Deletion of the Glutaredoxin-2 Gene Protects Mice from Diet-Induced Weight Gain, Which Correlates with Increased Mitochondrial Respiration and Proton Leaks in Skeletal Muscle.
Identifieur interne : 000178 ( Main/Exploration ); précédent : 000177; suivant : 000179Deletion of the Glutaredoxin-2 Gene Protects Mice from Diet-Induced Weight Gain, Which Correlates with Increased Mitochondrial Respiration and Proton Leaks in Skeletal Muscle.
Auteurs : Adrian Young [Canada] ; Danielle Gardiner [Canada] ; Nidhi Kuksal [Canada] ; Robert Gill [Canada] ; Marisa O'Brien [Canada] ; Ryan J. Mailloux [Canada]Source :
- Antioxidants & redox signaling [ 1557-7716 ] ; 2019.
Descripteurs français
- KwdFr :
- Alimentation riche en graisse (effets indésirables), Animaux (MeSH), Délétion de gène (MeSH), Femelle (MeSH), Glutarédoxines (déficit), Glutarédoxines (génétique), Glutarédoxines (métabolisme), Mitochondries (métabolisme), Muscles squelettiques (métabolisme), Mâle (MeSH), Prise de poids (effets des médicaments et des substances chimiques), Prise de poids (génétique), Protons (MeSH), Respiration cellulaire (MeSH), Souris (MeSH), Souris knockout (MeSH), Souris transgéniques (MeSH).
- MESH :
- déficit : Glutarédoxines.
- effets des médicaments et des substances chimiques : Prise de poids.
- effets indésirables : Alimentation riche en graisse.
- génétique : Glutarédoxines, Prise de poids.
- métabolisme : Glutarédoxines, Mitochondries, Muscles squelettiques.
- Animaux, Délétion de gène, Femelle, Mâle, Protons, Respiration cellulaire, Souris, Souris knockout, Souris transgéniques.
English descriptors
- KwdEn :
- Animals (MeSH), Cell Respiration (MeSH), Diet, High-Fat (adverse effects), Female (MeSH), Gene Deletion (MeSH), Glutaredoxins (deficiency), Glutaredoxins (genetics), Glutaredoxins (metabolism), Male (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Mice, Transgenic (MeSH), Mitochondria (metabolism), Muscle, Skeletal (metabolism), Protons (MeSH), Weight Gain (drug effects), Weight Gain (genetics).
- MESH :
- chemical , deficiency : Glutaredoxins.
- adverse effects : Diet, High-Fat.
- drug effects : Weight Gain.
- chemical , genetics : Glutaredoxins, Weight Gain.
- chemical , metabolism : Glutaredoxins, Mitochondria, Muscle, Skeletal.
- Animals, Cell Respiration, Female, Gene Deletion, Male, Mice, Mice, Knockout, Mice, Transgenic, Protons.
Abstract
Aims: The aim of this study was to determine whether deleting the gene encoding glutaredoxin-2 (GRX2) could protect mice from diet-induced weight gain. Results: Subjecting wild-type littermates to a high fat diet (HFD) induced a significant increase in overall body mass, white adipose tissue hypertrophy, lipid droplet accumulation in hepatocytes, and higher circulating insulin and triglyceride levels. In contrast, GRX2 heterozygotes (GRX2+/-) fed an HFD had a body mass, white adipose tissue weight, and hepatic and circulating lipid and insulin levels similar to littermates fed a control diet. Examination of the bioenergetics of muscle mitochondria revealed that this protective effect was associated with an increase in respiration and proton leaks. Muscle mitochondria from GRX2+/- mice had a ∼2- to 3-fold increase in state 3 (phosphorylating) respiration when pyruvate/malate or succinate served as substrates and a ∼4-fold increase when palmitoyl-carnitine was being oxidized. Proton leaks were ∼2- to 3-fold higher in GRX2+/- muscle mitochondria. Treatment of mitochondria with either guanosine diphosphate, genipin, or octanoyl-carnitine revealed that the higher rate of O2 consumption under state 4 conditions was associated with increased leaks through uncoupling protein-3 and adenine nucleotide translocase. GRX2+/- mitochondria also had better protection from oxidative distress. Innovation: For the first time, we demonstrate that deleting the Grx2 gene can protect from diet-induced weight gain and the development of obesity-related disorders. Conclusions: Deleting the Grx2 gene protects mice from diet-induced weight gain. This effect was related to an increase in muscle fuel combustion, mitochondrial respiration, proton leaks, and reactive oxygen species handling. Antioxid. Redox Signal. 31, 1272-1288.
DOI: 10.1089/ars.2018.7715
PubMed: 31317766
Affiliations:
Links toward previous steps (curation, corpus...)
