Augmented mitochondrial energy metabolism is an early response to chronic glucose stress in human pancreatic beta cells
Aims/hypothesis In islets from individuals with type 2 diabetes and in islets exposed to chronic elevated glucose, mitochondrial energy metabolism is impaired. Here, we studied early metabolic changes and mitochondrial adaptations in human beta cells during chronic glucose stress. Methods Respiratio...
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| Veröffentlicht in: | Diabetologia 2020-12, Vol.63 (12), p.2628-2640 |
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| creator | Chareyron, Isabelle Christen, Stefan Moco, Sofia Valsesia, Armand Lassueur, Steve Dayon, Loïc Wollheim, Claes B. Santo Domingo, Jaime Wiederkehr, Andreas |
| description | Aims/hypothesis
In islets from individuals with type 2 diabetes and in islets exposed to chronic elevated glucose, mitochondrial energy metabolism is impaired. Here, we studied early metabolic changes and mitochondrial adaptations in human beta cells during chronic glucose stress.
Methods
Respiration and cytosolic ATP changes were measured in human islet cell clusters after culture for 4 days in 11.1 mmol/l glucose. Metabolomics was applied to analyse intracellular metabolite changes as a result of glucose stress conditions. Alterations in beta cell function were followed using insulin secretion assays or cytosolic calcium signalling after expression of the calcium probe YC3.6 specifically in beta cells of islet clusters.
Results
At early stages of glucose stress, mitochondrial energy metabolism was augmented in contrast to the previously described mitochondrial dysfunction in beta cells from islets of diabetic donors. Following chronic glucose stress, mitochondrial respiration increased (by 52.4%,
p
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| doi_str_mv | 10.1007/s00125-020-05275-5 |
| format | Article |
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In islets from individuals with type 2 diabetes and in islets exposed to chronic elevated glucose, mitochondrial energy metabolism is impaired. Here, we studied early metabolic changes and mitochondrial adaptations in human beta cells during chronic glucose stress.
Methods
Respiration and cytosolic ATP changes were measured in human islet cell clusters after culture for 4 days in 11.1 mmol/l glucose. Metabolomics was applied to analyse intracellular metabolite changes as a result of glucose stress conditions. Alterations in beta cell function were followed using insulin secretion assays or cytosolic calcium signalling after expression of the calcium probe YC3.6 specifically in beta cells of islet clusters.
Results
At early stages of glucose stress, mitochondrial energy metabolism was augmented in contrast to the previously described mitochondrial dysfunction in beta cells from islets of diabetic donors. Following chronic glucose stress, mitochondrial respiration increased (by 52.4%,
p
< 0.001) and, as a consequence, the cytosolic ATP/ADP ratio in resting human pancreatic islet cells was elevated (by 27.8%,
p
< 0.05). Because of mitochondrial overactivation in the resting state, nutrient-induced beta cell activation was reduced. In addition, chronic glucose stress caused metabolic adaptations that resulted in the accumulation of intermediates of the glycolytic pathway, the pentose phosphate pathway and the TCA cycle; the most strongly augmented metabolite was glycerol 3-phosphate. The changes in metabolites observed are likely to be due to the inability of mitochondria to cope with continuous nutrient oversupply. To protect beta cells from chronic glucose stress, we inhibited mitochondrial pyruvate transport. Metabolite concentrations were partially normalised and the mitochondrial respiratory response to nutrients was markedly improved. Furthermore, stimulus–secretion coupling as assessed by cytosolic calcium signalling, was restored.
Conclusion/interpretation
We propose that metabolic changes and associated mitochondrial overactivation are early adaptations to glucose stress, and may reflect what happens as a result of poor blood glucose control. Inhibition of mitochondrial pyruvate transport reduces mitochondrial nutrient overload and allows beta cells to recover from chronic glucose stress.
