ATP-sensitive K+ channels: a link between B-cell metabolism and insulin secretion
Abstract
Conference Article| February 01 1990 ATP-sensitive K+ channels: a link between B-cell metabolism and insulin secretion FRANCES M. ASHCROFT; FRANCES M. ASHCROFT 1University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, U.K. Search for other works by this author on: This Site PubMed Google Scholar PATRIK RORSMAN PATRIK RORSMAN * 1University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1990) 18 (1): 109–111. https://doi.org/10.1042/bst0180109 Article history Received: July 24 1989 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation FRANCES M. ASHCROFT, PATRIK RORSMAN; ATP-sensitive K+ channels: a link between B-cell metabolism and insulin secretion. Biochem Soc Trans 1 February 1990; 18 (1): 109–111. doi: https://doi.org/10.1042/bst0180109 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search Keywords: KATP channel, ATP-sensitive K+channel, PKC, protein kinase C, PMA, phorbol 12-myristate 13-acetate This content is only available as a PDF. © 1990 Biochemical Society1990 Article PDF first page preview Close Modal You do not currently have access to this content.
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The KATP channel has a central function in glucose-stimulated insulin release, transducing an increase in ATP into depolarisation with voltage-dependent influx of Ca2+.
“The K ATP channel has a central function in glucosestimulated insulin release, transducing an increase in ATP into depolarisation with voltage-dependent influx of Ca 2+ [37].”
From Glucose inhibits glucagon secretion by a direct effect on mouse pancreatic alpha cells (2007) · cites this paper as [37]
Initiation of insulin secretion is generally attributed to depolarization with increase of [Ca2+]i after closure of KATP channels.
“Initiation of secretion is generally attributed to depolarization with increase of [Ca 2ϩ ] i after closure of K ATP channels (19).”
From Paradoxical Stimulation of Glucagon Secretion by High Glucose Concentrations (2006) · cites this paper as [19]
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“Indeed, closure of KATP is a crucial step in glucose-stimulated insulin secretion fromβ−cells (Ashcroft and Rorsman 1990).”
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“Over the years, the glucose-stimulated insulin secretion (GSIS) has been extensively studied, and its mechanism is well documented [3,4].”
BackgroundA key role for phosphorylated inositol compounds in pancreatic β-cell stimulus–secretion coupling
Berggren, P., & Barker, C. J. (2008) · Advances in Enzyme Regulation · doi:10.1016/j.advenzreg.2007.11.012 · Cited by 20 · see citing works
Nyblom, H. K., Nord, L. I., Andersson, R., Kenne, L., & Bergsten, P. (2007) · NMR in Biomedicine · doi:10.1002/nbm.1197 · Cited by 20 · see citing works
Grøndahl, M. F. G., Keating, D. J., Vilsbøll, T., & Knop, F. K. (2017) · Current Diabetes Reports · doi:10.1007/s11892-017-0967-z · Cited by 21 · see citing works
Sexual hormones and diabetes: The impact of estradiol in pancreatic β cell
Merino, B., & García‐Arévalo, M. (2021) · International review of cytology · doi:10.1016/bs.ircmb.2021.02.004 · Cited by 19 · see citing works
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“…pairs Glucose-stimulated insulin secretion from the pancreatic β cell is dependent upon the ability of the KATP channel to alter the voltage polarization of the cell membrane (Ashcroft and Rorsman, 1990), and mutations in KCNJ11 have been reported to cause pediatric diabetes (Ioannou et al., 2011).”
BackgroundTentonin 3/TMEM150C regulates glucose-stimulated insulin secretion in pancreatic β-cells.
Wee, J., Pak, S., Kim, T., Hong, G., Lee, J.-S., Nan, J., Kim, H., Lee, M.-O., Park, K., & Oh, U. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.110067 · Cited by 20 · see citing works
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New mechanisms for sulfonylurea control of insulin secretion
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ATP-Sensitive K+ Channel Signaling in Glucokinase-Deficient Diabetes
Remedi, M. S., Koster, J. C., Patton, B. L., & Nichols, C. G. (2005) · Diabetes · doi:10.2337/diabetes.54.10.2925 · Cited by 16 · see citing works
“2 / islets, the KATP-independent pathway (2) will be “off,” but the KATP-dependent pathway (1) should remain permanently “on.”
BackgroundInfluentialEssential fatty acids (EFA): Role in pancreatic hormone release and concomitant metabolic effect
Opara, E. C., & Hubbard, V. S. (1993) · The Journal of Nutritional Biochemistry · doi:10.1016/0955-2863(93)90085-b · Cited by 16 · see citing works
Beta-cell Ion Channels and Their Role in Regulating Insulin Secretion
Thompson, B. M., & Satin, L. S. (2021) · Comprehensive Physiology · doi:10.1002/j.2040-4603.2021.tb00189.x · Cited by 47 · see citing works
Devarakonda, K., & Mobbs, C. V. (2016) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2016.09.012 · Cited by 14 · see citing works
Impact of moderate exercise on fatty acid oxidation in pancreatic β-cells and skeletal muscle
Langlois, A., Forterre, A. V., Pinget, M., & Bouzakri, K. (2021) · Journal of Endocrinological Investigation · doi:10.1007/s40618-021-01551-2 · Cited by 14 · see citing works
“Then, FAs enter the cell through specific transporters, such as the tissue-specific fatty acid transporter protein CD36/FAT and fatty acid binding protein (FABP), which are located at the cell membrane [8, 18, 19].”
BackgroundUse of regulated secretion in protein production from animal cells: An overview
Grampp, G. E., Sambanis, A., & Stephanopoulos, G. N. (2005) · Springer eBooks · doi:10.1007/bfb0000704 · Cited by 14 · see citing works
Khulan, T. S., & Miegombo, A. (2015) · Journal of Diabetes & Metabolism · doi:10.4172/2155-6156.1000507 · Cited by 13 · see citing works
“Melittin initiates membrane depolarization which leads to increased inflow of Са2+ ion to beta cells, through calcium channel depending on the extracellular calcium [10,11].”
BackgroundChen, C., Wang, S.-H., Hu, Q., Zeng, L., Peng, H.-L., Liu, C., Huang, L.-P., Song, H., Li, Y.-P., Yao, L.-H., et al. (2018) · Cellular Physiology and Biochemistry · doi:10.1159/000486921 · Cited by 11 · see citing works
- Authors
- ASHCROFT, F. M., & RORSMAN, P.
- Affiliations
- University of Oxford (GB)
- Venue
- Biochemical Society Transactions
- Publisher
- Portland Press Ltd.
- Published
- 1990-02-01
- Volume
- 18
- Issue
- 1
- Pages
- 109-111
- ISSN
- 0300-5127 (ISSN-L)
- 1470-8752
- OpenAlex
- W2355414246
- Cited by
- 145
- References
- 0
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 9 · 2020: 3 · 2019: 1 · 2018: 5 · 2017: 4 · 2016: 3 · 2015: 2 · 2014: 7 · 2013: 5 · 2012: 8
- FWCI
- 3.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochemical Society Transactions (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Keywords
- ATP-sensitive potassium channels, B cell metabolism, insulin secretion, pancreatic beta cells, protein kinase C, phorbol myristate acetate
- MeSH terms
- Insulin Secretion, Adenosine Triphosphate, Animals, Humans, Insulin, Islets of Langerhans, Potassium Channels
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