Voltage-Gated Na+ Channels are Modulated by Glucose and Involved in Regulating Cellular Insulin Content of INS-1 Cells
Background/Aims: Islet beta cells (β-cells) are unique cells that play a critical role in glucose homeostasis by secreting insulin in response to increased glucose levels. Voltage-gated ion channels in β-cells, such as K + and Ca 2+ channels, contribute to insulin secretion. The response of voltage-...
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Veröffentlicht in: | Cellular Physiology and Biochemistry 2018-01, Vol.45 (2), p.446-457 |
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description | Background/Aims: Islet beta cells (β-cells) are unique cells that play a critical role in glucose homeostasis by secreting insulin in response to increased glucose levels. Voltage-gated ion channels in β-cells, such as K + and Ca 2+ channels, contribute to insulin secretion. The response of voltage-gated Na + channels (VGSCs) in β-cells to the changes in glucose levels remains unknown. This work aims to determine the role of extracellular glucose on the regulation of VGSC. Methods: The effect of glucose on VGSC currents (I Na ) was investigated in insulin-secreting β-cell line (INS-1) cells of rats using whole-cell patch clamp techniques, and the effects of glucose on insulin content and cell viability were determined using Enzyme-Linked Immunosorbent Assay (ELISA) and Methylthiazolyldiphenyl-tetrazolium Bromide (MTT) assay methods respectively. Results: Our results show that extracellular glucose application can inhibit the peak of I Na in a concentration-dependent manner. Glucose concentration of 18 mM reduced the amplitude of I Na , suppressed the I Na of steady-state activation, shifted the steady-state inactivation curves of I Na to negative potentials, and prolonged the time course of I Na recovery from inactivation. Glucose also enhanced the activity-dependent attenuation of I Na and reduced the fraction of activated channels. Furthermore, 18 mM glucose or low concentration of tetrodotoxin (TTX, a VGSC-specific blocker) partially inhibited the activity of VGSC and also improved insulin synthesis. Conclusion: These results revealed that extracellular glucose application enhances the insulin synthesis in INS-1 cells and the mechanism through the partial inhibition on I Na channel is involved. Our results innovatively suggest that VGSC plays a vital role in modulating glucose homeostasis. |
doi_str_mv | 10.1159/000486921 |
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Voltage-gated ion channels in β-cells, such as K + and Ca 2+ channels, contribute to insulin secretion. The response of voltage-gated Na + channels (VGSCs) in β-cells to the changes in glucose levels remains unknown. This work aims to determine the role of extracellular glucose on the regulation of VGSC. Methods: The effect of glucose on VGSC currents (I Na ) was investigated in insulin-secreting β-cell line (INS-1) cells of rats using whole-cell patch clamp techniques, and the effects of glucose on insulin content and cell viability were determined using Enzyme-Linked Immunosorbent Assay (ELISA) and Methylthiazolyldiphenyl-tetrazolium Bromide (MTT) assay methods respectively. Results: Our results show that extracellular glucose application can inhibit the peak of I Na in a concentration-dependent manner. Glucose concentration of 18 mM reduced the amplitude of I Na , suppressed the I Na of steady-state activation, shifted the steady-state inactivation curves of I Na to negative potentials, and prolonged the time course of I Na recovery from inactivation. Glucose also enhanced the activity-dependent attenuation of I Na and reduced the fraction of activated channels. Furthermore, 18 mM glucose or low concentration of tetrodotoxin (TTX, a VGSC-specific blocker) partially inhibited the activity of VGSC and also improved insulin synthesis. Conclusion: These results revealed that extracellular glucose application enhances the insulin synthesis in INS-1 cells and the mechanism through the partial inhibition on I Na channel is involved. Our results innovatively suggest that VGSC plays a vital role in modulating glucose homeostasis.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000486921</identifier><identifier>PMID: 29402835</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Cell Line ; Cell Survival - drug effects ; Dextrose ; Diabetes ; Endocrinology ; Enzyme-Linked Immunosorbent Assay ; Evoked Potentials - drug effects ; Gene expression ; Glucose ; Glucose - pharmacology ; Health aspects ; INS-1 cells ; Insulin ; Insulin - analysis ; Insulin-Secreting Cells - cytology ; Insulin-Secreting Cells - drug effects ; Insulin-Secreting Cells - physiology ; Kinases ; Original Paper ; Pancreatic beta cells ; Patch-Clamp Techniques ; Physiological aspects ; Protein synthesis ; Proteins ; Rats ; Sodium channels ; Tetrodotoxin ; Tetrodotoxin - toxicity ; Voltage-gated Na+ channel ; Voltage-Gated Sodium Channels - metabolism</subject><ispartof>Cellular Physiology and Biochemistry, 2018-01, Vol.45 (2), p.446-457</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><rights>COPYRIGHT 2018 S. Karger AG</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c530t-61e0a6faa700313fd6cb45f864cd7024e0e7907694e4c21ab11b0ba2332833d03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,2102,27635,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29402835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Chong</creatorcontrib><creatorcontrib>Wang, Songhua</creatorcontrib><creatorcontrib>Hu, Qingjuan</creatorcontrib><creatorcontrib>Zeng, Lvming</creatorcontrib><creatorcontrib>Peng, Hailong</creatorcontrib><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Huang, Li-Ping</creatorcontrib><creatorcontrib>Song, Hao</creatorcontrib><creatorcontrib>Li, Yuping</creatorcontrib><creatorcontrib>Yao, Li-Hua</creatorcontrib><creatorcontrib>Meng, Wei</creatorcontrib><title>Voltage-Gated Na+ Channels are Modulated by Glucose and Involved in Regulating Cellular Insulin Content of INS-1 Cells</title><title>Cellular Physiology and Biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Background/Aims: Islet beta cells (β-cells) are unique cells that play a critical role in glucose homeostasis by secreting insulin in response to increased glucose levels. Voltage-gated ion channels in β-cells, such as K + and Ca 2+ channels, contribute to insulin secretion. The response of voltage-gated Na + channels (VGSCs) in β-cells to the changes in glucose levels remains unknown. This work aims to determine the role of extracellular glucose on the regulation of VGSC. Methods: The effect of glucose on VGSC currents (I Na ) was investigated in insulin-secreting β-cell line (INS-1) cells of rats using whole-cell patch clamp techniques, and the effects of glucose on insulin content and cell viability were determined using Enzyme-Linked Immunosorbent Assay (ELISA) and Methylthiazolyldiphenyl-tetrazolium Bromide (MTT) assay methods respectively. Results: Our results show that extracellular glucose application can inhibit the peak of I Na in a concentration-dependent manner. Glucose concentration of 18 mM reduced the amplitude of I Na , suppressed the I Na of steady-state activation, shifted the steady-state inactivation curves of I Na to negative potentials, and prolonged the time course of I Na recovery from inactivation. Glucose also enhanced the activity-dependent attenuation of I Na and reduced the fraction of activated channels. Furthermore, 18 mM glucose or low concentration of tetrodotoxin (TTX, a VGSC-specific blocker) partially inhibited the activity of VGSC and also improved insulin synthesis. Conclusion: These results revealed that extracellular glucose application enhances the insulin synthesis in INS-1 cells and the mechanism through the partial inhibition on I Na channel is involved. Our results innovatively suggest that VGSC plays a vital role in modulating glucose homeostasis.</description><subject>Animals</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Dextrose</subject><subject>Diabetes</subject><subject>Endocrinology</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Evoked Potentials - drug effects</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Glucose - pharmacology</subject><subject>Health aspects</subject><subject>INS-1 cells</subject><subject>Insulin</subject><subject>Insulin - analysis</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Kinases</subject><subject>Original Paper</subject><subject>Pancreatic beta cells</subject><subject>Patch-Clamp Techniques</subject><subject>Physiological aspects</subject><subject>Protein synthesis</subject><subject>Proteins</subject><subject>Rats</subject><subject>Sodium channels</subject><subject>Tetrodotoxin</subject><subject>Tetrodotoxin - toxicity</subject><subject>Voltage-gated Na+ channel</subject><subject>Voltage-Gated Sodium Channels - metabolism</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNptkk1v1DAQhiMEoqVw4I6QpV5AKMVjO3F8LBEsK5WC-Lpajj9Clqy9tZOV-u9xN2UPCPng8czzjv3KUxTPAV8AVOItxpg1tSDwoDgFRqAUnDcPc4yhKhvR8JPiSUobnI9ckMfFCREMk4ZWp8X-Zxgn1dtypSZr0LV6g9pfyns7JqSiRZ-CmcdDqbtFq3HWIVmkvEFrvw_jPucHj77a_g4afI9aO445jrme5jHX2uAn6ycUHFpffyvhQKSnxSOnxmSf3e9nxY8P77-3H8urz6t1e3lV6oriqazBYlU7pTjGFKgzte5Y5ZqaacMxYRZbLjCvBbNME1AdQIc7RSjN7qjB9KxYL31NUBu5i8NWxVsZ1CAPiRB7qeI06NFKnrsyMFTrqmMOa8VdTTtwHcG4a1iVe71aeu1iuJltmuR2SDq7Ud6GOUkQooKKccEzev4Puglz9NmpJAAcagwH6mKhepXvH7wLU1Q6L2O3gw7euiHnL2vKK0KzKgteLwIdQ0rRuqMjwPJuEuRxEjL78v4Jc7e15kj-_foMvFiA3yr2Nh6Bo_78v-X2y7uFkDvj6B8YuL8X</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Chen, Chong</creator><creator>Wang, Songhua</creator><creator>Hu, Qingjuan</creator><creator>Zeng, Lvming</creator><creator>Peng, Hailong</creator><creator>Liu, Chao</creator><creator>Huang, Li-Ping</creator><creator>Song, Hao</creator><creator>Li, Yuping</creator><creator>Yao, Li-Hua</creator><creator>Meng, Wei</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Voltage-Gated Na+ Channels are Modulated by Glucose and Involved in Regulating Cellular Insulin Content of INS-1 Cells</title><author>Chen, Chong ; Wang, Songhua ; Hu, Qingjuan ; Zeng, Lvming ; Peng, Hailong ; Liu, Chao ; Huang, Li-Ping ; Song, Hao ; Li, Yuping ; Yao, Li-Hua ; Meng, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c530t-61e0a6faa700313fd6cb45f864cd7024e0e7907694e4c21ab11b0ba2332833d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Dextrose</topic><topic>Diabetes</topic><topic>Endocrinology</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Evoked Potentials - drug effects</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Glucose - pharmacology</topic><topic>Health aspects</topic><topic>INS-1 cells</topic><topic>Insulin</topic><topic>Insulin - analysis</topic><topic>Insulin-Secreting Cells - cytology</topic><topic>Insulin-Secreting Cells - drug effects</topic><topic>Insulin-Secreting Cells - physiology</topic><topic>Kinases</topic><topic>Original Paper</topic><topic>Pancreatic beta cells</topic><topic>Patch-Clamp Techniques</topic><topic>Physiological aspects</topic><topic>Protein synthesis</topic><topic>Proteins</topic><topic>Rats</topic><topic>Sodium channels</topic><topic>Tetrodotoxin</topic><topic>Tetrodotoxin - toxicity</topic><topic>Voltage-gated Na+ channel</topic><topic>Voltage-Gated Sodium Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chong</creatorcontrib><creatorcontrib>Wang, Songhua</creatorcontrib><creatorcontrib>Hu, Qingjuan</creatorcontrib><creatorcontrib>Zeng, Lvming</creatorcontrib><creatorcontrib>Peng, Hailong</creatorcontrib><creatorcontrib>Liu, Chao</creatorcontrib><creatorcontrib>Huang, Li-Ping</creatorcontrib><creatorcontrib>Song, Hao</creatorcontrib><creatorcontrib>Li, Yuping</creatorcontrib><creatorcontrib>Yao, Li-Hua</creatorcontrib><creatorcontrib>Meng, Wei</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular Physiology and Biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chong</au><au>Wang, Songhua</au><au>Hu, Qingjuan</au><au>Zeng, Lvming</au><au>Peng, Hailong</au><au>Liu, Chao</au><au>Huang, Li-Ping</au><au>Song, Hao</au><au>Li, Yuping</au><au>Yao, Li-Hua</au><au>Meng, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Voltage-Gated Na+ Channels are Modulated by Glucose and Involved in Regulating Cellular Insulin Content of INS-1 Cells</atitle><jtitle>Cellular Physiology and Biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>45</volume><issue>2</issue><spage>446</spage><epage>457</epage><pages>446-457</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Background/Aims: Islet beta cells (β-cells) are unique cells that play a critical role in glucose homeostasis by secreting insulin in response to increased glucose levels. Voltage-gated ion channels in β-cells, such as K + and Ca 2+ channels, contribute to insulin secretion. The response of voltage-gated Na + channels (VGSCs) in β-cells to the changes in glucose levels remains unknown. This work aims to determine the role of extracellular glucose on the regulation of VGSC. Methods: The effect of glucose on VGSC currents (I Na ) was investigated in insulin-secreting β-cell line (INS-1) cells of rats using whole-cell patch clamp techniques, and the effects of glucose on insulin content and cell viability were determined using Enzyme-Linked Immunosorbent Assay (ELISA) and Methylthiazolyldiphenyl-tetrazolium Bromide (MTT) assay methods respectively. Results: Our results show that extracellular glucose application can inhibit the peak of I Na in a concentration-dependent manner. Glucose concentration of 18 mM reduced the amplitude of I Na , suppressed the I Na of steady-state activation, shifted the steady-state inactivation curves of I Na to negative potentials, and prolonged the time course of I Na recovery from inactivation. Glucose also enhanced the activity-dependent attenuation of I Na and reduced the fraction of activated channels. Furthermore, 18 mM glucose or low concentration of tetrodotoxin (TTX, a VGSC-specific blocker) partially inhibited the activity of VGSC and also improved insulin synthesis. Conclusion: These results revealed that extracellular glucose application enhances the insulin synthesis in INS-1 cells and the mechanism through the partial inhibition on I Na channel is involved. Our results innovatively suggest that VGSC plays a vital role in modulating glucose homeostasis.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>29402835</pmid><doi>10.1159/000486921</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cell Line Cell Survival - drug effects Dextrose Diabetes Endocrinology Enzyme-Linked Immunosorbent Assay Evoked Potentials - drug effects Gene expression Glucose Glucose - pharmacology Health aspects INS-1 cells Insulin Insulin - analysis Insulin-Secreting Cells - cytology Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - physiology Kinases Original Paper Pancreatic beta cells Patch-Clamp Techniques Physiological aspects Protein synthesis Proteins Rats Sodium channels Tetrodotoxin Tetrodotoxin - toxicity Voltage-gated Na+ channel Voltage-Gated Sodium Channels - metabolism |
title | Voltage-Gated Na+ Channels are Modulated by Glucose and Involved in Regulating Cellular Insulin Content of INS-1 Cells |
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