NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic β-cells.
Identifieur interne : 000338 ( Main/Exploration ); précédent : 000337; suivant : 000339NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic β-cells.
Auteurs : Laila R B. Santos [Belgique] ; Carole Muller [Belgique] ; Arnaldo H. De Souza [Belgique] ; Hilton K. Takahashi [Belgique] ; Peter Spégel [Suède] ; Ian R. Sweet [États-Unis] ; Heeyoung Chae [Belgique] ; Hindrik Mulder [Suède] ; Jean-Christophe Jonas [Belgique]Source :
- Molecular metabolism [ 2212-8778 ] ; 2017.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Calcium (métabolisme), Cellules cultivées (MeSH), Cellules à insuline (métabolisme), Exocytose (MeSH), Femelle (MeSH), Glucose (métabolisme), Glutathion (métabolisme), Insuline (métabolisme), NADP (métabolisme), NADP transhydrogenase, AB-specific (génétique), NADP transhydrogenase, AB-specific (métabolisme), Oxydoréduction (MeSH), Protéines mitochondriales (génétique), Protéines mitochondriales (métabolisme), Souris (MeSH), Souris de lignée C57BL (MeSH).
- MESH :
- génétique : NADP transhydrogenase, AB-specific, Protéines mitochondriales.
- métabolisme : Calcium, Cellules à insuline, Glucose, Glutathion, Insuline, NADP, NADP transhydrogenase, AB-specific, Protéines mitochondriales.
- Animaux, Cellules cultivées, Exocytose, Femelle, Oxydoréduction, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals (MeSH), Calcium (metabolism), Cells, Cultured (MeSH), Exocytosis (MeSH), Female (MeSH), Glucose (metabolism), Glutathione (metabolism), Insulin (metabolism), Insulin-Secreting Cells (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mitochondrial Proteins (genetics), Mitochondrial Proteins (metabolism), NADP (metabolism), NADP Transhydrogenase, AB-Specific (genetics), NADP Transhydrogenase, AB-Specific (metabolism), Oxidation-Reduction (MeSH).
- MESH :
- chemical , genetics : Mitochondrial Proteins, NADP Transhydrogenase, AB-Specific.
- chemical , metabolism : Calcium, Glucose, Glutathione, Insulin, Mitochondrial Proteins, NADP, NADP Transhydrogenase, AB-Specific.
- metabolism : Insulin-Secreting Cells.
- Animals, Cells, Cultured, Exocytosis, Female, Mice, Mice, Inbred C57BL, Oxidation-Reduction.
Abstract
OBJECTIVE
The glucose stimulation of insulin secretion (GSIS) by pancreatic β-cells critically depends on increased production of metabolic coupling factors, including NADPH. Nicotinamide nucleotide transhydrogenase (NNT) typically produces NADPH at the expense of NADH and ΔpH in energized mitochondria. Its spontaneous inactivation in C57BL/6J mice was previously shown to alter ATP production, Ca
METHODS
Islets were isolated from female C57BL/6J mice (J-islets), which lack functional NNT, and genetically close C57BL/6N mice (N-islets). Wild-type mouse NNT was expressed in J-islets by adenoviral infection. Mitochondrial and cytosolic glutathione oxidation was measured with glutaredoxin 1-fused roGFP2 probes targeted or not to the mitochondrial matrix. NADPH and NADH redox state was measured biochemically. Insulin secretion and upstream coupling events were measured under dynamic or static conditions by standard procedures.
RESULTS
NNT is largely responsible for the acute glucose-induced rise in islet NADPH/NADP
CONCLUSION
These results drastically modify current views on NNT operation and mitochondrial function in pancreatic β-cells.
DOI: 10.1016/j.molmet.2017.04.004
PubMed: 28580284
PubMed Central: PMC5444111
Affiliations:
- Belgique, Suède, États-Unis
- Province du Brabant wallon, Région wallonne
- Louvain-la-Neuve
- Université catholique de Louvain
Links toward previous steps (curation, corpus...)
