Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 최호순 | - |
dc.date.accessioned | 2018-04-11T14:47:22Z | - |
dc.date.available | 2018-04-11T14:47:22Z | - |
dc.date.issued | 2011-12 | - |
dc.identifier.citation | Liver International, 2011, 31(9), P.1315-1324 | en_US |
dc.identifier.issn | 1478-3223 | - |
dc.identifier.uri | https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1478-3231.2011.02602.x | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/65597 | - |
dc.description.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. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Blackwell Publishing Ltd | en_US |
dc.subject | carnitine | en_US |
dc.subject | lipotoxicity | en_US |
dc.subject | mitochondria | en_US |
dc.title | Prevention of free fatty acid-induced hepatic lipotoxicity by carnitine via reversal of mitochondrial dysfunction | en_US |
dc.type | Article | en_US |
dc.relation.no | 9 | - |
dc.relation.volume | 31 | - |
dc.identifier.doi | 10.1111/j.1478-3231.2011.02602.x | - |
dc.relation.page | 1315-1324 | - |
dc.relation.journal | LIVER INTERNATIONAL | - |
dc.contributor.googleauthor | JunJun, D. W.Cho, W. K.Jun, J. H.Kwon, H. J.Jang, K. S.Kim, H. J.Jeon, H. J.Lee, K. N.Lee, H. L.Lee, O. Y. D. W. | - |
dc.contributor.googleauthor | Cho, W. K. | - |
dc.contributor.googleauthor | Jun, J. H. | - |
dc.contributor.googleauthor | Kwon, H. J. | - |
dc.contributor.googleauthor | Jang, K. S. | - |
dc.contributor.googleauthor | Kim, H. J. | - |
dc.contributor.googleauthor | Jeon, H. J. | - |
dc.contributor.googleauthor | Lee, K. N. | - |
dc.contributor.googleauthor | Lee, H. L. | - |
dc.contributor.googleauthor | Lee, O. Y. | - |
dc.relation.code | 2011211589 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | hschoi96 | - |
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