Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction
Background: Mitochondria are the main sites for fatty acid oxidation and play a central role in lipotoxicity and nonalcoholic steatohepatitis. Aims: We investigated whether carnitine prevents free fatty acid (FFA)‐induced lipotoxicity in vitro and in vivo. Methods: HepG2 cells were incubated with FF...
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| Veröffentlicht in: | Liver international 2011-10, Vol.31 (9), p.1315-1324 |
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| creator | Jun, Dae Won Cho, Won Kyeong Jun, Jin Hyun Kwon, Hyuk Jin Jang, Ki-Seok Kim, Hyun-Jeong Jeon, Hye Jun Lee, Kang Nyeong Lee, Hang Lak Lee, Oh Young Yoon, Byung Chul Choi, Ho Soon Hahm, Joon Soo Lee, Min Ho |
| description | Background:
Mitochondria are the main sites for fatty acid oxidation and play a central role in lipotoxicity and nonalcoholic steatohepatitis.
Aims:
We investigated whether carnitine prevents free fatty acid (FFA)‐induced lipotoxicity in vitro and in vivo.
Methods:
HepG2 cells were incubated with FFA, along with carnitine and carnitine complexes. Mitochondrial β‐oxidation, transmembrane potential, intracellular ATP levels and changes in mitochondrial copy number and morphology were analysed. Otsuka Long‐Evans Tokushima Fatty and Long‐Evans Tokushima Otsuka rats were segregated into three experimental groups and fed for 8 weeks with (i) normal chow, (ii) a methionine choline‐deficient (MCD) diet or (iii) an l‐carnitine‐supplemented MCD diet.
Results:
Carnitine prevented FFA‐induced apoptosis (16% vs. 3%, P |
| doi_str_mv | 10.1111/j.1478-3231.2011.02602.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_905669861</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>905669861</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5222-2c618e70f01fd902be8952fe434c409ab8536d2495203e9f8d21c8a3197da5b63</originalsourceid><addsrcrecordid>eNqNkE9v1DAQxS1ERUvhKyDfOCX4T-LEBw6olNJqaYsE9Gg59lj1ko23tlM2374JW_bMXGY0894b6YcQpqSkc31Yl7Rq2oIzTktGKC0JE4SVuxfo5HB4eZgZP0avU1oTQqWs6St0zBiRvKqrE_RwG-ERhuzDgIPDLgJgp3OesDbeFn6wowGL72Grsze499uQw84bPyu6CRsdB5_9APjRa7xExaT7JWnjczD3YbDRzws7JTcOZnnzBh053Sd4-9xP0c8v5z_Ovharm4vLs0-rwtSMsYIZQVtoiCPUWUlYB62smYOKV6YiUndtzYVl1bwkHKRrLaOm1ZzKxuq6E_wUvd_nbmN4GCFltfHJQN_rAcKYlCS1ELIVdFa2e6WJIaUITm2j3-g4KUrUwlut1YJSLVjVwlv95a12s_Xd85Ox24A9GP8BngUf94I_vofpv4PV6vLXMs3-Yu_3KcPu4NfxtxINb2p1d32hrvj3O8G_fVacPwFdvJ8g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>905669861</pqid></control><display><type>article</type><title>Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Jun, Dae Won ; Cho, Won Kyeong ; Jun, Jin Hyun ; Kwon, Hyuk Jin ; Jang, Ki-Seok ; Kim, Hyun-Jeong ; Jeon, Hye Jun ; Lee, Kang Nyeong ; Lee, Hang Lak ; Lee, Oh Young ; Yoon, Byung Chul ; Choi, Ho Soon ; Hahm, Joon Soo ; Lee, Min Ho</creator><creatorcontrib>Jun, Dae Won ; Cho, Won Kyeong ; Jun, Jin Hyun ; Kwon, Hyuk Jin ; Jang, Ki-Seok ; Kim, Hyun-Jeong ; Jeon, Hye Jun ; Lee, Kang Nyeong ; Lee, Hang Lak ; Lee, Oh Young ; Yoon, Byung Chul ; Choi, Ho Soon ; Hahm, Joon Soo ; Lee, Min Ho</creatorcontrib><description>Background:
Mitochondria are the main sites for fatty acid oxidation and play a central role in lipotoxicity and nonalcoholic steatohepatitis.