Le document en format XML
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Sweet</name><affiliation wicri:level="1"><nlm:affiliation>University of Washington Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, 98195, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>University of Washington Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, 98195</wicri:regionArea><wicri:noRegion>98195</wicri:noRegion></affiliation></author><author><name sortKey="Chae, Heeyoung" sort="Chae, Heeyoung" uniqKey="Chae H" first="Heeyoung" last="Chae">Heeyoung Chae</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author><author><name sortKey="Mulder, Hindrik" sort="Mulder, Hindrik" uniqKey="Mulder H" first="Hindrik" last="Mulder">Hindrik Mulder</name><affiliation wicri:level="1"><nlm:affiliation>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02</wicri:regionArea><wicri:noRegion>205 02</wicri:noRegion></affiliation></author><author><name sortKey="Jonas, Jean Christophe" sort="Jonas, Jean Christophe" uniqKey="Jonas J" first="Jean-Christophe" last="Jonas">Jean-Christophe Jonas</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28580284</idno><idno type="pmid">28580284</idno><idno type="doi">10.1016/j.molmet.2017.04.004</idno><idno type="pmc">PMC5444111</idno><idno type="wicri:Area/Main/Corpus">000335</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000335</idno><idno type="wicri:Area/Main/Curation">000335</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000335</idno><idno type="wicri:Area/Main/Exploration">000335</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic β-cells.</title><author><name sortKey="Santos, Laila R B" sort="Santos, Laila R B" uniqKey="Santos L" first="Laila R B" last="Santos">Laila R B. Santos</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author><author><name sortKey="Muller, Carole" sort="Muller, Carole" uniqKey="Muller C" first="Carole" last="Muller">Carole Muller</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author><author><name sortKey="De Souza, Arnaldo H" sort="De Souza, Arnaldo H" uniqKey="De Souza A" first="Arnaldo H" last="De Souza">Arnaldo H. De Souza</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author><author><name sortKey="Takahashi, Hilton K" sort="Takahashi, Hilton K" uniqKey="Takahashi H" first="Hilton K" last="Takahashi">Hilton K. Takahashi</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author><author><name sortKey="Spegel, Peter" sort="Spegel, Peter" uniqKey="Spegel P" first="Peter" last="Spégel">Peter Spégel</name><affiliation wicri:level="1"><nlm:affiliation>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02</wicri:regionArea><wicri:noRegion>205 02</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Lund University, Department of Chemistry, Centre for Analysis and Synthesis, Lund, 221 00, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Lund University, Department of Chemistry, Centre for Analysis and Synthesis, Lund, 221 00</wicri:regionArea><wicri:noRegion>221 00</wicri:noRegion></affiliation></author><author><name sortKey="Sweet, Ian R" sort="Sweet, Ian R" uniqKey="Sweet I" first="Ian R" last="Sweet">Ian R. Sweet</name><affiliation wicri:level="1"><nlm:affiliation>University of Washington Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, 98195, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>University of Washington Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, 98195</wicri:regionArea><wicri:noRegion>98195</wicri:noRegion></affiliation></author><author><name sortKey="Chae, Heeyoung" sort="Chae, Heeyoung" uniqKey="Chae H" first="Heeyoung" last="Chae">Heeyoung Chae</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author><author><name sortKey="Mulder, Hindrik" sort="Mulder, Hindrik" uniqKey="Mulder H" first="Hindrik" last="Mulder">Hindrik Mulder</name><affiliation wicri:level="1"><nlm:affiliation>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02</wicri:regionArea><wicri:noRegion>205 02</wicri:noRegion></affiliation></author><author><name sortKey="Jonas, Jean Christophe" sort="Jonas, Jean Christophe" uniqKey="Jonas J" first="Jean-Christophe" last="Jonas">Jean-Christophe Jonas</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</nlm:affiliation><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200</wicri:regionArea><orgName type="university">Université catholique de Louvain</orgName><placeName><settlement type="city">Louvain-la-Neuve</settlement><region type="region" nuts="1">Région wallonne</region><region type="province" nuts="1">Province du Brabant wallon</region></placeName></affiliation></author></analytic><series><title level="j">Molecular metabolism</title><idno type="eISSN">2212-8778</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Calcium (metabolism)</term><term>Cells, Cultured (MeSH)</term><term>Exocytosis (MeSH)</term><term>Female (MeSH)</term><term>Glucose (metabolism)</term><term>Glutathione (metabolism)</term><term>Insulin (metabolism)</term><term>Insulin-Secreting Cells (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mitochondrial Proteins (genetics)</term><term>Mitochondrial Proteins (metabolism)</term><term>NADP (metabolism)</term><term>NADP Transhydrogenase, AB-Specific (genetics)</term><term>NADP Transhydrogenase, AB-Specific (metabolism)</term><term>Oxidation-Reduction (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Calcium (métabolisme)</term><term>Cellules cultivées (MeSH)</term><term>Cellules à insuline (métabolisme)</term><term>Exocytose (MeSH)</term><term>Femelle (MeSH)</term><term>Glucose (métabolisme)</term><term>Glutathion (métabolisme)</term><term>Insuline (métabolisme)</term><term>NADP (métabolisme)</term><term>NADP transhydrogenase, AB-specific (génétique)</term><term>NADP transhydrogenase, AB-specific (métabolisme)</term><term>Oxydoréduction (MeSH)</term><term>Protéines mitochondriales (génétique)</term><term>Protéines mitochondriales (métabolisme)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Mitochondrial Proteins</term><term>NADP Transhydrogenase, AB-Specific</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term><term>Glucose</term><term>Glutathione</term><term>Insulin</term><term>Mitochondrial Proteins</term><term>NADP</term><term>NADP Transhydrogenase, AB-Specific</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>NADP transhydrogenase, AB-specific</term><term>Protéines mitochondriales</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Insulin-Secreting Cells</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Calcium</term><term>Cellules à insuline</term><term>Glucose</term><term>Glutathion</term><term>Insuline</term><term>NADP</term><term>NADP transhydrogenase, AB-specific</term><term>Protéines mitochondriales</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Exocytosis</term><term>Female</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Oxidation-Reduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Exocytose</term><term>Femelle</term><term>Oxydoréduction</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>OBJECTIVE</b></p><p>The glucose stimulation of insulin secretion (GSIS) by pancreatic β-cells critically depends on increased production of metabolic coupling factors, including NADPH. Nicotinamide nucleotide transhydrogenase (NNT) typically produces NADPH at the expense of NADH and ΔpH in energized mitochondria. Its spontaneous inactivation in C57BL/6J mice was previously shown to alter ATP production, Ca</p></div><div type="abstract" xml:lang="en"><p><b>METHODS</b></p><p>Islets were isolated from female C57BL/6J mice (J-islets), which lack functional NNT, and genetically close C57BL/6N mice (N-islets). Wild-type mouse NNT was expressed in J-islets by adenoviral infection. Mitochondrial and cytosolic glutathione oxidation was measured with glutaredoxin 1-fused roGFP2 probes targeted or not to the mitochondrial matrix. NADPH and NADH redox state was measured biochemically. Insulin secretion and upstream coupling events were measured under dynamic or static conditions by standard procedures.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>NNT is largely responsible for the acute glucose-induced rise in islet NADPH/NADP</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSION</b></p><p>These results drastically modify current views on NNT operation and mitochondrial function in pancreatic β-cells.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28580284</PMID><DateCompleted><Year>2018</Year><Month>12</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>12</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">2212-8778</ISSN><JournalIssue CitedMedium="Internet"><Volume>6</Volume><Issue>6</Issue><PubDate><Year>2017</Year><Month>06</Month></PubDate></JournalIssue><Title>Molecular metabolism</Title><ISOAbbreviation>Mol Metab</ISOAbbreviation></Journal><ArticleTitle>NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic β-cells.</ArticleTitle><Pagination><MedlinePgn>535-547</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.molmet.2017.04.004</ELocationID><Abstract><AbstractText Label="OBJECTIVE">The glucose stimulation of insulin secretion (GSIS) by pancreatic β-cells critically depends on increased production of metabolic coupling factors, including NADPH. Nicotinamide nucleotide transhydrogenase (NNT) typically produces NADPH at the expense of NADH and ΔpH in energized mitochondria. Its spontaneous inactivation in C57BL/6J mice was previously shown to alter ATP production, Ca<sup>2+</sup> influx, and GSIS, thereby leading to glucose intolerance. Here, we tested the role of NNT in the glucose regulation of mitochondrial NADPH and glutathione redox state and reinvestigated its role in GSIS coupling events in mouse pancreatic islets.</AbstractText><AbstractText Label="METHODS">Islets were isolated from female C57BL/6J mice (J-islets), which lack functional NNT, and genetically close C57BL/6N mice (N-islets). Wild-type mouse NNT was expressed in J-islets by adenoviral infection. Mitochondrial and cytosolic glutathione oxidation was measured with glutaredoxin 1-fused roGFP2 probes targeted or not to the mitochondrial matrix. NADPH and NADH redox state was measured biochemically. Insulin secretion and upstream coupling events were measured under dynamic or static conditions by standard procedures.