NADPH oxidase-2 does not contribute to β-cell glucotoxicity in cultured pancreatic islets from C57BL/6J mice.
Identifieur interne : 000339 ( Main/Exploration ); précédent : 000338; suivant : 000340NADPH oxidase-2 does not contribute to β-cell glucotoxicity in cultured pancreatic islets from C57BL/6J mice.
Auteurs : Arnaldo H. De Souza [Brésil] ; Laila R B. Santos [Belgique] ; Leticia P. Roma [Brésil] ; Mohammed Bensellam [Belgique] ; Angelo R. Carpinelli [Brésil] ; Jean-Christophe Jonas [Belgique]Source :
- Molecular and cellular endocrinology [ 1872-8057 ] ; 2017.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Animaux (MeSH), Apoptose (effets des médicaments et des substances chimiques), Cellules à insuline (anatomopathologie), Cellules à insuline (effets des médicaments et des substances chimiques), Cellules à insuline (enzymologie), Cytosol (métabolisme), Glucose (toxicité), Glutarédoxines (métabolisme), Glutathion (métabolisme), Heme oxygenase-1 (génétique), Heme oxygenase-1 (métabolisme), Insuline (métabolisme), Mâle (MeSH), NADPH Oxidase 2 (déficit), NADPH Oxidase 2 (métabolisme), Oxydoréduction (MeSH), Protéines à fluorescence verte (métabolisme), Souris de lignée C57BL (MeSH), Souris knockout (MeSH), Survie cellulaire (effets des médicaments et des substances chimiques), Sécrétion d'insuline (MeSH), Techniques de culture de tissus (MeSH), Thiols (métabolisme), Transporteur de glucose de type 2 (génétique), Transporteur de glucose de type 2 (métabolisme).
- MESH :
- anatomopathologie : Cellules à insuline.
- déficit : NADPH Oxidase 2.
- effets des médicaments et des substances chimiques : Apoptose, Cellules à insuline, Survie cellulaire.
- enzymologie : Cellules à insuline.
- génétique : ARN messager, Heme oxygenase-1, Transporteur de glucose de type 2.
- métabolisme : ARN messager, Cytosol, Glutarédoxines, Glutathion, Heme oxygenase-1, Insuline, NADPH Oxidase 2, Protéines à fluorescence verte, Thiols, Transporteur de glucose de type 2.
- toxicité : Glucose.
- Animaux, Mâle, Oxydoréduction, Souris de lignée C57BL, Souris knockout, Sécrétion d'insuline, Techniques de culture de tissus.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (drug effects), Cell Survival (drug effects), Cytosol (metabolism), Glucose (toxicity), Glucose Transporter Type 2 (genetics), Glucose Transporter Type 2 (metabolism), Glutaredoxins (metabolism), Glutathione (metabolism), Green Fluorescent Proteins (metabolism), Heme Oxygenase-1 (genetics), Heme Oxygenase-1 (metabolism), Insulin (metabolism), Insulin Secretion (MeSH), Insulin-Secreting Cells (drug effects), Insulin-Secreting Cells (enzymology), Insulin-Secreting Cells (pathology), Male (MeSH), Mice, Inbred C57BL (MeSH), Mice, Knockout (MeSH), NADPH Oxidase 2 (deficiency), NADPH Oxidase 2 (metabolism), Oxidation-Reduction (MeSH), RNA, Messenger (genetics), RNA, Messenger (metabolism), Sulfhydryl Compounds (metabolism), Tissue Culture Techniques (MeSH).
- MESH :
- chemical , deficiency : NADPH Oxidase 2.
- chemical , genetics : Glucose Transporter Type 2, Heme Oxygenase-1, RNA, Messenger.
- chemical , metabolism : Glucose Transporter Type 2, Glutaredoxins, Glutathione, Green Fluorescent Proteins, Heme Oxygenase-1, Insulin, NADPH Oxidase 2, RNA, Messenger, Sulfhydryl Compounds.
- chemical , toxicity : Glucose.
- drug effects : Apoptosis, Cell Survival, Insulin-Secreting Cells.