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Mailloux</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's</wicri:regionArea><wicri:noRegion>St. John's</wicri:noRegion></affiliation></author></analytic><series><title level="j">Antioxidants & redox signaling</title><idno type="eISSN">1557-7716</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cell Respiration (MeSH)</term><term>Diet, High-Fat (adverse effects)</term><term>Female (MeSH)</term><term>Gene Deletion (MeSH)</term><term>Glutaredoxins (deficiency)</term><term>Glutaredoxins (genetics)</term><term>Glutaredoxins (metabolism)</term><term>Male (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Mice, Transgenic (MeSH)</term><term>Mitochondria (metabolism)</term><term>Muscle, Skeletal (metabolism)</term><term>Protons (MeSH)</term><term>Weight Gain (drug effects)</term><term>Weight Gain (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Alimentation riche en graisse (effets indésirables)</term><term>Animaux (MeSH)</term><term>Délétion de gène (MeSH)</term><term>Femelle (MeSH)</term><term>Glutarédoxines (déficit)</term><term>Glutarédoxines (génétique)</term><term>Glutarédoxines (métabolisme)</term><term>Mitochondries (métabolisme)</term><term>Muscles squelettiques (métabolisme)</term><term>Mâle (MeSH)</term><term>Prise de poids (effets des médicaments et des substances chimiques)</term><term>Prise de poids (génétique)</term><term>Protons (MeSH)</term><term>Respiration cellulaire (MeSH)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Souris transgéniques (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutaredoxins</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Diet, High-Fat</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Weight Gain</term></keywords><keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Glutarédoxines</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Prise de poids</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Alimentation riche en graisse</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glutaredoxins</term><term>Weight Gain</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Glutarédoxines</term><term>Prise de poids</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutaredoxins</term><term>Mitochondria</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutarédoxines</term><term>Mitochondries</term><term>Muscles squelettiques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Respiration</term><term>Female</term><term>Gene Deletion</term><term>Male</term><term>Mice</term><term>Mice, Knockout</term><term>Mice, Transgenic</term><term>Protons</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Délétion de gène</term><term>Femelle</term><term>Mâle</term><term>Protons</term><term>Respiration cellulaire</term><term>Souris</term><term>Souris knockout</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><b><i>Aims:</i></b> The aim of this study was to determine whether deleting the gene encoding glutaredoxin-2 (GRX2) could protect mice from diet-induced weight gain. <b><i>Results:</i></b> Subjecting wild-type littermates to a high fat diet (HFD) induced a significant increase in overall body mass, white adipose tissue hypertrophy, lipid droplet accumulation in hepatocytes, and higher circulating insulin and triglyceride levels. In contrast, GRX2 heterozygotes (GRX2<sup>+/-</sup>) fed an HFD had a body mass, white adipose tissue weight, and hepatic and circulating lipid and insulin levels similar to littermates fed a control diet. Examination of the bioenergetics of muscle mitochondria revealed that this protective effect was associated with an increase in respiration and proton leaks. Muscle mitochondria from GRX2<sup>+/-</sup> mice had a ∼2- to 3-fold increase in state 3 (phosphorylating) respiration when pyruvate/malate or succinate served as substrates and a ∼4-fold increase when palmitoyl-carnitine was being oxidized. Proton leaks were ∼2- to 3-fold higher in GRX2<sup>+/-</sup> muscle mitochondria. Treatment of mitochondria with either guanosine diphosphate, genipin, or octanoyl-carnitine revealed that the higher rate of O<sub>2</sub> consumption under state 4 conditions was associated with increased leaks through uncoupling protein-3 and adenine nucleotide translocase. GRX2<sup>+/-</sup> mitochondria also had better protection from oxidative distress. <b><i>Innovation:</i></b> For the first time, we demonstrate that deleting the <i>Grx2</i> gene can protect from diet-induced weight gain and the development of obesity-related disorders. <b><i>Conclusions:</i></b> Deleting the <i>Grx2</i> gene protects mice from diet-induced weight gain. This effect was related to an increase in muscle fuel combustion, mitochondrial respiration, proton leaks, and reactive oxygen species handling. <i>Antioxid. Redox Signal.</i> 31, 1272-1288.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31317766</PMID><DateCompleted><Year>2020</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1557-7716</ISSN><JournalIssue CitedMedium="Internet"><Volume>31</Volume><Issue>17</Issue><PubDate><Year>2019</Year><Month>12</Month></PubDate></JournalIssue><Title>Antioxidants & redox signaling</Title><ISOAbbreviation>Antioxid Redox Signal</ISOAbbreviation></Journal><ArticleTitle>Deletion of the Glutaredoxin-2 Gene Protects Mice from Diet-Induced Weight Gain, Which Correlates with Increased Mitochondrial Respiration and Proton Leaks in Skeletal Muscle.