</AbstractText><AbstractText Label="RESULTS">NNT is largely responsible for the acute glucose-induced rise in islet NADPH/NADP<sup>+</sup> ratio and decrease in mitochondrial glutathione oxidation, with a small impact on cytosolic glutathione. However, contrary to current views on NNT in β-cells, these effects resulted from a glucose-dependent reduction in NADPH consumption by NNT reverse mode of operation, rather than from a stimulation of its forward mode of operation. Accordingly, the lack of NNT in J-islets decreased their sensitivity to exogenous H<sub>2</sub>O<sub>2</sub> at non-stimulating glucose. Surprisingly, the lack of NNT did not alter the glucose-stimulation of Ca<sup>2+</sup> influx and upstream mitochondrial events, but it markedly reduced both phases of GSIS by altering Ca<sup>2+</sup>-induced exocytosis and its metabolic amplification.</AbstractText><AbstractText Label="CONCLUSION">These results drastically modify current views on NNT operation and mitochondrial function in pancreatic β-cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Santos</LastName><ForeName>Laila R B</ForeName><Initials>LRB</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Muller</LastName><ForeName>Carole</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>de Souza</LastName><ForeName>Arnaldo H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takahashi</LastName><ForeName>Hilton K</ForeName><Initials>HK</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Spégel</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Lund University, Department of Chemistry, Centre for Analysis and Synthesis, Lund, 221 00, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sweet</LastName><ForeName>Ian R</ForeName><Initials>IR</Initials><AffiliationInfo><Affiliation>University of Washington Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, 98195, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chae</LastName><ForeName>Heeyoung</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mulder</LastName><ForeName>Hindrik</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Lund University, Department of Clinical Sciences in Malmö, Unit of Molecular Metabolism, Malmö, 205 02, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jonas</LastName><ForeName>Jean-Christophe</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, B-1200, Belgium.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P30 DK017047</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>04</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Mol Metab</MedlineTA><NlmUniqueID>101605730</NlmUniqueID><ISSNLinking>2212-8778</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D024101">Mitochondrial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>53-59-8</RegistryNumber><NameOfSubstance UI="D009249">NADP</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.6.1.2</RegistryNumber><NameOfSubstance UI="D061087">NADP Transhydrogenase, AB-Specific</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.6.1.2</RegistryNumber><NameOfSubstance UI="C556048">Nnt protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002118" MajorTopicYN="N">Calcium</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005089" MajorTopicYN="N">Exocytosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="N">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024101" MajorTopicYN="N">Mitochondrial Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009249" MajorTopicYN="N">NADP</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D061087" MajorTopicYN="N">NADP Transhydrogenase, AB-Specific</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">AT2, aldrithiol</Keyword><Keyword MajorTopicYN="Y">C57BL/6J mice</Keyword><Keyword MajorTopicYN="Y">C57BL/6N mice</Keyword><Keyword MajorTopicYN="Y">CMV, cytomegalovirus</Keyword><Keyword MajorTopicYN="Y">DTT, dithiotreitol</Keyword><Keyword MajorTopicYN="Y">Dz, diazoxide</Keyword><Keyword MajorTopicYN="Y">FCCP, carbonyl cyanide-p-trifluoromethoxyphenylhydrazone</Keyword><Keyword MajorTopicYN="Y">GRX1, glutaredoxin 1</Keyword><Keyword MajorTopicYN="Y">GRX1-roGFP2</Keyword><Keyword MajorTopicYN="Y">GSIS, glucose stimulation of insulin secretion</Keyword><Keyword MajorTopicYN="Y">Glucose metabolism</Keyword><Keyword MajorTopicYN="Y">IDH, isocitrate dehydrogenase</Keyword><Keyword MajorTopicYN="Y">Insulin secretion</Keyword><Keyword MajorTopicYN="Y">KRB, Krebs solution</Keyword><Keyword MajorTopicYN="Y">ME, malic enzyme</Keyword><Keyword MajorTopicYN="Y">Mitochondrial shuttles</Keyword><Keyword MajorTopicYN="Y">NNT, nicotinamide nucleotide transhydrogenase</Keyword><Keyword MajorTopicYN="Y">OCR, oxygen consumption rate</Keyword><Keyword MajorTopicYN="Y">Pancreatic islet</Keyword><Keyword MajorTopicYN="Y">Redox-sensitive GFP</Keyword><Keyword MajorTopicYN="Y">Stimulus-secretion coupling</Keyword><Keyword MajorTopicYN="Y">WT, 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