- Glucose appetition in C57BL/6J mice: Influence of nonnutritive sweetener experience, food deprivation state and sex differences.Physiology & behavior · 2024Article
- 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
- Activation and inhibition of the sweet taste receptor TAS1R2-TAS1R3 differentially affect glucose tolerance in humans.PloS one · 2024Article
- TRPM4 and PLCβ3 contribute to normal behavioral responses to an array of sweeteners and carbohydrates but PLCβ3 is not needed for taste-driven licking for glucose.Chemical senses · 2024Article
- Sugar signals from oral glucose transporters elicit cephalic-phase insulin release in mice.The journal of physiological sciences : JPS · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The taste of sugar elicits cephalic-phase insulin release (CPIR), which limits the rise in blood glucose associated with meals. Little is known, however, about the gustatory mechanisms that trigger CPIR. We asked whether oral stimulation with any of the following taste stimuli elicited CPIR in mice: glucose, sucrose, maltose, fructose, Polycose, saccharin, sucralose, AceK, SC45647, or a nonmetabolizable sugar analog. The only taste stimuli that elicited CPIR were glucose and the glucose-containing saccharides (sucrose, maltose, Polycose). When we mixed an α-glucosidase inhibitor (acarbose) with the latter three saccharides, the mice no longer exhibited CPIR. This revealed that the carbohydrates were hydrolyzed in the mouth, and that the liberated glucose triggered CPIR. We also found that increasing the intensity or duration of oral glucose stimulation caused a corresponding increase in CPIR magnitude. To identify the components of the glucose-specific taste-signaling pathway, we examined the necessity of Calhm1, P2X2+P2X3, SGLT1, and Sur1. Among these proteins, only Sur1 was necessary for CPIR. Sur1 was not necessary, however, for taste-mediated attraction to sugars. Given that Sur1 is a subunit of the ATP-sensitive K
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.