- enzymology : Insulin-Secreting Cells.
- metabolism : Cytosol.
- pathology : Insulin-Secreting Cells.
- Animals, Insulin Secretion, Male, Mice, Inbred C57BL, Mice, Knockout, Oxidation-Reduction, Tissue Culture Techniques.
Abstract
High glucose-induced oxidative stress and increased NADPH oxidase-2 (NOX2) activity may contribute to the progressive decline of the functional β-cell mass in type 2 diabetes. To test that hypothesis, we characterized, in islets from male NOX2 knockout (NOX2-KO) and wild-type (WT) C57BL/6J mice cultured for up to 3 weeks at 10 or 30 mmol/l glucose (G10 or G30), the in vitro effects of glucose on cytosolic oxidative stress using probes sensing glutathione oxidation (GRX1-roGFP2), thiol oxidation (roGFP1) or H2O2 (roGFP2-Orp1), on β-cell stimulus-secretion coupling events and on β-cell apoptosis. After 1-2 days of culture in G10, the glucose stimulation of insulin secretion (GSIS) was ∼1.7-fold higher in NOX2-KO vs. WT islets at 20-30 mmol/l glucose despite similar rises in NAD(P)H and intracellular calcium concentration ([Ca2+]i) and no differences in cytosolic GRX1-roGFP2 oxidation. After long-term culture at G10, roGFP1 and roGFP2-Orp1 oxidation and β-cell apoptosis remained low, and the glucose-induced rises in NAD(P)H, [Ca2+]i and GSIS were similarly preserved in both islet types. After prolonged culture at G30, roGFP1 and roGFP2-Orp1 oxidation increased in parallel with β-cell apoptosis, the glucose sensitivity of the NADPH, [Ca2+]i and insulin secretion responses increased, the maximal [Ca2+]i response decreased, but maximal GSIS was preserved. These responses were almost identical in both islet types. In conclusion, NOX2 is a negative regulator of maximal GSIS in C57BL/6J mouse islets, but it does not detectably contribute to the in vitro glucotoxic induction of cytosolic oxidative stress and alterations of β-cell survival and function.
DOI: 10.1016/j.mce.2016.09.022
PubMed: 27664519
Affiliations:
- Belgique, Brésil
- Région de Bruxelles-Capitale, État de São Paulo
- Bruxelles, São Paulo
- Université catholique de Louvain, Université de São Paulo
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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, Belgium; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, Belgium; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author><author><name sortKey="Santos, Laila R B" sort="Santos, Laila R B" uniqKey="Santos L" first="Laila R B" last="Santos">Laila R B. 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Roma</name><affiliation wicri:level="4"><nlm:affiliation>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName><orgName type="university">Université de São Paulo</orgName></affiliation></author><author><name sortKey="Bensellam, Mohammed" sort="Bensellam, Mohammed" uniqKey="Bensellam M" first="Mohammed" last="Bensellam">Mohammed Bensellam</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, 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</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author><author><name sortKey="Carpinelli, Angelo R" sort="Carpinelli, Angelo R" uniqKey="Carpinelli A" first="Angelo R" last="Carpinelli">Angelo R. 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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, Belgium; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, Belgium; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author><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, 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</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author><author><name sortKey="Roma, Leticia P" sort="Roma, Leticia P" uniqKey="Roma L" first="Leticia P" last="Roma">Leticia P. Roma</name><affiliation wicri:level="4"><nlm:affiliation>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName><orgName type="university">Université de São Paulo</orgName></affiliation></author><author><name sortKey="Bensellam, Mohammed" sort="Bensellam, Mohammed" uniqKey="Bensellam M" first="Mohammed" last="Bensellam">Mohammed Bensellam</name><affiliation wicri:level="4"><nlm:affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, 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</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author><author><name sortKey="Carpinelli, Angelo R" sort="Carpinelli, Angelo R" uniqKey="Carpinelli A" first="Angelo R" last="Carpinelli">Angelo R. Carpinelli</name><affiliation wicri:level="4"><nlm:affiliation>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo</wicri:regionArea><placeName><settlement type="city">São Paulo</settlement><region type="state">État de São Paulo</region></placeName><orgName type="university">Université de São Paulo</orgName></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, Belgium. Electronic address: jean-christophe.jonas@uclouvain.be.