Graphical abstract</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-020-05275-5</identifier><identifier>PMID: 32960311</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adaptation ; Beta cells ; Calcium signalling ; Cell activation ; Cell culture ; Diabetes mellitus (non-insulin dependent) ; Electron transport ; Energy metabolism ; Glucose ; Glucose metabolism ; Glycerol ; Glycolysis ; Human Physiology ; Insulin ; Insulin secretion ; Intermediates ; Internal Medicine ; Islet cells ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Metabolites ; Metabolomics ; Mitochondria ; Nutrients ; Pancreas ; Pentose phosphate pathway ; Pyruvic acid ; Respiration ; Secretion ; Signal transduction ; Tricarboxylic acid cycle</subject><ispartof>Diabetologia, 2020-12, Vol.63 (12), p.2628-2640</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-837c41012bd3c7edfa36aba33c3325bb8d7c73e29b9eb0ae40dbb6533ea043ae3</citedby><cites>FETCH-LOGICAL-c540t-837c41012bd3c7edfa36aba33c3325bb8d7c73e29b9eb0ae40dbb6533ea043ae3</cites><orcidid>0000-0003-0964-1210 ; 0000-0001-8170-8876 ; 0000-0002-8499-270X ; 0000-0002-4570-9879 ; 0000-0003-0746-9664 ; 0000-0002-2121-8215 ; 0000-0001-5501-0482 ; 0000-0003-2685-7558</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-020-05275-5$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-020-05275-5$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32960311$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chareyron, Isabelle</creatorcontrib><creatorcontrib>Christen, Stefan</creatorcontrib><creatorcontrib>Moco, Sofia</creatorcontrib><creatorcontrib>Valsesia, Armand</creatorcontrib><creatorcontrib>Lassueur, Steve</creatorcontrib><creatorcontrib>Dayon, Loïc</creatorcontrib><creatorcontrib>Wollheim, Claes B.</creatorcontrib><creatorcontrib>Santo Domingo, Jaime</creatorcontrib><creatorcontrib>Wiederkehr, Andreas</creatorcontrib><title>Augmented mitochondrial energy metabolism is an early response to chronic glucose stress in human pancreatic beta cells</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
In islets from individuals with type 2 diabetes and in islets exposed to chronic elevated glucose, mitochondrial energy metabolism is impaired. Here, we studied early metabolic changes and mitochondrial adaptations in human beta cells during chronic glucose stress.
Methods
Respiration and cytosolic ATP changes were measured in human islet cell clusters after culture for 4 days in 11.1 mmol/l glucose. Metabolomics was applied to analyse intracellular metabolite changes as a result of glucose stress conditions. Alterations in beta cell function were followed using insulin secretion assays or cytosolic calcium signalling after expression of the calcium probe YC3.6 specifically in beta cells of islet clusters.
Results
At early stages of glucose stress, mitochondrial energy metabolism was augmented in contrast to the previously described mitochondrial dysfunction in beta cells from islets of diabetic donors. Following chronic glucose stress, mitochondrial respiration increased (by 52.4%,
p
< 0.001) and, as a consequence, the cytosolic ATP/ADP ratio in resting human pancreatic islet cells was elevated (by 27.8%,
p
< 0.05). Because of mitochondrial overactivation in the resting state, nutrient-induced beta cell activation was reduced. In addition, chronic glucose stress caused metabolic adaptations that resulted in the accumulation of intermediates of the glycolytic pathway, the pentose phosphate pathway and the TCA cycle; the most strongly augmented metabolite was glycerol 3-phosphate. The changes in metabolites observed are likely to be due to the inability of mitochondria to cope with continuous nutrient oversupply. To protect beta cells from chronic glucose stress, we inhibited mitochondrial pyruvate transport. Metabolite concentrations were partially normalised and the mitochondrial respiratory response to nutrients was markedly improved. Furthermore, stimulus–secretion coupling as assessed by cytosolic calcium signalling, was restored.
Conclusion/interpretation
We propose that metabolic changes and associated mitochondrial overactivation are early adaptations to glucose stress, and may reflect what happens as a result of poor blood glucose control. Inhibition of mitochondrial pyruvate transport reduces mitochondrial nutrient overload and allows beta cells to recover from chronic glucose stress.
