Impaired mitochondrial medium-chain fatty acid oxidation drives periportal macrovesicular steatosis in sirtuin-5 knockout mice
Medium-chain triglycerides (MCT), containing C 8 –C 12 fatty acids, are used to treat several pediatric disorders and are widely consumed as a nutritional supplement. Here, we investigated the role of the sirtuin deacylase Sirt5 in MCT metabolism by feeding Sirt5 knockout mice (Sirt5KO) high-fat die...
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| creator | Goetzman, Eric S. Bharathi, Sivakama S. Zhang, Yuxun Zhao, Xue-Jun Dobrowolski, Steven F. Peasley, Kevin Sims-Lucas, Sunder Monga, Satdarshan P. |
| description | Medium-chain triglycerides (MCT), containing C
8
–C
12
fatty acids, are used to treat several pediatric disorders and are widely consumed as a nutritional supplement. Here, we investigated the role of the sirtuin deacylase Sirt5 in MCT metabolism by feeding Sirt5 knockout mice (Sirt5KO) high-fat diets containing either C
8
/C
10
fatty acids or coconut oil, which is rich in C
12
, for five weeks. Coconut oil, but not C
8
/C
10
feeding, induced periportal macrovesicular steatosis in Sirt5KO mice.
14
C–C
12
degradation was significantly reduced in Sirt5KO liver. This decrease was localized to the mitochondrial β-oxidation pathway, as Sirt5KO mice exhibited no change in peroxisomal C
12
β-oxidation. Endoplasmic reticulum ω-oxidation, a minor fatty acid degradation pathway known to be stimulated by C
12
accumulation, was increased in Sirt5KO liver. Mice lacking another mitochondrial C
12
oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macrovesicular steatosis when fed coconut oil, confirming that defective mitochondrial C
12
oxidation is sufficient to induce the steatosis phenotype. Sirt5KO liver exhibited normal LCAD activity but reduced mitochondrial acyl-CoA synthetase activity with C
12
. These studies reveal a role for Sirt5 in regulating the hepatic response to MCT and may shed light into the pathogenesis of periportal steatosis, a hallmark of human pediatric non-alcoholic fatty liver disease. |
| doi_str_mv | 10.1038/s41598-020-75615-3 |
| format | Article |
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8
–C
12
fatty acids, are used to treat several pediatric disorders and are widely consumed as a nutritional supplement. Here, we investigated the role of the sirtuin deacylase Sirt5 in MCT metabolism by feeding Sirt5 knockout mice (Sirt5KO) high-fat diets containing either C
8
/C
10
fatty acids or coconut oil, which is rich in C
12
, for five weeks. Coconut oil, but not C
8
/C
10
feeding, induced periportal macrovesicular steatosis in Sirt5KO mice.
14
C–C
12
degradation was significantly reduced in Sirt5KO liver. This decrease was localized to the mitochondrial β-oxidation pathway, as Sirt5KO mice exhibited no change in peroxisomal C
12
β-oxidation. Endoplasmic reticulum ω-oxidation, a minor fatty acid degradation pathway known to be stimulated by C
12
accumulation, was increased in Sirt5KO liver. Mice lacking another mitochondrial C
12
oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macrovesicular steatosis when fed coconut oil, confirming that defective mitochondrial C
12
oxidation is sufficient to induce the steatosis phenotype. Sirt5KO liver exhibited normal LCAD activity but reduced mitochondrial acyl-CoA synthetase activity with C
12
. These studies reveal a role for Sirt5 in regulating the hepatic response to MCT and may shed light into the pathogenesis of periportal steatosis, a hallmark of human pediatric non-alcoholic fatty liver disease.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-020-75615-3</identifier><identifier>PMID: 33110171</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/443 ; 631/45 ; 692/4017 ; Acyl-CoA dehydrogenase ; Acyl-CoA Dehydrogenase, Long-Chain - metabolism ; Animals ; Coconut oil ; Coconut Oil - administration & dosage ; Dietary Fats - administration & dosage ; Endoplasmic reticulum ; Fatty acids ; Fatty Acids - metabolism ; Fatty liver ; Female ; High fat diet ; Humanities and Social Sciences ; Liver ; Liver diseases ; Male ; Mice ; Mice, Knockout ; Mitochondria ; Mitochondria, Liver - metabolism ; multidisciplinary ; Non-alcoholic Fatty Liver Disease - genetics ; Non-alcoholic Fatty Liver Disease - metabolism ; Oxidation ; Oxidation-Reduction ; Pediatrics ; Phenotypes ; Science ; Science (multidisciplinary) ; Sirtuins - genetics ; Steatosis ; Triglycerides ; Triglycerides - metabolism</subject><ispartof>Scientific reports, 2020-10, Vol.10 (1), p.18367-18367, Article 18367</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-4e621a776667b300fa779e9b7c13070c53eb042e183bd3056559de2321cca8a13</citedby><cites>FETCH-LOGICAL-c577t-4e621a776667b300fa779e9b7c13070c53eb042e183bd3056559de2321cca8a13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7591893/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7591893/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,41119,42188,51575,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33110171$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Goetzman, Eric S.</creatorcontrib><creatorcontrib>Bharathi, Sivakama S.</creatorcontrib><creatorcontrib>Zhang, Yuxun</creatorcontrib><creatorcontrib>Zhao, Xue-Jun</creatorcontrib><creatorcontrib>Dobrowolski, Steven F.</creatorcontrib><creatorcontrib>Peasley, Kevin</creatorcontrib><creatorcontrib>Sims-Lucas, Sunder</creatorcontrib><creatorcontrib>Monga, Satdarshan P.</creatorcontrib><title>Impaired mitochondrial medium-chain fatty acid oxidation drives periportal macrovesicular steatosis in sirtuin-5 knockout mice</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Medium-chain triglycerides (MCT), containing C
8
–C
12
fatty acids, are used to treat several pediatric disorders and are widely consumed as a nutritional supplement. Here, we investigated the role of the sirtuin deacylase Sirt5 in MCT metabolism by feeding Sirt5 knockout mice (Sirt5KO) high-fat diets containing either C
8
/C
10
fatty acids or coconut oil, which is rich in C
12
, for five weeks. Coconut oil, but not C
8
/C
10
feeding, induced periportal macrovesicular steatosis in Sirt5KO mice.