</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</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author></analytic><series><title level="j">Molecular and cellular endocrinology</title><idno type="eISSN">1872-8057</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>Apoptosis (drug effects)</term><term>Cell Survival (drug effects)</term><term>Cytosol (metabolism)</term><term>Glucose (toxicity)</term><term>Glucose Transporter Type 2 (genetics)</term><term>Glucose Transporter Type 2 (metabolism)</term><term>Glutaredoxins (metabolism)</term><term>Glutathione (metabolism)</term><term>Green Fluorescent Proteins (metabolism)</term><term>Heme Oxygenase-1 (genetics)</term><term>Heme Oxygenase-1 (metabolism)</term><term>Insulin (metabolism)</term><term>Insulin Secretion (MeSH)</term><term>Insulin-Secreting Cells (drug effects)</term><term>Insulin-Secreting Cells (enzymology)</term><term>Insulin-Secreting Cells (pathology)</term><term>Male (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>NADPH Oxidase 2 (deficiency)</term><term>NADPH Oxidase 2 (metabolism)</term><term>Oxidation-Reduction (MeSH)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Sulfhydryl Compounds (metabolism)</term><term>Tissue Culture Techniques (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Animaux (MeSH)</term><term>Apoptose (effets des médicaments et des substances chimiques)</term><term>Cellules à insuline (anatomopathologie)</term><term>Cellules à insuline (effets des médicaments et des substances chimiques)</term><term>Cellules à insuline (enzymologie)</term><term>Cytosol (métabolisme)</term><term>Glucose (toxicité)</term><term>Glutarédoxines (métabolisme)</term><term>Glutathion (métabolisme)</term><term>Heme oxygenase-1 (génétique)</term><term>Heme oxygenase-1 (métabolisme)</term><term>Insuline (métabolisme)</term><term>Mâle (MeSH)</term><term>NADPH Oxidase 2 (déficit)</term><term>NADPH Oxidase 2 (métabolisme)</term><term>Oxydoréduction (MeSH)</term><term>Protéines à fluorescence verte (métabolisme)</term><term>Souris de lignée C57BL (MeSH)</term><term>Souris knockout (MeSH)</term><term>Survie cellulaire (effets des médicaments et des substances chimiques)</term><term>Sécrétion d'insuline (MeSH)</term><term>Techniques de culture de tissus (MeSH)</term><term>Thiols (métabolisme)</term><term>Transporteur de glucose de type 2 (génétique)</term><term>Transporteur de glucose de type 2 (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>NADPH Oxidase 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glucose Transporter Type 2</term><term>Heme Oxygenase-1</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glucose Transporter Type 2</term><term>Glutaredoxins</term><term>Glutathione</term><term>Green Fluorescent Proteins</term><term>Heme Oxygenase-1</term><term>Insulin</term><term>NADPH Oxidase 2</term><term>RNA, Messenger</term><term>Sulfhydryl Compounds</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Glucose</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules à insuline</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Cell Survival</term><term>Insulin-Secreting Cells</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>NADPH Oxidase 2</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Cellules à insuline</term><term>Survie cellulaire</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Cellules à insuline</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Insulin-Secreting Cells</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Heme oxygenase-1</term><term>Transporteur de glucose de type 2</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Cytosol</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Cytosol</term><term>Glutarédoxines</term><term>Glutathion</term><term>Heme oxygenase-1</term><term>Insuline</term><term>NADPH Oxidase 2</term><term>Protéines à fluorescence verte</term><term>Thiols</term><term>Transporteur de glucose de type 2</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Insulin-Secreting Cells</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Glucose</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Insulin Secretion</term><term>Male</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Oxidation-Reduction</term><term>Tissue Culture Techniques</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Mâle</term><term>Oxydoréduction</term><term>Souris