Aims:
We investigated whether carnitine prevents free fatty acid (FFA)‐induced lipotoxicity in vitro and in vivo.
Methods:
HepG2 cells were incubated with FFA, along with carnitine and carnitine complexes. Mitochondrial β‐oxidation, transmembrane potential, intracellular ATP levels and changes in mitochondrial copy number and morphology were analysed. Otsuka Long‐Evans Tokushima Fatty and Long‐Evans Tokushima Otsuka rats were segregated into three experimental groups and fed for 8 weeks with (i) normal chow, (ii) a methionine choline‐deficient (MCD) diet or (iii) an l‐carnitine‐supplemented MCD diet.
Results:
Carnitine prevented FFA‐induced apoptosis (16% vs. 3%, P < 0.05). FFA treatment resulted in swollen mitochondria with increased inner matrix density and loss of cristae. However, mitochondria co‐treated with carnitine had normal ultrastructure. The mitochondrial DNA copy number was higher in the carnitine treatment group than in the palmitic acid treatment group (375 vs. 221 copies, P < 0.05). The carnitine group showed higher mitochondrial β‐oxidation than did the control and palmitic acid treatment groups (597 vs. 432 and 395 ccpm, P < 0.05). Carnitine treatment increased the mRNA expression of carnitine palmitoyltransferase 1A and peroxisome proliferator‐activated receptor‐γ, and carnitine‐lipoic acid further augmented the mRNA expression. In the in vivo model, carnitine‐treated rats showed lower alanine transaminase levels and lesser lobular inflammation than did the MCD‐treated rats.
Conclusions:
Carnitine and carnitine‐lipoic acid prevent lipotoxicity by increasing mitochondrial β‐oxidation and reducing intracellular oxidative stress.</description><identifier>ISSN: 1478-3223</identifier><identifier>EISSN: 1478-3231</identifier><identifier>DOI: 10.1111/j.1478-3231.2011.02602.x</identifier><identifier>PMID: 22093454</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adenosine Triphosphate - metabolism ; Animals ; Apoptosis - drug effects ; carnitine ; Carnitine - analogs & derivatives ; Carnitine - pharmacology ; Carnitine O-Palmitoyltransferase - genetics ; Carnitine O-Palmitoyltransferase - metabolism ; Choline Deficiency - complications ; Disease Models, Animal ; DNA, Mitochondrial - metabolism ; Fatty Acids, Nonesterified - metabolism ; Fatty Liver - etiology ; Fatty Liver - genetics ; Fatty Liver - metabolism ; Fatty Liver - pathology ; Fatty Liver - prevention & control ; Gene Expression Regulation - drug effects ; Hep G2 Cells ; Humans ; lipotoxicity ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Lysosomes - drug effects ; Lysosomes - metabolism ; Membrane Potential, Mitochondrial - drug effects ; Methionine - deficiency ; mitochondria ; Mitochondria, Liver - drug effects ; Mitochondria, Liver - metabolism ; Mitochondria, Liver - pathology ; Non-alcoholic Fatty Liver Disease ; Oxidation-Reduction ; Oxidative Stress - drug effects ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Rats ; Rats, Inbred OLETF ; Rats, Long-Evans ; RNA, Messenger - metabolism ; Thioctic Acid - analogs & derivatives ; Thioctic Acid - pharmacology ; Time Factors</subject><ispartof>Liver international, 2011-10, Vol.31 (9), p.1315-1324</ispartof><rights>2011 John Wiley & Sons A/S</rights><rights>2011 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5222-2c618e70f01fd902be8952fe434c409ab8536d2495203e9f8d21c8a3197da5b63</citedby><cites>FETCH-LOGICAL-c5222-2c618e70f01fd902be8952fe434c409ab8536d2495203e9f8d21c8a3197da5b63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1478-3231.2011.02602.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1478-3231.2011.02602.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22093454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jun, Dae Won</creatorcontrib><creatorcontrib>Cho, Won Kyeong</creatorcontrib><creatorcontrib>Jun, Jin Hyun</creatorcontrib><creatorcontrib>Kwon, Hyuk Jin</creatorcontrib><creatorcontrib>Jang, Ki-Seok</creatorcontrib><creatorcontrib>Kim, Hyun-Jeong</creatorcontrib><creatorcontrib>Jeon, Hye Jun</creatorcontrib><creatorcontrib>Lee, Kang Nyeong</creatorcontrib><creatorcontrib>Lee, Hang Lak</creatorcontrib><creatorcontrib>Lee, Oh Young</creatorcontrib><creatorcontrib>Yoon, Byung Chul</creatorcontrib><creatorcontrib>Choi, Ho Soon</creatorcontrib><creatorcontrib>Hahm, Joon Soo</creatorcontrib><creatorcontrib>Lee, Min Ho</creatorcontrib><title>Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction</title><title>Liver international</title><addtitle>Liver International</addtitle><description>Background:
Mitochondria are the main sites for fatty acid oxidation and play a central role in lipotoxicity and nonalcoholic steatohepatitis.