14
C–C
12
degradation was significantly reduced in Sirt5KO liver. This decrease was localized to the mitochondrial β-oxidation pathway, as Sirt5KO mice exhibited no change in peroxisomal C
12
β-oxidation. Endoplasmic reticulum ω-oxidation, a minor fatty acid degradation pathway known to be stimulated by C
12
accumulation, was increased in Sirt5KO liver. Mice lacking another mitochondrial C
12
oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macrovesicular steatosis when fed coconut oil, confirming that defective mitochondrial C
12
oxidation is sufficient to induce the steatosis phenotype. Sirt5KO liver exhibited normal LCAD activity but reduced mitochondrial acyl-CoA synthetase activity with C
12
. These studies reveal a role for Sirt5 in regulating the hepatic response to MCT and may shed light into the pathogenesis of periportal steatosis, a hallmark of human pediatric non-alcoholic fatty liver disease.</description><subject>631/443</subject><subject>631/45</subject><subject>692/4017</subject><subject>Acyl-CoA dehydrogenase</subject><subject>Acyl-CoA Dehydrogenase, Long-Chain - metabolism</subject><subject>Animals</subject><subject>Coconut oil</subject><subject>Coconut Oil - administration & dosage</subject><subject>Dietary Fats - administration & dosage</subject><subject>Endoplasmic reticulum</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty liver</subject><subject>Female</subject><subject>High fat diet</subject><subject>Humanities and Social Sciences</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mitochondria</subject><subject>Mitochondria, Liver - metabolism</subject><subject>multidisciplinary</subject><subject>Non-alcoholic Fatty Liver Disease - genetics</subject><subject>Non-alcoholic Fatty Liver Disease - metabolism</subject><subject>Oxidation</subject><subject>Oxidation-Reduction</subject><subject>Pediatrics</subject><subject>Phenotypes</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Sirtuins - genetics</subject><subject>Steatosis</subject><subject>Triglycerides</subject><subject>Triglycerides - metabolism</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9UU1v1DAQtRCIVkv_AAdkiQsXgz_iOLkgoYqWSpW4wNlynNmu28QOtlPRC7-dWbaUwgFfPJp582bePEJeCv5WcNW9K43Qfce45MzoVmimnpBjyRvNpJLy6aP4iJyUcs3xadk3on9OjpQSggsjjsmPi3lxIcNI51CT36U45uAmOsMY1pn5nQuRbl2td9T5MNL0PYyuhhQp4m6h0AVyWFKu-x7nc8Jc8OvkMi0VXE0lFIoUJeS6hsg0vYnJ36S14kAPL8izrZsKnNz_G_L17OOX00_s8vP5xemHS-a1MZU10ErhjGnb1gyK8y3GPfSD8UJxw71WMPBGgujUMCquW637EVC88N51TqgNeX_gXdYBpXmINbvJLjnMLt_Z5IL9uxLDzl6lW2t0L7peIcGbe4Kcvq1Qqp1D8TBNLkJai5WN1nhQhRtsyOt_oNdpzRHlIcoILU3PDaLkAYU3KyXD9mEZwe3eYXtw2KLD9pfDdr_Fq8cyHlp--4kAdQAULMUryH9m_4f2J6Cds88</recordid><startdate>20201027</startdate><enddate>20201027</enddate><creator>Goetzman, Eric S.</creator><creator>Bharathi, Sivakama S.</creator><creator>Zhang, Yuxun</creator><creator>Zhao, Xue-Jun</creator><creator>Dobrowolski, Steven F.</creator><creator>Peasley, Kevin</creator><creator>Sims-Lucas, Sunder</creator><creator>Monga, Satdarshan P.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20201027</creationdate><title>Impaired mitochondrial medium-chain fatty acid oxidation drives periportal macrovesicular steatosis in sirtuin-5 knockout mice</title><author>Goetzman, Eric S. ; Bharathi, Sivakama S. ; Zhang, Yuxun ; Zhao, Xue-Jun ; Dobrowolski, Steven F. ; Peasley, Kevin ; Sims-Lucas, Sunder ; Monga, Satdarshan P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-4e621a776667b300fa779e9b7c13070c53eb042e183bd3056559de2321cca8a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>631/443</topic><topic>631/45</topic><topic>692/4017</topic><topic>Acyl-CoA dehydrogenase</topic><topic>Acyl-CoA Dehydrogenase, Long-Chain - metabolism</topic><topic>Animals</topic><topic>Coconut oil</topic><topic>Coconut Oil - administration & dosage</topic><topic>Dietary Fats - administration & dosage</topic><topic>Endoplasmic reticulum</topic><topic>Fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty liver</topic><topic>Female</topic><topic>High fat diet</topic><topic>Humanities and Social Sciences</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mitochondria</topic><topic>Mitochondria, Liver - metabolism</topic><topic>multidisciplinary</topic><topic>Non-alcoholic Fatty Liver Disease - genetics</topic><topic>Non-alcoholic Fatty Liver Disease - metabolism</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Pediatrics</topic><topic>Phenotypes</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Sirtuins - genetics</topic><topic>Steatosis</topic><topic>Triglycerides</topic><topic>Triglycerides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Goetzman, Eric S.