TRPC3 Regulates Islet Beta‐Cell Insulin Secretion
Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose‐stimulated insulin secr...
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| Published in | Advanced science Vol. 10; no. 6; pp. e2204846 - n/a |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Germany
John Wiley & Sons, Inc
01.02.2023
John Wiley and Sons Inc Wiley |
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| Abstract | Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose‐stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3‐dependent in vivo insulin secretion is investigated using pharmacological tools and Trpc3−/− mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2‐[N‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl) amino]‐2‐deoxy‐D‐glucose and calcium imaging. TRPC3 modulation by a small‐molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3‐controlled insulin secretion is KATP‐independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small‐molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes.
TRPC3, a non‐selective calcium channel, is identified as a regulator of glucose‐stimulated insulin release in human and mouse beta cells via a KATP‐independent mechanism. Small‐molecule TRPC3 modulation improves insulin secretion and diabetic hallmarks in animals. These findings advance the understanding of insulin secretion physiology and render the TRPC3 channel an appealing diabetes treatment target. |
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| AbstractList | Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose‐stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3‐dependent in vivo insulin secretion is investigated using pharmacological tools and
Trpc3
−/−
mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2‐[
N
‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl) amino]‐2‐deoxy‐D‐glucose and calcium imaging. TRPC3 modulation by a small‐molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3‐controlled insulin secretion is K
ATP
‐independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small‐molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes.
TRPC3, a non‐selective calcium channel, is identified as a regulator of glucose‐stimulated insulin release in human and mouse beta cells via a K
ATP
‐independent mechanism. Small‐molecule TRPC3 modulation improves insulin secretion and diabetic hallmarks in animals. These findings advance the understanding of insulin secretion physiology and render the TRPC3 channel an appealing diabetes treatment target. Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose‐stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3‐dependent in vivo insulin secretion is investigated using pharmacological tools and Trpc3−/− mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2‐[N‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl) amino]‐2‐deoxy‐D‐glucose and calcium imaging. TRPC3 modulation by a small‐molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3‐controlled insulin secretion is KATP‐independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small‐molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes. TRPC3, a non‐selective calcium channel, is identified as a regulator of glucose‐stimulated insulin release in human and mouse beta cells via a KATP‐independent mechanism. Small‐molecule TRPC3 modulation improves insulin secretion and diabetic hallmarks in animals. These findings advance the understanding of insulin secretion physiology and render the TRPC3 channel an appealing diabetes treatment target. Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose‐stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3‐dependent in vivo insulin secretion is investigated using pharmacological tools and Trpc3 −/− mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2‐[ N ‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl) amino]‐2‐deoxy‐D‐glucose and calcium imaging. TRPC3 modulation by a small‐molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3‐controlled insulin secretion is K ATP ‐independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small‐molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes. Insulin release is tightly controlled by glucose-stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non-selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose-stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3-dependent in vivo insulin secretion is investigated using pharmacological tools and Trpc3 mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose and calcium imaging. TRPC3 modulation by a small-molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3-controlled insulin secretion is K -independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small-molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes. Insulin release is tightly controlled by glucose-stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non-selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose-stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3-dependent in vivo insulin secretion is investigated using pharmacological tools and Trpc3−/− mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose and calcium imaging. TRPC3 modulation by a small-molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3-controlled insulin secretion is