Graphical abstract</description><subject>Adaptation</subject><subject>Beta cells</subject><subject>Calcium signalling</subject><subject>Cell activation</subject><subject>Cell culture</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Electron transport</subject><subject>Energy metabolism</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>Glycerol</subject><subject>Glycolysis</subject><subject>Human Physiology</subject><subject>Insulin</subject><subject>Insulin secretion</subject><subject>Intermediates</subject><subject>Internal Medicine</subject><subject>Islet cells</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolomics</subject><subject>Mitochondria</subject><subject>Nutrients</subject><subject>Pancreas</subject><subject>Pentose phosphate pathway</subject><subject>Pyruvic acid</subject><subject>Respiration</subject><subject>Secretion</subject><subject>Signal transduction</subject><subject>Tricarboxylic acid cycle</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kUuLFDEUhYMoTjv6B1xIwI2b0ptXpWojDIOjwoAbBXchSd2uzlCVtEmV0v_e9PQ4PhYuQiDnu-fmcAh5zuA1A9BvCgDjqgEODSiuVaMekA2TgjcgefeQbI56w7r26xl5UsoNAAgl28fkTPC-BcHYhvy4WMcZ44IDncOS_C7FIQc7UYyYxwOdcbEuTaHMNBRqI0WbpwPNWPYpFqRLon6XUwyejtPqU30qS1ULDZHu1rlO7G30Ge1SEVfdqMdpKk_Jo62dCj67u8_Jl6t3ny8_NNef3n-8vLhuvJKwNJ3QXrIaww3Caxy2VrTWWSG8EFw51w3aa4G8dz06sChhcK5VQqAFKSyKc_L25Ltf3YyDr1Gzncw-h9nmg0k2mL-VGHZmTN-NbiXrlawGr-4Mcvq2YlnMHMoxgo2Y1mK4lLLTbaugoi__QW_SmmONVynNel4PqxQ_UT6nUjJu7z_DwBx7NadeTe3V3PZqVB168WeM-5FfRVZAnIBSpThi_r37P7Y_AX96sWM</recordid><startdate>20201201</startdate><enddate>20201201</enddate><creator>Chareyron, Isabelle</creator><creator>Christen, Stefan</creator><creator>Moco, Sofia</creator><creator>Valsesia, Armand</creator><creator>Lassueur, Steve</creator><creator>Dayon, Loïc</creator><creator>Wollheim, Claes B.</creator><creator>Santo Domingo, Jaime</creator><creator>Wiederkehr, Andreas</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>H94</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>5PM</scope><orcidid>https://orcid.org/0000-0003-0964-1210</orcidid><orcidid>https://orcid.org/0000-0001-8170-8876</orcidid><orcidid>https://orcid.org/0000-0002-8499-270X</orcidid><orcidid>https://orcid.org/0000-0002-4570-9879</orcidid><orcidid>https://orcid.org/0000-0003-0746-9664</orcidid><orcidid>https://orcid.org/0000-0002-2121-8215</orcidid><orcidid>https://orcid.org/0000-0001-5501-0482</orcidid><orcidid>https://orcid.org/0000-0003-2685-7558</orcidid></search><sort><creationdate>20201201</creationdate><title>Augmented mitochondrial energy metabolism is an early response to chronic glucose stress in human pancreatic beta cells</title><author>Chareyron, Isabelle ; Christen, Stefan ; Moco, Sofia ; Valsesia, Armand ; Lassueur, Steve ; Dayon, Loïc ; Wollheim, Claes B. ; Santo Domingo, Jaime ; Wiederkehr, Andreas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-837c41012bd3c7edfa36aba33c3325bb8d7c73e29b9eb0ae40dbb6533ea043ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adaptation</topic><topic>Beta cells</topic><topic>Calcium signalling</topic><topic>Cell activation</topic><topic>Cell culture</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Electron transport</topic><topic>Energy metabolism</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>Glycerol</topic><topic>Glycolysis</topic><topic>Human Physiology</topic><topic>Insulin</topic><topic>Insulin secretion</topic><topic>Intermediates</topic><topic>Internal Medicine</topic><topic>Islet cells</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metabolomics</topic><topic>Mitochondria</topic><topic>Nutrients</topic><topic>Pancreas</topic><topic>Pentose phosphate pathway</topic><topic>Pyruvic acid</topic><topic>Respiration</topic><topic>Secretion</topic><topic>Signal transduction</topic><topic>Tricarboxylic acid cycle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chareyron, Isabelle</creatorcontrib><creatorcontrib>Christen, Stefan</creatorcontrib><creatorcontrib>Moco, Sofia</creatorcontrib><creatorcontrib>Valsesia, Armand</creatorcontrib><creatorcontrib>Lassueur, Steve</creatorcontrib><creatorcontrib>Dayon, Loïc</creatorcontrib><creatorcontrib>Wollheim, Claes B.</creatorcontrib><creatorcontrib>Santo Domingo, Jaime</creatorcontrib><creatorcontrib>Wiederkehr, Andreas</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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>AIDS and Cancer Research Abstracts</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>PubMed Central (Full Participant titles)</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chareyron, Isabelle</au><au>Christen, Stefan</au><au>Moco, Sofia</au><au>Valsesia, Armand</au><au>Lassueur, Steve</au><au>Dayon, Loïc</au><au>Wollheim, Claes B.</au><au>Santo Domingo, Jaime</au><au>Wiederkehr, Andreas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Augmented mitochondrial energy metabolism is an early response to chronic glucose stress in human pancreatic beta cells</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2020-12-01</date><risdate>2020</risdate><volume>63</volume><issue>12</issue><spage>2628</spage><epage>2640</epage><pages>2628-2640</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
In islets from individuals with type 2 diabetes and in islets exposed to chronic elevated glucose, mitochondrial energy metabolism is impaired. Here, we studied early metabolic changes and mitochondrial adaptations in human beta cells during chronic glucose stress.