de lignée C57BL</term><term>Souris knockout</term><term>Sécrétion d'insuline</term><term>Techniques de culture de tissus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">High glucose-induced oxidative stress and increased NADPH oxidase-2 (NOX2) activity may contribute to the progressive decline of the functional β-cell mass in type 2 diabetes. To test that hypothesis, we characterized, in islets from male NOX2 knockout (NOX2-KO) and wild-type (WT) C57BL/6J mice cultured for up to 3 weeks at 10 or 30 mmol/l glucose (G10 or G30), the in vitro effects of glucose on cytosolic oxidative stress using probes sensing glutathione oxidation (GRX1-roGFP2), thiol oxidation (roGFP1) or H<sub>2</sub>O<sub>2</sub> (roGFP2-Orp1), on β-cell stimulus-secretion coupling events and on β-cell apoptosis. After 1-2 days of culture in G10, the glucose stimulation of insulin secretion (GSIS) was ∼1.7-fold higher in NOX2-KO vs. WT islets at 20-30 mmol/l glucose despite similar rises in NAD(P)H and intracellular calcium concentration ([Ca<sup>2+</sup>]<sub>i</sub>) and no differences in cytosolic GRX1-roGFP2 oxidation. After long-term culture at G10, roGFP1 and roGFP2-Orp1 oxidation and β-cell apoptosis remained low, and the glucose-induced rises in NAD(P)H, [Ca<sup>2+</sup>]<sub>i</sub> and GSIS were similarly preserved in both islet types. After prolonged culture at G30, roGFP1 and roGFP2-Orp1 oxidation increased in parallel with β-cell apoptosis, the glucose sensitivity of the NADPH, [Ca<sup>2+</sup>]<sub>i</sub> and insulin secretion responses increased, the maximal [Ca<sup>2+</sup>]<sub>i</sub> response decreased, but maximal GSIS was preserved. These responses were almost identical in both islet types. In conclusion, NOX2 is a negative regulator of maximal GSIS in C57BL/6J mouse islets, but it does not detectably contribute to the in vitro glucotoxic induction of cytosolic oxidative stress and alterations of β-cell survival and function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27664519</PMID><DateCompleted><Year>2017</Year><Month>11</Month><Day>17</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8057</ISSN><JournalIssue CitedMedium="Internet"><Volume>439</Volume><PubDate><Year>2017</Year><Month>01</Month><Day>05</Day></PubDate></JournalIssue><Title>Molecular and cellular endocrinology</Title><ISOAbbreviation>Mol Cell Endocrinol</ISOAbbreviation></Journal><ArticleTitle>NADPH oxidase-2 does not contribute to β-cell glucotoxicity in cultured pancreatic islets from C57BL/6J mice.</ArticleTitle><Pagination><MedlinePgn>354-362</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0303-7207(16)30387-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.mce.2016.09.022</ELocationID><Abstract><AbstractText>High glucose-induced oxidative stress and increased NADPH oxidase-2 (NOX2) activity may contribute to the progressive decline of the functional β-cell mass in type 2 diabetes. To test that hypothesis, we characterized, in islets from male NOX2 knockout (NOX2-KO) and wild-type (WT) C57BL/6J mice cultured for up to 3 weeks at 10 or 30 mmol/l glucose (G10 or G30), the in vitro effects of glucose on cytosolic oxidative stress using probes sensing glutathione oxidation (GRX1-roGFP2), thiol oxidation (roGFP1) or H<sub>2</sub>O<sub>2</sub> (roGFP2-Orp1), on β-cell stimulus-secretion coupling events and on β-cell apoptosis. After 1-2 days of culture in G10, the glucose stimulation of insulin secretion (GSIS) was ∼1.7-fold higher in NOX2-KO vs. WT islets at 20-30 mmol/l glucose despite similar rises in NAD(P)H and intracellular calcium concentration ([Ca<sup>2+</sup>]<sub>i</sub>) and no differences in cytosolic GRX1-roGFP2 oxidation. After long-term culture at G10, roGFP1 and roGFP2-Orp1 oxidation and β-cell apoptosis remained low, and the glucose-induced rises in NAD(P)H, [Ca<sup>2+</sup>]<sub>i</sub> and GSIS were similarly preserved in both islet types. After prolonged culture at G30, roGFP1 and roGFP2-Orp1 oxidation increased in parallel with β-cell apoptosis, the glucose sensitivity of the NADPH, [Ca<sup>2+</sup>]<sub>i</sub> and insulin secretion responses increased, the maximal [Ca<sup>2+</sup>]<sub>i</sub> response decreased, but maximal GSIS was preserved. These responses were almost identical in both islet types. In conclusion, NOX2 is a negative regulator of maximal GSIS in C57BL/6J mouse islets, but it does not detectably contribute to the in vitro glucotoxic induction of cytosolic oxidative stress and alterations of β-cell survival and function.