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[PMID]:29176803
[Au] Autor:Pan JH; Lim Y; Kim JH; Heo W; Lee KY; Shin HJ; Kim JK; Lee JH; Kim YJ
[Ad] Endereço:Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea.
[Ti] Título:Root bark of Ulmus davidiana var. japonica restrains acute alcohol-induced hepatic steatosis onset in mice by inhibiting ROS accumulation.
[So] Source:PLoS One;12(11):e0188381, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcohol-induced hepatic steatosis and inflammation are key drivers of alcohol-induced liver injury, mainly caused by oxidative stress. The roots bark of Ulmus davidiana var. japonica is well known for its substantial antioxidative and antitumorigenic potency. In this study, we examined whether this plant can ameliorate alcohol-induced liver injuries characterized by hepatic steatosis and inflammation through its antioxidative activity. C57BL/6J mice were treated with the root bark extract of Ulmus davidiana var. japonica (RUE; 100 mg of extract/kg bodyweight; oral gavage) and alcohol (1 g/kg of bodyweight; oral gavage) for 5 days. Markers of acute alcohol-induced hepatic steatosis were determined and putative molecular mechanisms responsible for the protection of RUE were investigated. RUE noticeably protected against alcohol-induced hepatic steatosis and inflammation. Reactive oxygen species (ROS), over-produced by alcohol, negatively orchestrated various signaling pathways involved in the lipid metabolism and inflammation. These pathways were restored through the ROS scavenging activity of RUE in the liver. In particular, the expression of lipogenic genes (e.g., SREBP-1, ACC, and FAS) and inflammatory cytokines (e.g., IL-1ß, and NF-κB p65) significantly decreased with RUE treatment. Conversely, the expression of fatty acid oxidation-related genes (e.g., SIRT1, AMPKα, and PGC1α) were increased in mice treated with RUE. Thus, the results indicate that RUE counteracts and thus attenuates alcoholic hepatic steatosis onset in mice, possibly by suppressing ROS-mediated steatosis and inflammation.
[Mh] Termos MeSH primário: Fígado Gorduroso Alcoólico/tratamento farmacológico
Casca de Planta/química
Extratos Vegetais/uso terapêutico
Raízes de Plantas/química
Espécies Reativas de Oxigênio/metabolismo
Ulmus/química
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Catequina/análise
Citocinas/metabolismo
Etanol
Fígado Gorduroso Alcoólico/genética
Fígado Gorduroso Alcoólico/patologia
Regulação da Expressão Gênica/efeitos dos fármacos
Inflamação/patologia
Metabolismo dos Lipídeos/efeitos dos fármacos
Metabolismo dos Lipídeos/genética
Fígado/efeitos dos fármacos
Fígado/patologia
Camundongos Endogâmicos C57BL
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Extratos Vegetais/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cytokines); 0 (NF-kappa B); 0 (Plant Extracts); 0 (Reactive Oxygen Species); 3K9958V90M (Ethanol); 8R1V1STN48 (Catechin); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188381


  2 / 1302 MEDLINE  
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[PMID]:28467182
[Au] Autor:Li Y; Zhou J
[Ad] Endereço:Department of Infectious Disease, the Third Hospital of Hebei Medical University, Shijiazhuang 050051, China.
[Ti] Título:Roles of silent information regulator 1-serine/arginine-rich splicing factor 10-lipin 1 axis in the pathogenesis of alcohol fatty liver disease.
