The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
β-Cell Secretory Products Activate α-Cell ATP-Dependent Potassium Channels to Inhibit Glucagon Release
Abstract
Glucagon, secreted from islet α-cells, mobilizes liver glucose. During hyperglycemia, glucagon secretion is inhibited by paracrine factors from other islet cells, but in type 1 and type 2 diabetic patients, this suppression is lost. We investigated the effects of β-cell secretory products zinc and insulin on isolated rat α-cells, intact islets, and perfused pancreata. Islet glucagon secretion was markedly zinc sensitive (IC50 = 2.7 μmol/l) more than insulin release (IC50 = 10.7 μmol/l). Glucose, the mitochondrial substrate pyruvate, and the ATP-sensitive K+ channel (KATP channel) inhibitor tolbutamide stimulated isolated α-cell electrical activity and glucagon secretion. Zinc opened KATP channels and inhibited both electrical activity and pyruvate (but not arginine)-stimulated glucagon secretion in α-cells. Insulin tran-siently increased KATP channel activity, inhibited electrical activity and glucagon secretion in α-cells, and inhibited pancreatic glucagon output. Insulin receptor and KATP channel subunit transcripts were more abundant in α- than β-cells. Transcript for the glucagon-like peptide 1 (GLP-1) receptor was not detected in α-cells nor did GLP-1 stimulate α-cell glucagon release. β-Cell secretory products zinc and insulin therefore inhibit glucagon secretion most probably by direct activation of KATP channels, thereby masking an α-cell metabolism secretion coupling pathway similar to β-cells.
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Cites
Glucagon and regulation of glucose metabolism
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Mitochondrial glutamate acts as a messenger in glucose-induced insulin exocytosis
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Self-citationInsulin activates ATP-sensitive K+ channels in hypothalamic neurons of lean, but not obese rats
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Cited by
Glucagon-like peptide 1 (GLP-1)
Müller, T. D., Finan, B., Bloom, S. R., D'Alessio, D., Drucker, D. J., Flatt, P. R., Fritsche, A., Gribble, F., Grill, H. J., Habener, J. F., et al. (2019) · Molecular Metabolism · doi:10.1016/j.molmet.2019.09.010 · Cited by 1,868
The role of incretins in glucose homeostasis and diabetes treatment
Kim, W., & Egan, J. M. (2008) · Pharmacological Reviews · doi:10.1124/pr.108.000604 · Cited by 824
Zinc as a Gatekeeper of Immune Function
Wessels, I., Maywald, M., & Rink, L. (2017) · Nutrients · doi:10.3390/nu9121286 · Cited by 747
Physiology of Proglucagon Peptides: Role of Glucagon and GLP-1 in Health and Disease
Sandoval, D. A., & D'Alessio, D. A. (2015) · Physiological Reviews · doi:10.1152/physrev.00013.2014 · Cited by 498
The metabolic actions of glucagon revisited
Habegger, K. M., Heppner, K. M., Geary, N., Bartness, T. J., DiMarchi, R., & Tschöp, M. H. (2010) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2010.187 · Cited by 406
Metadata
- Authors
- Franklin, I., Gromada, J., Gjinovci, A., Theander, S., & Wollheim, C. B.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-06-01
- Volume
- 54
- Issue
- 6
- Pages
- 1808-1815
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2148175667
- Cited by
- 299
- References
- 52
- FWCI
- 16.47
- Type
- journal article
- Language
- en
- Open access
- closed
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- Franklin, I., Gromada, J., Gjinovci, A., Theander, S., & Wollheim, C. B. (2005). β-Cell Secretory Products Activate α-Cell ATP-Dependent Potassium Channels to Inhibit Glucagon Release. Diabetes. https://doi.org/10.2337/diabetes.54.6.1808
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