Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue
Identifieur interne : 000A86 ( Ncbi/Merge ); précédent : 000A85; suivant : 000A87Arsenite 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
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<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>
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<journal-title-group><journal-title>Scientific Reports</journal-title>
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<article-id pub-id-type="publisher-id">50965</article-id>
<article-id pub-id-type="doi">10.1038/s41598-019-50965-9</article-id>
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<title-group><article-title>Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue</article-title>
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<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</aff>
<aff id="Aff4"><label>4</label>
<institution-wrap><institution-id institution-id-type="ISNI">0000 0001 0666 4105</institution-id>
<institution-id institution-id-type="GRID">grid.266813.8</institution-id>
<institution>College of Medicine,</institution>
<institution>University of Nebraska Medical Center,</institution>
</institution-wrap>
Omaha, NE 68198 USA</aff>
<aff id="Aff5"><label>5</label>
<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</aff>
</contrib-group>
<pub-date pub-type="epub"><day>8</day>
<month>10</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>8</day>
<month>10</month>
<year>2019</year>
</pub-date>
<pub-date pub-type="collection"><year>2019</year>
</pub-date>
<volume>9</volume>
<elocation-id>14464</elocation-id>
<history><date date-type="received"><day>11</day>
<month>2</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>20</day>
<month>9</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© The Author(s) 2019</copyright-statement>
<license license-type="OpenAccess"><license-p><bold>Open Access</bold>
This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
.</license-p>
</license>
</permissions>
<abstract id="Abs1"><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>
</abstract>
<kwd-group kwd-group-type="npg-subject"><title>Subject terms</title>
<kwd>Mechanisms of disease</kwd>
<kwd>Diseases</kwd>
</kwd-group>
<funding-group><award-group><funding-source><institution-wrap><institution-id institution-id-type="FundRef">https://doi.org/10.13039/100008114</institution-id>
<institution>University of Nebraska-Lincoln (UNL)</institution>
</institution-wrap>
</funding-source>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution>Undergraduate Creative Activities and Research Experience (UCARE) program-scholarship from the Pepsi Quasi Endowment and Union Bank & Trust</institution>
</funding-source>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution>Undergraduate Creative Activities and Research Experience (UCARE) program-scholarship from the Pepsi Quasi Endowment and Union Bank & Trust</institution>
</funding-source>
</award-group>
</funding-group>
<funding-group><award-group><funding-source><institution>University of Nebraska ARD/ORED/BIOC grants, Layman awards, Nebraska Tobacco Settlement-Biomedical research enhancement funds and Nebraska Center for the Prevention of Obesity Diseases (NPOD) seed grant from NIH (P20GM104320)</institution>
</funding-source>
</award-group>
</funding-group>
<custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name>
<meta-value>© The Author(s) 2019</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<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>
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