</creatorcontrib><creatorcontrib>Bharathi, Sivakama S.</creatorcontrib><creatorcontrib>Zhang, Yuxun</creatorcontrib><creatorcontrib>Zhao, Xue-Jun</creatorcontrib><creatorcontrib>Dobrowolski, Steven F.</creatorcontrib><creatorcontrib>Peasley, Kevin</creatorcontrib><creatorcontrib>Sims-Lucas, Sunder</creatorcontrib><creatorcontrib>Monga, Satdarshan P.</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Goetzman, Eric S.</au><au>Bharathi, Sivakama S.</au><au>Zhang, Yuxun</au><au>Zhao, Xue-Jun</au><au>Dobrowolski, Steven F.</au><au>Peasley, Kevin</au><au>Sims-Lucas, Sunder</au><au>Monga, Satdarshan P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired mitochondrial medium-chain fatty acid oxidation drives periportal macrovesicular steatosis in sirtuin-5 knockout mice</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2020-10-27</date><risdate>2020</risdate><volume>10</volume><issue>1</issue><spage>18367</spage><epage>18367</epage><pages>18367-18367</pages><artnum>18367</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Medium-chain triglycerides (MCT), containing C
8
–C
12
fatty acids, are used to treat several pediatric disorders and are widely consumed as a nutritional supplement. Here, we investigated the role of the sirtuin deacylase Sirt5 in MCT metabolism by feeding Sirt5 knockout mice (Sirt5KO) high-fat diets containing either C
8
/C
10
fatty acids or coconut oil, which is rich in C
12
, for five weeks. Coconut oil, but not C
8
/C
10
feeding, induced periportal macrovesicular steatosis in Sirt5KO mice.
14
C–C
12
degradation was significantly reduced in Sirt5KO liver. This decrease was localized to the mitochondrial β-oxidation pathway, as Sirt5KO mice exhibited no change in peroxisomal C
12
β-oxidation. Endoplasmic reticulum ω-oxidation, a minor fatty acid degradation pathway known to be stimulated by C
12
accumulation, was increased in Sirt5KO liver. Mice lacking another mitochondrial C
12
oxidation enzyme, long-chain acyl-CoA dehydrogenase (LCAD), also developed periportal macrovesicular steatosis when fed coconut oil, confirming that defective mitochondrial C
12
oxidation is sufficient to induce the steatosis phenotype. Sirt5KO liver exhibited normal LCAD activity but reduced mitochondrial acyl-CoA synthetase activity with C
12
. These studies reveal a role for Sirt5 in regulating the hepatic response to MCT and may shed light into the pathogenesis of periportal steatosis, a hallmark of human pediatric non-alcoholic fatty liver disease.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>33110171</pmid><doi>10.1038/s41598-020-75615-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals; Nature Free; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | 631/443 631/45 692/4017 Acyl-CoA dehydrogenase Acyl-CoA Dehydrogenase, Long-Chain - metabolism Animals Coconut oil Coconut Oil - administration & dosage Dietary Fats - administration & dosage Endoplasmic reticulum Fatty acids Fatty Acids - metabolism Fatty liver Female High fat diet Humanities and Social Sciences Liver Liver diseases Male Mice Mice, Knockout Mitochondria Mitochondria, Liver - metabolism multidisciplinary Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - metabolism Oxidation Oxidation-Reduction Pediatrics Phenotypes Science Science (multidisciplinary) Sirtuins - genetics Steatosis Triglycerides Triglycerides - metabolism |
| title | Impaired mitochondrial medium-chain fatty acid oxidation drives periportal macrovesicular steatosis in sirtuin-5 knockout mice |
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