[So] Source:Exp Biol Med (Maywood);242(11):1117-1125, 2017 06.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Alcohol exposure is a major reason of morbidity and mortality all over the world, with much of detrimental consequences attributing to alcoholic liver disease (ALD). With the continued ethanol consumption, alcoholic fatty liver disease (AFLD, the earliest and reversible form of ALD) can further develop to more serious forms of alcoholic liver damage, including alcoholic steatohepatitis, fibrosis/cirrhosis, and even eventually progress to hepatocellular carcinoma and liver failure. Furthermore, cell trauma, inflammation, oxidative stress, regeneration, and bacterial translocation are crucial promoters of ethanol-mediated liver lesions. AFLD is characterized by excessive fat deposition in liver induced by excessive drinking, which is related closely to the raised synthesis of fatty acids and triglyceride, reduction of mitochondrial fatty acid ß-oxidation, and the aggregation of very-low-density lipoprotein (VLDL). Although little is known about the cellular and molecular mechanisms of AFLD, it seems to be correlated to diverse signal channels. Massive studies have suggested that liver steatosis is closely associated with the inhibition of silent information regulator 1 (SIRT1) and the augment of lipin1 ß/α ratio mediated by ethanol. Recently, serine/arginine-rich splicing factor 10 (SFRS10), a specific molecule functioning in alternative splicing of lipin 1 (LPIN1) pre-mRNAs, has emerged as the central connection between SIRT1 and lipin1 signaling. It seems a new signaling axis, SIRT1-SFRS10-LPIN1 axis, acting in the pathogenesis of AFLD exists. This article aims to further explore the interactions among the above three molecules and their influences on the development of AFLD. Impact statement ALD is a major health burden in industrialized countries as well as China. AFLD, the earliest and reversible form of ALD, can progress to hepatitis, fibrosis/cirrhosis, even hepatoma. While the mechanisms, by which ethanol consumption leads to AFLD, are complicated and multiple, and remain incompletely understood. SIRT1, SFRS10, and LIPIN1 had been separately reported to participate in lipid metabolism and the pathogenesis of AFLD. Noteworthy, we found the connection among them via searching articles in PubMed and we had elaborated the connection in detail in this minireview. It seems a new signaling axis, SIRT1-SFRS10-LIPIN1 axis, acting in the pathogenesis of AFLD exists. Further study aimed at SIRT1-SFRS10-LIPIN1 signaling system will possibly offer a more effective therapeutic target for AFLD.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Fígado Gorduroso Alcoólico/fisiopatologia
Fígado/patologia
Fosfatidato Fosfatase/metabolismo
Proteínas Repressoras/metabolismo
Fatores de Processamento de Serina-Arginina/metabolismo
Transdução de Sinais
Sirtuína 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica
Seres Humanos
Metabolismo dos Lipídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Repressor Proteins); 0 (SRSF10 protein, human); 170974-22-8 (Serine-Arginine Splicing Factors); EC 3.1.3.4 (LPIN1 protein, human); EC 3.1.3.4 (Phosphatidate Phosphatase); EC 3.5.1.- (SIRT1 protein, human); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1177/1535370217707729


  3 / 1302 MEDLINE  
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[PMID]:28964808
[Au] Autor:Yao YL; Han X; Song J; Zhang J; Li YM; Lian LH; Wu YL; Nan JX
[Ad] Endereço:Key Laboratory for Natural Resource of Changbai Mountain & Functional Molecules, Ministry of Education, College of Pharmacy, Yanbian University, Yanji 133002, Jilin Province, China.
[Ti] Título:Acanthoic acid protectsagainst ethanol-induced liver injury: Possible role of AMPK activation and IRAK4 inhibition.
[So] Source:Toxicol Lett;281:127-138, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to investigate the effects of acanthoic acid (AA) on the regulation of inflammatory response, lipid accumulation, and fibrosis via AMPK- IRAK4 signaling against chronic alcohol consumption in mice. Ethanol-induced liver injury was induced in male mice by Lieber-DeCarli diet for 28d. And mice in AA groups were gavaged with AA (20 or 40mg/kg) for 28d. AA treatment significantly decreased serum AST and TG, hepatic TG levels, serum ethanol and LPS levels compared with chronic ethanol administration. AA ameliorated histological changes, lipid droplets, hepatic fibrosis, and inflammation induced by ethanol. AA significantly increased the expressions of p-LKB1, p-AMPK, and SIRT1 caused by chronic ethanol administration, and attenuated the increasing protein expressions of IRAK1 and IRAK4.siRNA against AMPKα1 blocked AMPKα1 and increased IRAK4 protein expressions, compared with control-siRNA-transfected group, while AA treatment significantly decreased IRAK4 expressions compared with AMPKα1-siRNA-transfected group. AMPK-siRNA also blocked the decreased effect of AA on inflammatory factors. AA decreased over-expression of IRAK4 and inflammation under ethanol plus LPS challenge. AA recruited LKB1-AMPK phosphorylation and activated SIRT1 to regulate alcoholic liver injury, especially, inhibited IRAK1/4 signaling pathway to regulate lipid metabolism, hepatic fibrosis and inflammation caused by alcohol consumption.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Diterpenos/farmacologia
Etanol/toxicidade
Fígado Gorduroso Alcoólico/tratamento farmacológico
Quinases Associadas a Receptores de Interleucina-1/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Animais
Aspartato Aminotransferases/sangue
Células Cultivadas
Quinases Associadas a Receptores de Interleucina-1/antagonistas & inibidores
Quinases Associadas a Receptores de Interleucina-1/genética
Metabolismo dos Lipídeos/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fosforilação
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Transdução de Sinais
Sirtuína 1/genética
Sirtuína 1/metabolismo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diterpenes); 0 (RNA, Small Interfering); 0 (Triglycerides); 0 (acanthoic acid); 3K9958V90M (Ethanol); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.7.1.- (Stk11 protein, mouse); EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases); EC 2.7.11.1 (Irak1 protein, mouse); EC 2.7.11.1 (Irak4 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


  4 / 1302 MEDLINE  
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[PMID]:28882574
[Au] Autor:Zhao YY; Yang R; Xiao M; Guan MJ; Zhao N; Zeng T
[Ad] Endereço:Institute of Toxicology, School of Public Health, Shandong University, 44 Wenhua West Road, Jinan, Shandong Province, PR China.