Aims:
We investigated whether carnitine prevents free fatty acid (FFA)‐induced lipotoxicity in vitro and in vivo.
Methods:
HepG2 cells were incubated with FFA, along with carnitine and carnitine complexes. Mitochondrial β‐oxidation, transmembrane potential, intracellular ATP levels and changes in mitochondrial copy number and morphology were analysed. Otsuka Long‐Evans Tokushima Fatty and Long‐Evans Tokushima Otsuka rats were segregated into three experimental groups and fed for 8 weeks with (i) normal chow, (ii) a methionine choline‐deficient (MCD) diet or (iii) an l‐carnitine‐supplemented MCD diet.
Results:
Carnitine prevented FFA‐induced apoptosis (16% vs. 3%, P < 0.05). FFA treatment resulted in swollen mitochondria with increased inner matrix density and loss of cristae. However, mitochondria co‐treated with carnitine had normal ultrastructure. The mitochondrial DNA copy number was higher in the carnitine treatment group than in the palmitic acid treatment group (375 vs. 221 copies, P < 0.05). The carnitine group showed higher mitochondrial β‐oxidation than did the control and palmitic acid treatment groups (597 vs. 432 and 395 ccpm, P < 0.05). Carnitine treatment increased the mRNA expression of carnitine palmitoyltransferase 1A and peroxisome proliferator‐activated receptor‐γ, and carnitine‐lipoic acid further augmented the mRNA expression. In the in vivo model, carnitine‐treated rats showed lower alanine transaminase levels and lesser lobular inflammation than did the MCD‐treated rats.
Conclusions:
Carnitine and carnitine‐lipoic acid prevent lipotoxicity by increasing mitochondrial β‐oxidation and reducing intracellular oxidative stress.</description><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>carnitine</subject><subject>Carnitine - analogs & derivatives</subject><subject>Carnitine - pharmacology</subject><subject>Carnitine O-Palmitoyltransferase - genetics</subject><subject>Carnitine O-Palmitoyltransferase - metabolism</subject><subject>Choline Deficiency - complications</subject><subject>Disease Models, Animal</subject><subject>DNA, Mitochondrial - metabolism</subject><subject>Fatty Acids, Nonesterified - metabolism</subject><subject>Fatty Liver - etiology</subject><subject>Fatty Liver - genetics</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - pathology</subject><subject>Fatty Liver - prevention & control</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hep G2 Cells</subject><subject>Humans</subject><subject>lipotoxicity</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Lysosomes - drug effects</subject><subject>Lysosomes - metabolism</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Methionine - deficiency</subject><subject>mitochondria</subject><subject>Mitochondria, Liver - drug effects</subject><subject>Mitochondria, Liver - metabolism</subject><subject>Mitochondria, Liver - pathology</subject><subject>Non-alcoholic Fatty Liver Disease</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress - drug effects</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred OLETF</subject><subject>Rats, Long-Evans</subject><subject>RNA, Messenger - metabolism</subject><subject>Thioctic Acid - analogs & derivatives</subject><subject>Thioctic Acid - pharmacology</subject><subject>Time Factors</subject><issn>1478-3223</issn><issn>1478-3231</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE9v1DAQxS1ERUvhKyDfOCX4T-LEBw6olNJqaYsE9Gg59lj1ko23tlM2374JW_bMXGY0894b6YcQpqSkc31Yl7Rq2oIzTktGKC0JE4SVuxfo5HB4eZgZP0avU1oTQqWs6St0zBiRvKqrE_RwG-ERhuzDgIPDLgJgp3OesDbeFn6wowGL72Grsze499uQw84bPyu6CRsdB5_9APjRa7xExaT7JWnjczD3YbDRzws7JTcOZnnzBh053Sd4-9xP0c8v5z_Ovharm4vLs0-rwtSMsYIZQVtoiCPUWUlYB62smYOKV6YiUndtzYVl1bwkHKRrLaOm1ZzKxuq6E_wUvd_nbmN4GCFltfHJQN_rAcKYlCS1ELIVdFa2e6WJIaUITm2j3-g4KUrUwlut1YJSLVjVwlv95a12s_Xd85Ox24A9GP8BngUf94I_vofpv4PV6vLXMs3-Yu_3KcPu4NfxtxINb2p1d32hrvj3O8G_fVacPwFdvJ8g</recordid><startdate>201110</startdate><enddate>201110</enddate><creator>Jun, Dae Won</creator><creator>Cho, Won