Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue
Identifieur interne : 000A62 ( Main/Exploration ); précédent : 000A61; suivant : 000A63Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue
Auteurs : Jiyoung Bae [États-Unis] ; Yura Jang [États-Unis] ; Heejeong Kim [États-Unis] ; Kalika Mahato [États-Unis] ; Cameron Schaecher [États-Unis] ; Isaac M. Kim [États-Unis] ; Eunju Kim [États-Unis] ; Seung-Hyun Ro [États-Unis]Source :
- Scientific Reports [ 2045-2322 ] ; 2019.
Abstract
Arsenite, a trivalent form of arsenic, is an element that occurs naturally in the environment. Humans are exposed to high dose of arsenite through consuming arsenite-contaminated drinking water and food, and the arsenite can accumulate in the human tissues. Arsenite induces oxidative stress, which is linked to metabolic disorders such as obesity and diabetes. Brown adipocytes dissipating energy as heat have emerging roles for obesity treatment and prevention. Therefore, understanding the pathophysiological role of brown adipocytes can provide effective strategies delineating the link between arsenite exposure and metabolic disorders. Our study revealed that arsenite significantly reduced differentiation of murine brown adipocytes and mitochondrial biogenesis and respiration, leading to attenuated thermogenesis via decreasing UCP1 expression. Oral administration of arsenite in mice resulted in heavy accumulation in brown adipose tissue and suppression of lipogenesis, mitochondrial biogenesis and thermogenesis. Mechanistically, arsenite exposure significantly inhibited autophagy necessary for homeostasis of brown adipose tissue through suppression of Sestrin2 and ULK1. These results clearly confirm the emerging mechanisms underlying the implications of arsenite exposure in metabolic disorders.
Url:
DOI: 10.1038/s41598-019-50965-9
PubMed: 31594991
PubMed Central: 6783448
Affiliations:
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Nebraska,</institution></institution-wrap>Lincoln, NE 68588 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nebraska</region></placeName><wicri:cityArea>Lincoln</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0001 2171 9311</institution-id><institution-id institution-id-type="GRID">grid.21107.35</institution-id><institution>Department of Neurology,</institution><institution>The Johns Hopkins University School of Medicine,</institution></institution-wrap>Baltimore, MD 21205 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Kim, Heejeong" sort="Kim, Heejeong" uniqKey="Kim H" first="Heejeong" last="Kim">Heejeong Kim</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id 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Kim</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0060</institution-id><institution-id institution-id-type="GRID">grid.24434.35</institution-id><institution>Department of Biochemistry,</institution><institution>University of Nebraska,</institution></institution-wrap>Lincoln, NE 68588 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nebraska</region></placeName><wicri:cityArea>Lincoln</wicri:cityArea></affiliation></author><author><name sortKey="Kim, Eunju" sort="Kim, Eunju" uniqKey="Kim E" first="Eunju" last="Kim">Eunju Kim</name><affiliation wicri:level="2"><nlm:aff id="Aff5"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0060</institution-id><institution-id institution-id-type="GRID">grid.24434.35</institution-id><institution>Department of Mechanical and Materials Engineering,</institution><institution>University of Nebraska,</institution></institution-wrap>Lincoln, NE 68588 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nebraska</region></placeName><wicri:cityArea>Lincoln</wicri:cityArea></affiliation></author><author><name sortKey="Ro, Seung Hyun" sort="Ro, Seung Hyun" uniqKey="Ro S" first="Seung-Hyun" last="Ro">Seung-Hyun Ro</name><affiliation wicri:level="2"><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1937 0060</institution-id><institution-id institution-id-type="GRID">grid.24434.35</institution-id><institution>Department of Biochemistry,</institution><institution>University of Nebraska,</institution></institution-wrap>Lincoln, NE 68588 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Nebraska</region></placeName><wicri:cityArea>Lincoln</wicri:cityArea></affiliation></author></analytic><series><title level="j">Scientific Reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Arsenite, a trivalent form of arsenic, is an element that occurs naturally in the environment. Humans are exposed to high dose of arsenite through consuming arsenite-contaminated drinking water and food, and the arsenite can accumulate in the human tissues. Arsenite induces oxidative stress, which is linked to metabolic disorders such as obesity and diabetes. Brown adipocytes dissipating energy as heat have emerging roles for obesity treatment and prevention. Therefore, understanding the pathophysiological role of brown adipocytes can provide effective strategies delineating the link between arsenite exposure and metabolic disorders. Our study revealed that arsenite significantly reduced differentiation of murine brown adipocytes and mitochondrial biogenesis and respiration, leading to attenuated thermogenesis via decreasing UCP1 expression. Oral administration of arsenite in mice resulted in heavy accumulation in brown adipose tissue and suppression of lipogenesis, mitochondrial biogenesis and thermogenesis. Mechanistically, arsenite exposure significantly inhibited autophagy necessary for homeostasis of brown adipose tissue through suppression of Sestrin2 and ULK1. These results clearly confirm the emerging mechanisms underlying the implications of arsenite exposure in metabolic disorders.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Shigetoh, Y" uniqKey="Shigetoh Y">Y Shigetoh</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Re, Rn" uniqKey="Re R">RN Re</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Apovian, Cm" uniqKey="Apovian C">CM Apovian</name></author><author><name sortKey="Gokce, N" uniqKey="Gokce N">N Gokce</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Basen Engquist, K" uniqKey="Basen Engquist K">K Basen-Engquist</name></author><author><name sortKey="Chang, M" uniqKey="Chang M">M Chang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, Yh" uniqKey="Lee Y">YH Lee</name></author><author><name sortKey="Mottillo, Ep" uniqKey="Mottillo 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Rodriguez</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li><li>Nebraska</li><li>Wisconsin</li></region></list><tree><country name="États-Unis"><region name="Nebraska"><name sortKey="Bae, Jiyoung" sort="Bae, Jiyoung" uniqKey="Bae J" first="Jiyoung" last="Bae">Jiyoung Bae</name></region><name sortKey="Bae, Jiyoung" sort="Bae, Jiyoung" uniqKey="Bae J" first="Jiyoung" last="Bae">Jiyoung Bae</name><name sortKey="Jang, Yura" sort="Jang, Yura" uniqKey="Jang Y" first="Yura" last="Jang">Yura Jang</name><name sortKey="Jang, Yura" sort="Jang, Yura" uniqKey="Jang Y" first="Yura" last="Jang">Yura Jang</name><name sortKey="Kim, Eunju" sort="Kim, Eunju" uniqKey="Kim E" first="Eunju" last="Kim">Eunju Kim</name><name sortKey="Kim, Heejeong" sort="Kim, Heejeong" uniqKey="Kim H" first="Heejeong" last="Kim">Heejeong Kim</name><name sortKey="Kim, Isaac M" sort="Kim, Isaac M" uniqKey="Kim I" first="Isaac M." last="Kim">Isaac M. Kim</name><name sortKey="Mahato, Kalika" sort="Mahato, Kalika" uniqKey="Mahato K" first="Kalika" last="Mahato">Kalika Mahato</name><name sortKey="Ro, Seung Hyun" sort="Ro, Seung Hyun" uniqKey="Ro S" first="Seung-Hyun" last="Ro">Seung-Hyun Ro</name><name sortKey="Schaecher, Cameron" sort="Schaecher, Cameron" uniqKey="Schaecher C" first="Cameron" last="Schaecher">Cameron Schaecher</name><name sortKey="Schaecher, Cameron" sort="Schaecher, Cameron" uniqKey="Schaecher C" first="Cameron" last="Schaecher">Cameron Schaecher</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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