Metformin ameliorates skeletal muscle atrophy in Grx1 KO mice by regulating intramuscular lipid accumulation and glucose utilization.
Identifieur interne : 000047 ( Main/Exploration ); précédent : 000046; suivant : 000048Metformin ameliorates skeletal muscle atrophy in Grx1 KO mice by regulating intramuscular lipid accumulation and glucose utilization.
Auteurs : Yunfei Yang [République populaire de Chine] ; Zhiyin Liao [République populaire de Chine] ; Qian Xiao [République populaire de Chine]Source :
- Biochemical and biophysical research communications [ 1090-2104 ] ; 2020.
Abstract
Skeletal muscle is the largest tissue in the body, and plays a remarkable role in energy and metabolic homeostasis. Disorder in lipid metabolism and glucose utilization could impair the quality and function of skeletal muscle. Glutaredoxin-1 (Grx1) acts as a vital metabolic regulator of redox homeostasis. Recent studies have shown that Grx1 regulates hepatic lipid metabolism. The skeletal muscle also contains abundant Grx1, but the role of Grx1 in skeletal muscle remains unknown. Therefore, we investigated the effect of Grx1 on skeletal muscle. In this study, we found that Grx1-deficient mice (Grx1-/-) spontaneously developed muscle atrophy by 3 months of age. And the p-AMPK activity and Sirt1 activity were inhibited in Grx1-/- mice, which led to intramuscular lipid deposition and glucose utilization disorder in skeletal muscle. However, intraperitoneal injection of metformin for 15 consecutive days ameliorated skeletal muscle atrophy caused by Grx1 deficiency to a certain extent. Taken together, these findings indicate that Grx1 deficiency might induce skeletal muscle atrophy by regulating the intramuscular lipid deposition and glucose utilization, which could be attenuated by metformin. Therefore, the expression or activity of Grx1 may be a pharmacological approach to ameliorate muscle atrophy diseases, such as sarcopenia.
DOI: 10.1016/j.bbrc.2020.09.119
PubMed: 33069361
Affiliations:
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Electronic address: xiaoqian1956@126.com.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016</wicri:regionArea><wicri:noRegion>400016</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical and biophysical research communications</title><idno type="eISSN">1090-2104</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Skeletal muscle is the largest tissue in the body, and plays a remarkable role in energy and metabolic homeostasis. Disorder in lipid metabolism and glucose utilization could impair the quality and function of skeletal muscle. Glutaredoxin-1 (Grx1) acts as a vital metabolic regulator of redox homeostasis. Recent studies have shown that Grx1 regulates hepatic lipid metabolism. The skeletal muscle also contains abundant Grx1, but the role of Grx1 in skeletal muscle remains unknown. Therefore, we investigated the effect of Grx1 on skeletal muscle. In this study, we found that Grx1-deficient mice (Grx1<sup>-/-</sup>) spontaneously developed muscle atrophy by 3 months of age. And the p-AMPK activity and Sirt1 activity were inhibited in Grx1<sup>-/-</sup> mice, which led to intramuscular lipid deposition and glucose utilization disorder in skeletal muscle. However, intraperitoneal injection of metformin for 15 consecutive days ameliorated skeletal muscle atrophy caused by Grx1 deficiency to a certain extent. Taken together, these findings indicate that Grx1 deficiency might induce skeletal muscle atrophy by regulating the intramuscular lipid deposition and glucose utilization, which could be attenuated by metformin. Therefore, the expression or activity of Grx1 may be a pharmacological approach to ameliorate muscle atrophy diseases, such as sarcopenia.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">33069361</PMID><DateRevised><Year>2020</Year><Month>10</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2104</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Oct</Month><Day>14</Day></PubDate></JournalIssue><Title>Biochemical and biophysical research communications</Title><ISOAbbreviation>Biochem Biophys Res Commun</ISOAbbreviation></Journal><ArticleTitle>Metformin ameliorates skeletal muscle atrophy in Grx1 KO mice by regulating intramuscular lipid accumulation and glucose utilization.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0006-291X(20)31872-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbrc.2020.09.119</ELocationID><Abstract><AbstractText>Skeletal muscle is the largest tissue in the body, and plays a remarkable role in energy and metabolic homeostasis. Disorder in lipid metabolism and glucose utilization could impair the quality and function of skeletal muscle. Glutaredoxin-1 (Grx1) acts as a vital metabolic regulator of redox homeostasis. Recent studies have shown that Grx1 regulates hepatic lipid metabolism. The skeletal muscle also contains abundant Grx1, but the role of Grx1 in skeletal muscle remains unknown. Therefore, we investigated the effect of Grx1 on skeletal muscle. In this study, we found that Grx1-deficient mice (Grx1<sup>-/-</sup>) spontaneously developed muscle atrophy by 3 months of age. And the p-AMPK activity and Sirt1 activity were inhibited in Grx1<sup>-/-</sup> mice, which led to intramuscular lipid deposition and glucose utilization disorder in skeletal muscle. However, intraperitoneal injection of metformin for 15 consecutive days ameliorated skeletal muscle atrophy caused by Grx1 deficiency to a certain extent. Taken together, these findings indicate that Grx1 deficiency might induce skeletal muscle atrophy by regulating the intramuscular lipid deposition and glucose utilization, which could be attenuated by metformin. Therefore, the expression or activity of Grx1 may be a pharmacological approach to ameliorate muscle atrophy diseases, such as sarcopenia.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Yunfei</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liao</LastName><ForeName>Zhiyin</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Qian</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. Electronic address: xiaoqian1956@126.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>10</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Biochem Biophys Res Commun</MedlineTA><NlmUniqueID>0372516</NlmUniqueID><ISSNLinking>0006-291X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Glucose utilization</Keyword><Keyword MajorTopicYN="N">Grx1</Keyword><Keyword MajorTopicYN="N">Intramuscular lipid accumulation</Keyword><Keyword MajorTopicYN="N">Muscle atrophy</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare that there are no conflicts of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>09</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>09</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>10</Month><Day>18</Day><Hour>20</Hour><Minute>22</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>10</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33069361</ArticleId><ArticleId IdType="pii">S0006-291X(20)31872-6</ArticleId><ArticleId IdType="doi">10.1016/j.bbrc.2020.09.119</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Yang, Yunfei" sort="Yang, Yunfei" uniqKey="Yang Y" first="Yunfei" last="Yang">Yunfei Yang</name></noRegion><name sortKey="Liao, Zhiyin" sort="Liao, Zhiyin" uniqKey="Liao Z" first="Zhiyin" last="Liao">Zhiyin Liao</name><name sortKey="Xiao, Qian" sort="Xiao, Qian" uniqKey="Xiao Q" first="Qian" last="Xiao">Qian Xiao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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