Kyeong</creator><creator>Jun, Jin Hyun</creator><creator>Kwon, Hyuk Jin</creator><creator>Jang, Ki-Seok</creator><creator>Kim, Hyun-Jeong</creator><creator>Jeon, Hye Jun</creator><creator>Lee, Kang Nyeong</creator><creator>Lee, Hang Lak</creator><creator>Lee, Oh Young</creator><creator>Yoon, Byung Chul</creator><creator>Choi, Ho Soon</creator><creator>Hahm, Joon Soo</creator><creator>Lee, Min Ho</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>201110</creationdate><title>Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction</title><author>Jun, Dae Won ; Cho, Won Kyeong ; Jun, Jin Hyun ; Kwon, Hyuk Jin ; Jang, Ki-Seok ; Kim, Hyun-Jeong ; Jeon, Hye Jun ; Lee, Kang Nyeong ; Lee, Hang Lak ; Lee, Oh Young ; Yoon, Byung Chul ; Choi, Ho Soon ; Hahm, Joon Soo ; Lee, Min Ho</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5222-2c618e70f01fd902be8952fe434c409ab8536d2495203e9f8d21c8a3197da5b63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>carnitine</topic><topic>Carnitine - analogs & derivatives</topic><topic>Carnitine - pharmacology</topic><topic>Carnitine O-Palmitoyltransferase - genetics</topic><topic>Carnitine O-Palmitoyltransferase - metabolism</topic><topic>Choline Deficiency - complications</topic><topic>Disease Models, Animal</topic><topic>DNA, Mitochondrial - metabolism</topic><topic>Fatty Acids, Nonesterified - metabolism</topic><topic>Fatty Liver - etiology</topic><topic>Fatty Liver - genetics</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - pathology</topic><topic>Fatty Liver - prevention & control</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hep G2 Cells</topic><topic>Humans</topic><topic>lipotoxicity</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Lysosomes - drug effects</topic><topic>Lysosomes - metabolism</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Methionine - deficiency</topic><topic>mitochondria</topic><topic>Mitochondria, Liver - drug effects</topic><topic>Mitochondria, Liver - metabolism</topic><topic>Mitochondria, Liver - pathology</topic><topic>Non-alcoholic Fatty Liver Disease</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress - drug effects</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred OLETF</topic><topic>Rats, Long-Evans</topic><topic>RNA, Messenger - metabolism</topic><topic>Thioctic Acid - analogs & derivatives</topic><topic>Thioctic Acid - pharmacology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jun, Dae Won</creatorcontrib><creatorcontrib>Cho, Won Kyeong</creatorcontrib><creatorcontrib>Jun, Jin Hyun</creatorcontrib><creatorcontrib>Kwon, Hyuk Jin</creatorcontrib><creatorcontrib>Jang, Ki-Seok</creatorcontrib><creatorcontrib>Kim, Hyun-Jeong</creatorcontrib><creatorcontrib>Jeon, Hye Jun</creatorcontrib><creatorcontrib>Lee, Kang Nyeong</creatorcontrib><creatorcontrib>Lee, Hang Lak</creatorcontrib><creatorcontrib>Lee, Oh Young</creatorcontrib><creatorcontrib>Yoon, Byung Chul</creatorcontrib><creatorcontrib>Choi, Ho Soon</creatorcontrib><creatorcontrib>Hahm, Joon Soo</creatorcontrib><creatorcontrib>Lee, Min Ho</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Liver international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jun, Dae Won</au><au>Cho, Won Kyeong</au><au>Jun, Jin Hyun</au><au>Kwon, Hyuk Jin</au><au>Jang, Ki-Seok</au><au>Kim, Hyun-Jeong</au><au>Jeon, Hye Jun</au><au>Lee, Kang Nyeong</au><au>Lee, Hang Lak</au><au>Lee, Oh Young</au><au>Yoon, Byung Chul</au><au>Choi, Ho Soon</au><au>Hahm, Joon Soo</au><au>Lee, Min Ho</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction</atitle><jtitle>Liver international</jtitle><addtitle>Liver International</addtitle><date>2011-10</date><risdate>2011</risdate><volume>31</volume><issue>9</issue><spage>1315</spage><epage>1324</epage><pages>1315-1324</pages><issn>1478-3223</issn><eissn>1478-3231</eissn><abstract>Background:
Mitochondria are the main sites for fatty acid oxidation and play a central role in lipotoxicity and nonalcoholic steatohepatitis.