[Ti] Título:Kupffer cells activation promoted binge drinking-induced fatty liver by activating lipolysis in white adipose tissues.
[So] Source:Toxicology;390:53-60, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Kupffer cells (KCs) have been suggested to play critical roles in chronic ethanol induced early liver injury, but the role of KCs in binge drinking-induced hepatic steatosis remains unclear. This study was designed to investigate the roles of KCs inhibitor (GdCl ) and TNF-α antagonist (etanercept) on binge drinking-induced liver steatosis and to explore the underlying mechanisms. C57BL/6 mice were exposed to three doses of ethanol (6g/kg body weight) to mimic binge drinking-induced fatty liver. The results showed that both GdCl and etanercept partially but significantly alleviated binge drinking-induced increase of hepatic triglyceride (TG) level, and reduced fat droplets accumulation in mice liver. GdCl but not etanercept significantly blocked binge drinking-induced activation of KCs. However, neither GdCl nor etanercept could affect binge drinking-induced decrease of PPAR-α, ACOX, FAS, ACC and SCD protein levels, or increase of the LC3 II/LC3 I ratio and p62 protein level. Interestingly, both GdCl and etanercept significantly suppressed binge drinking-induced phosphorylation of HSL in epididymal adipose tissues. Results of in vitro studies with cultured epididymal adipose tissues showed that TNF-α could increase the phosphorylation of HSL in adipose tissues and upgrade the secretion of free fatty acid (FFA) in the culture medium. Taken together, KCs inhibitor and TNF-α antagonist could partially attenuate binge drinking-induced liver steatosis, which might be attributed to the suppression of mobilization of white adipose tissues. These results suggest that KCs activation may promote binge drinking-induced fatty liver by TNF-α mediated activation of lipolysis in white adipose tissues.
[Mh] Termos MeSH primário: Tecido Adiposo Branco/metabolismo
Bebedeira
Etanol
Fígado Gorduroso Alcoólico/metabolismo
Macrófagos do Fígado/metabolismo
Lipólise
Fígado/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo Branco/efeitos dos fármacos
Tecido Adiposo Branco/patologia
Animais
Autofagia/efeitos dos fármacos
Modelos Animais de Doenças
Etanercepte/farmacologia
Fígado Gorduroso Alcoólico/etiologia
Fígado Gorduroso Alcoólico/patologia
Fígado Gorduroso Alcoólico/prevenção & controle
Gadolínio/farmacologia
Macrófagos do Fígado/efeitos dos fármacos
Macrófagos do Fígado/patologia
Gotículas Lipídicas/metabolismo
Lipogênese/efeitos dos fármacos
Lipólise/efeitos dos fármacos
Fígado/efeitos dos fármacos
Fígado/patologia
Masculino
Camundongos Endogâmicos C57BL
PPAR alfa/genética
PPAR alfa/metabolismo
Proteína de Ligação a Elemento Regulador de Esterol 1/genética
Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
Técnicas de Cultura de Tecidos
Triglicerídeos/metabolismo
Fator de Necrose Tumoral alfa/antagonistas & inibidores
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR alpha); 0 (Srebf1 protein, mouse); 0 (Sterol Regulatory Element Binding Protein 1); 0 (Triglycerides); 0 (Tumor Necrosis Factor-alpha); 3K9958V90M (Ethanol); AU0V1LM3JT (Gadolinium); OP401G7OJC (Etanercept); P7082WY76D (gadolinium chloride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  5 / 1302 MEDLINE  
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[PMID]:28817659
[Au] Autor:Ma Z; Zhang Y; Li Q; Xu M; Bai J; Wu S
[Ad] Endereço:Department of Hepatobiliary Surgery, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
[Ti] Título:Resveratrol improves alcoholic fatty liver disease by downregulating HIF-1α expression and mitochondrial ROS production.