</ArticleTitle><Pagination><MedlinePgn>1272-1288</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1089/ars.2018.7715</ELocationID><Abstract><AbstractText><b><i>Aims:</i></b> The aim of this study was to determine whether deleting the gene encoding glutaredoxin-2 (GRX2) could protect mice from diet-induced weight gain. <b><i>Results:</i></b> Subjecting wild-type littermates to a high fat diet (HFD) induced a significant increase in overall body mass, white adipose tissue hypertrophy, lipid droplet accumulation in hepatocytes, and higher circulating insulin and triglyceride levels. In contrast, GRX2 heterozygotes (GRX2<sup>+/-</sup>) fed an HFD had a body mass, white adipose tissue weight, and hepatic and circulating lipid and insulin levels similar to littermates fed a control diet. Examination of the bioenergetics of muscle mitochondria revealed that this protective effect was associated with an increase in respiration and proton leaks. Muscle mitochondria from GRX2<sup>+/-</sup> mice had a ∼2- to 3-fold increase in state 3 (phosphorylating) respiration when pyruvate/malate or succinate served as substrates and a ∼4-fold increase when palmitoyl-carnitine was being oxidized. Proton leaks were ∼2- to 3-fold higher in GRX2<sup>+/-</sup> muscle mitochondria. Treatment of mitochondria with either guanosine diphosphate, genipin, or octanoyl-carnitine revealed that the higher rate of O<sub>2</sub> consumption under state 4 conditions was associated with increased leaks through uncoupling protein-3 and adenine nucleotide translocase. GRX2<sup>+/-</sup> mitochondria also had better protection from oxidative distress. <b><i>Innovation:</i></b> For the first time, we demonstrate that deleting the <i>Grx2</i> gene can protect from diet-induced weight gain and the development of obesity-related disorders. <b><i>Conclusions:</i></b> Deleting the <i>Grx2</i> gene protects mice from diet-induced weight gain. This effect was related to an increase in muscle fuel combustion, mitochondrial respiration, proton leaks, and reactive oxygen species handling. <i>Antioxid. Redox Signal.</i> 31, 1272-1288.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Young</LastName><ForeName>Adrian</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gardiner</LastName><ForeName>Danielle</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuksal</LastName><ForeName>Nidhi</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gill</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>O'Brien</LastName><ForeName>Marisa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mailloux</LastName><ForeName>Ryan J</ForeName><Initials>RJ</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Faculty of Science, Memorial University of Newfoundland, St. John's, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>08</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Antioxid Redox Signal</MedlineTA><NlmUniqueID>100888899</NlmUniqueID><ISSNLinking>1523-0864</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516009">Glrx2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011522">Protons</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019069" MajorTopicYN="Y">Cell Respiration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017353" MajorTopicYN="N">Gene Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="N">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011522" MajorTopicYN="Y">Protons</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015430" MajorTopicYN="N">Weight Gain</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">fuel metabolism</Keyword><Keyword MajorTopicYN="Y">glutaredoxin-2</Keyword><Keyword MajorTopicYN="Y">mitochondria</Keyword><Keyword MajorTopicYN="Y">obesity</Keyword><Keyword MajorTopicYN="Y">reactive oxygen species</Keyword><Keyword MajorTopicYN="Y">respiration</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>7</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>7</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31317766</ArticleId><ArticleId IdType="doi">10.1089/ars.2018.7715</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Young, Adrian" sort="Young, Adrian" uniqKey="Young A" first="Adrian" last="Young">Adrian Young</name></noRegion><name sortKey="Gardiner, Danielle" sort="Gardiner, Danielle" uniqKey="Gardiner D" first="Danielle" last="Gardiner">Danielle Gardiner</name><name sortKey="Gill, Robert" sort="Gill, Robert" uniqKey="Gill R" first="Robert" last="Gill">Robert Gill</name><name sortKey="Kuksal, Nidhi" sort="Kuksal, Nidhi" uniqKey="Kuksal N" first="Nidhi" last="Kuksal">Nidhi Kuksal</name><name sortKey="Mailloux, Ryan J" sort="Mailloux, Ryan J" uniqKey="Mailloux R" first="Ryan J" last="Mailloux">Ryan J. Mailloux</name><name sortKey="O Brien, Marisa" sort="O Brien, Marisa" uniqKey="O Brien M" first="Marisa" last="O'Brien">Marisa O'Brien</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:31317766" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a GlutaredoxinV1
| This area was generated with Dilib version V0.6.37. |  |