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><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, Belgium; Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><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, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roma</LastName><ForeName>Leticia P</ForeName><Initials>LP</Initials><AffiliationInfo><Affiliation>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bensellam</LastName><ForeName>Mohammed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Université catholique de Louvain, Institute of Experimental and Clinical Research, Pole of Endocrinology, Diabetes and Nutrition, Brussels, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carpinelli</LastName><ForeName>Angelo R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.</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, Belgium. Electronic address: jean-christophe.jonas@uclouvain.be.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>09</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Mol Cell Endocrinol</MedlineTA><NlmUniqueID>7500844</NlmUniqueID><ISSNLinking>0303-7207</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516006">Glrx protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051273">Glucose Transporter Type 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007328">Insulin</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013438">Sulfhydryl Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>147336-22-9</RegistryNumber><NameOfSubstance UI="D049452">Green Fluorescent Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.18</RegistryNumber><NameOfSubstance UI="D051547">Heme Oxygenase-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.6.3.-</RegistryNumber><NameOfSubstance UI="C488842">Cybb protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.6.3.-</RegistryNumber><NameOfSubstance UI="D000074662">NADPH Oxidase 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003600" MajorTopicYN="N">Cytosol</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051273" MajorTopicYN="N">Glucose Transporter Type 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049452" MajorTopicYN="N">Green Fluorescent Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051547" MajorTopicYN="N">Heme Oxygenase-1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000078790" MajorTopicYN="N">Insulin Secretion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050417" MajorTopicYN="N">Insulin-Secreting Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000074662" MajorTopicYN="N">NADPH Oxidase 2</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013438" MajorTopicYN="N">Sulfhydryl Compounds</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D046509" MajorTopicYN="N">Tissue Culture Techniques</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Apoptosis</Keyword><Keyword MajorTopicYN="Y">Insulin secretion</Keyword><Keyword MajorTopicYN="Y">NOX2</Keyword><Keyword MajorTopicYN="Y">Pancreatic β-cell</Keyword><Keyword MajorTopicYN="Y">roGFP sensors</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>04</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>08</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>9</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27664519</ArticleId><ArticleId IdType="pii">S0303-7207(16)30387-2</ArticleId><ArticleId IdType="doi">10.1016/j.mce.2016.09.022</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Belgique</li><li>Brésil</li></country><region><li>Région de Bruxelles-Capitale</li><li>État de São Paulo</li></region><settlement><li>Bruxelles</li><li>São Paulo</li></settlement><orgName><li>Université catholique de Louvain</li><li>Université de São Paulo</li></orgName></list><tree><country name="Brésil"><region name="État de São Paulo"><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></region><name sortKey="Carpinelli, Angelo R" sort="Carpinelli, Angelo R" uniqKey="Carpinelli A" first="Angelo R" last="Carpinelli">Angelo R. Carpinelli</name><name sortKey="Roma, Leticia P" sort="Roma, Leticia P" uniqKey="Roma L" first="Leticia P" last="Roma">Leticia P. Roma</name></country><country name="Belgique"><region name="Région de Bruxelles-Capitale"><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></region><name sortKey="Bensellam, Mohammed" sort="Bensellam, Mohammed" uniqKey="Bensellam M" first="Mohammed" last="Bensellam">Mohammed Bensellam</name><name sortKey="Jonas, Jean Christophe" sort="Jonas, Jean Christophe" uniqKey="Jonas J" first="Jean-Christophe" last="Jonas">Jean-Christophe Jonas</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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