Methods
Respiration and cytosolic ATP changes were measured in human islet cell clusters after culture for 4 days in 11.1 mmol/l glucose. Metabolomics was applied to analyse intracellular metabolite changes as a result of glucose stress conditions. Alterations in beta cell function were followed using insulin secretion assays or cytosolic calcium signalling after expression of the calcium probe YC3.6 specifically in beta cells of islet clusters.
Results
At early stages of glucose stress, mitochondrial energy metabolism was augmented in contrast to the previously described mitochondrial dysfunction in beta cells from islets of diabetic donors. Following chronic glucose stress, mitochondrial respiration increased (by 52.4%,
p
< 0.001) and, as a consequence, the cytosolic ATP/ADP ratio in resting human pancreatic islet cells was elevated (by 27.8%,
p
< 0.05). Because of mitochondrial overactivation in the resting state, nutrient-induced beta cell activation was reduced. In addition, chronic glucose stress caused metabolic adaptations that resulted in the accumulation of intermediates of the glycolytic pathway, the pentose phosphate pathway and the TCA cycle; the most strongly augmented metabolite was glycerol 3-phosphate. The changes in metabolites observed are likely to be due to the inability of mitochondria to cope with continuous nutrient oversupply. To protect beta cells from chronic glucose stress, we inhibited mitochondrial pyruvate transport. Metabolite concentrations were partially normalised and the mitochondrial respiratory response to nutrients was markedly improved. Furthermore, stimulus–secretion coupling as assessed by cytosolic calcium signalling, was restored.
Conclusion/interpretation
We propose that metabolic changes and associated mitochondrial overactivation are early adaptations to glucose stress, and may reflect what happens as a result of poor blood glucose control. Inhibition of mitochondrial pyruvate transport reduces mitochondrial nutrient overload and allows beta cells to recover from chronic glucose stress.
Graphical abstract</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>32960311</pmid><doi>10.1007/s00125-020-05275-5</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-0964-1210</orcidid><orcidid>https://orcid.org/0000-0001-8170-8876</orcidid><orcidid>https://orcid.org/0000-0002-8499-270X</orcidid><orcidid>https://orcid.org/0000-0002-4570-9879</orcidid><orcidid>https://orcid.org/0000-0003-0746-9664</orcidid><orcidid>https://orcid.org/0000-0002-2121-8215</orcidid><orcidid>https://orcid.org/0000-0001-5501-0482</orcidid><orcidid>https://orcid.org/0000-0003-2685-7558</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptation Beta cells Calcium signalling Cell activation Cell culture Diabetes mellitus (non-insulin dependent) Electron transport Energy metabolism Glucose Glucose metabolism Glycerol Glycolysis Human Physiology Insulin Insulin secretion Intermediates Internal Medicine Islet cells Medicine Medicine & Public Health Metabolic Diseases Metabolism Metabolites Metabolomics Mitochondria Nutrients Pancreas Pentose phosphate pathway Pyruvic acid Respiration Secretion Signal transduction Tricarboxylic acid cycle |
| title | Augmented mitochondrial energy metabolism is an early response to chronic glucose stress in human pancreatic beta cells |
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