Glucose elicits cephalic-phase insulin release in mice by activating KATPchannels in taste cells
| Autor: | Gabrielle S. Lubitz, John I. Glendinning, Yonina G. Frim, Anthony Sclafani, Anthony J. Basile, Ayelet Hochman |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
endocrine system medicine.medical_specialty Taste Physiology medicine.medical_treatment Administration Oral Stimulation Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine KATP Channels Physiology (medical) Internal medicine Insulin Secretion medicine Diazoxide Animals Insulin Fructose Maltose Cephalic phase Taste Buds Mice Inbred C57BL Glucose 030104 developmental biology Endocrinology chemistry Female CALHM1 Ion Channel Gating 030217 neurology & neurosurgery Research Article medicine.drug |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 312:R597-R610 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.00433.2016 |
| Popis: | 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+channel (KATP) channel and that this channel functions as a part of a glucose-sensing pathway in pancreatic β-cells, we asked whether the KATPchannel serves an analogous role in taste cells. We discovered that oral stimulation with drugs known to increase (glyburide) or decrease (diazoxide) KATPsignaling produced corresponding changes in glucose-stimulated CPIR. We propose that the KATPchannel is part of a novel signaling pathway in taste cells that mediates glucose-induced CPIR. |
| Databáze: | OpenAIRE |
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