Aims:
We investigated whether carnitine prevents free fatty acid (FFA)‐induced lipotoxicity in vitro and in vivo.
Methods:
HepG2 cells were incubated with FFA, along with carnitine and carnitine complexes. Mitochondrial β‐oxidation, transmembrane potential, intracellular ATP levels and changes in mitochondrial copy number and morphology were analysed. Otsuka Long‐Evans Tokushima Fatty and Long‐Evans Tokushima Otsuka rats were segregated into three experimental groups and fed for 8 weeks with (i) normal chow, (ii) a methionine choline‐deficient (MCD) diet or (iii) an l‐carnitine‐supplemented MCD diet.
Results:
Carnitine prevented FFA‐induced apoptosis (16% vs. 3%, P < 0.05). FFA treatment resulted in swollen mitochondria with increased inner matrix density and loss of cristae. However, mitochondria co‐treated with carnitine had normal ultrastructure. The mitochondrial DNA copy number was higher in the carnitine treatment group than in the palmitic acid treatment group (375 vs. 221 copies, P < 0.05). The carnitine group showed higher mitochondrial β‐oxidation than did the control and palmitic acid treatment groups (597 vs. 432 and 395 ccpm, P < 0.05). Carnitine treatment increased the mRNA expression of carnitine palmitoyltransferase 1A and peroxisome proliferator‐activated receptor‐γ, and carnitine‐lipoic acid further augmented the mRNA expression. In the in vivo model, carnitine‐treated rats showed lower alanine transaminase levels and lesser lobular inflammation than did the MCD‐treated rats.
Conclusions:
Carnitine and carnitine‐lipoic acid prevent lipotoxicity by increasing mitochondrial β‐oxidation and reducing intracellular oxidative stress.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>22093454</pmid><doi>10.1111/j.1478-3231.2011.02602.x</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Liver international, 2011-10, Vol.31 (9), p.1315-1324 |
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| language | eng |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adenosine Triphosphate - metabolism Animals Apoptosis - drug effects carnitine Carnitine - analogs & derivatives Carnitine - pharmacology Carnitine O-Palmitoyltransferase - genetics Carnitine O-Palmitoyltransferase - metabolism Choline Deficiency - complications Disease Models, Animal DNA, Mitochondrial - metabolism Fatty Acids, Nonesterified - metabolism Fatty Liver - etiology Fatty Liver - genetics Fatty Liver - metabolism Fatty Liver - pathology Fatty Liver - prevention & control Gene Expression Regulation - drug effects Hep G2 Cells Humans lipotoxicity Liver - drug effects Liver - metabolism Liver - pathology Lysosomes - drug effects Lysosomes - metabolism Membrane Potential, Mitochondrial - drug effects Methionine - deficiency mitochondria Mitochondria, Liver - drug effects Mitochondria, Liver - metabolism Mitochondria, Liver - pathology Non-alcoholic Fatty Liver Disease Oxidation-Reduction Oxidative Stress - drug effects PPAR gamma - genetics PPAR gamma - metabolism Rats Rats, Inbred OLETF Rats, Long-Evans RNA, Messenger - metabolism Thioctic Acid - analogs & derivatives Thioctic Acid - pharmacology Time Factors |
| title | Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction |
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