KATP-independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small-molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes. Abstract Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective cation channel, as a critical regulator of insulin secretion and glucose control. TRPC3's involvement in glucose‐stimulated insulin secretion (GSIS) is studied in human and animal islets. TRPC3‐dependent in vivo insulin secretion is investigated using pharmacological tools and Trpc3−/− mice. TRPC3's involvement in islet glucose uptake and GSCa is explored using fluorescent glucose analogue 2‐[N‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl) amino]‐2‐deoxy‐D‐glucose and calcium imaging. TRPC3 modulation by a small‐molecule activator, GSK1702934A, is evaluated in type 2 diabetic mice. TRPC3 is functionally expressed in human and mouse islet beta cells. TRPC3‐controlled insulin secretion is KATP‐independent and primarily mediated by diacylglycerol channel regulation of the cytosolic calcium oscillations following glucose stimulation. Conversely, glucose uptake in islets is independent of TRPC3. TRPC3 pharmacologic inhibition and knockout in mice lead to defective insulin secretion and glucose intolerance. Subsequently, TRPC3 activation through targeted small‐molecule enhances insulin secretion and alleviates diabetes hallmarks in animals. This study imputes a function for TRPC3 at the onset of GSIS. These insights strengthen one's knowledge of insulin secretion physiology and set forth the TRPC3 channel as an appealing candidate for drug development in the treatment of diabetes. |
| Author | Bakhos, Jules‐Joel Saliba, Youakim Maddah, Dina Groschner, Klaus Fares, Nassim Smayra, Viviane Birnbaumer, Lutz Rached, Gaëlle Hajal, Joelle |
| AuthorAffiliation | 5 Signal Transduction Laboratory National Institute of Environmental Health Sciences Research Triangle Park Durham NC C1107AAZ USA 2 Faculty of Medicine Saint Joseph University Saint Joseph University of Beirut POBox. 17‐5208 ‐ Mar Mikhaël Beirut 1104 2020 Lebanon 1 Physiology and Pathophysiology Research Laboratory Pole of Technology and Health Faculty of Medicine Saint Joseph University of Beirut POBox. 17‐5208 ‐ Mar Mikhaël Beirut 1104 2020 Lebanon 4 School of Medical Sciences Institute of Biomedical Research (BIOMED) Catholic University of Argentina Buenos Aires C1107AAZ Argentina 3 Gottfried‐Schatz‐Research‐Centre‐Biophysics Medical University of Graz Graz 8010 Austria |
| AuthorAffiliation_xml | – name: 1 Physiology and Pathophysiology Research Laboratory Pole of Technology and Health Faculty of Medicine Saint Joseph University of Beirut POBox. 17‐5208 ‐ Mar Mikhaël Beirut 1104 2020 Lebanon – name: 2 Faculty of Medicine Saint Joseph University Saint Joseph University of Beirut POBox. 17‐5208 ‐ Mar Mikhaël Beirut 1104 2020 Lebanon – name: 3 Gottfried‐Schatz‐Research‐Centre‐Biophysics Medical University of Graz Graz 8010 Austria – name: 4 School of Medical Sciences Institute of Biomedical Research (BIOMED) Catholic University of Argentina Buenos Aires C1107AAZ Argentina – name: 5 Signal Transduction Laboratory National Institute of Environmental Health Sciences Research Triangle Park Durham NC C1107AAZ USA |
| Author_xml | – sequence: 1 givenname: Gaëlle surname: Rached fullname: Rached, Gaëlle organization: Saint Joseph University of Beirut – sequence: 2 givenname: Youakim surname: Saliba fullname: Saliba, Youakim email: youakim.saliba@usj.edu.lb organization: Saint Joseph University of Beirut – sequence: 3 givenname: Dina surname: Maddah fullname: Maddah, Dina organization: Saint Joseph University of Beirut – sequence: 4 givenname: Joelle surname: Hajal fullname: Hajal, Joelle organization: Saint Joseph University of Beirut – sequence: 5 givenname: Viviane surname: Smayra fullname: Smayra, Viviane organization: Saint Joseph University of Beirut – sequence: 6 givenname: Jules‐Joel surname: Bakhos fullname: Bakhos, Jules‐Joel organization: Saint Joseph University of Beirut – sequence: 7 givenname: Klaus surname: Groschner fullname: Groschner, Klaus organization: Medical University of Graz – sequence: 8 givenname: Lutz surname: Birnbaumer fullname: Birnbaumer, Lutz organization: Research Triangle Park – sequence: 9 givenname: Nassim orcidid: 0000-0002-2935-2611 surname: Fares fullname: Fares, Nassim email: nassim.fares@usj.edu.lb organization: Saint Joseph University of Beirut |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/36642838$$D View this record in MEDLINE/PubMed |
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| Keywords | calcium TRPC3 insulin diabetes beta cells |
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| Snippet | Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non‐selective... Insulin release is tightly controlled by glucose-stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a non-selective... Abstract Insulin release is tightly controlled by glucose‐stimulated calcium (GSCa) through hitherto equivocal pathways. This study investigates TRPC3, a... |
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| SubjectTerms | Animals Antibodies beta cells calcium Calcium - metabolism diabetes Diabetes Mellitus, Experimental - metabolism Glucose Glucose - metabolism Humans Insulin Insulin - metabolism Insulin Secretion Insulin-Secreting Cells Mice Molecular weight Physiology Plasma TRPC3 |
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| Title | TRPC3 Regulates Islet Beta‐Cell Insulin Secretion |
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