[So] Source:PLoS One;12(8):e0183426, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress has been demonstrated to be involved in the etiology of alcoholic fatty liver disease (AFLD). Previous studies had demonstrated that resveratrol (RES) could reduce oxidative stress by different mechanisms. However, the effect of RES on alcohol-induced fatty liver remains unclear. In the present study, a total of 48 male SD rats were divided into three groups: Control, AFLD, and RES groups. Rats were administered with either nothing or 65% vol/vol alcohol (5 ml/kg/day in the first three days, and then 10 ml/kg/day in the following days) with or without RES supplementation (250 mg/kg/day) for 4 weeks. Blood and liver tissue samples were collected and subjected to biochemical assays, histological examination, Western blot, and mitochondrial radical oxygen species (ROS) assays. In RES group, significant decreases in serum ALT and AST concentrations, fat deposition, triglyceride (TG) content, HIF-1α protein expression as well as mitochondrial ROS production in liver were observed when compared with AFLD group (all p <0.05). These results indicated that RES could alleviate the liver injury induced by alcohol and prevent the progression of AFLD. Down regulation of HIF-1α protein expression and mitochondrial ROS production in liver might be, at least part of, the underlying mechanisms.
[Mh] Termos MeSH primário: Fígado Gorduroso Alcoólico/prevenção & controle
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Mitocôndrias Hepáticas/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Aspartato Aminotransferases/sangue
Biomarcadores/sangue
Etanol/sangue
Fígado Gorduroso Alcoólico/metabolismo
Masculino
Mitocôndrias Hepáticas/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Hif1a protein, rat); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Reactive Oxygen Species); 0 (Stilbenes); 3K9958V90M (Ethanol); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); Q369O8926L (resveratrol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183426


  6 / 1302 MEDLINE  
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[PMID]:28515323
[Au] Autor:Schott MB; Rasineni K; Weller SG; Schulze RJ; Sletten AC; Casey CA; McNiven MA
[Ad] Endereço:From the Department of Biochemistry and Molecular Biology and.
[Ti] Título:ß-Adrenergic induction of lipolysis in hepatocytes is inhibited by ethanol exposure.
[So] Source:J Biol Chem;292(28):11815-11828, 2017 Jul 14.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In liver steatosis ( fatty liver), hepatocytes accumulate many large neutral lipid storage organelles known as lipid droplets (LDs). LDs are important in the maintenance of energy homeostasis, but the signaling mechanisms that stimulate LD metabolism in hepatocytes are poorly defined. In adipocytes, catecholamines target the ß-adrenergic (ß-AR)/cAMP pathway to activate cytosolic lipases and induce their recruitment to the LD surface. Therefore, the goal of this study was to determine whether hepatocytes, like adipocytes, also undergo cAMP-mediated lipolysis in response to ß-AR stimulation. Using primary rat hepatocytes and human hepatoma cells, we found that treatment with the ß-AR agent isoproterenol caused substantial LD loss via activation of cytosolic lipases adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL). ß-Adrenergic stimulation rapidly activated PKA, which led to the phosphorylation of ATGL and HSL and their recruitment to the LD surface. To test whether this ß-AR-dependent lipolysis pathway was altered in a model of alcoholic fatty liver, primary hepatocytes from rats fed a 6-week EtOH-containing Lieber-DeCarli diet were treated with cAMP agonists. Compared with controls, EtOH-exposed hepatocytes showed a drastic inhibition in ß-AR/cAMP-induced LD breakdown and the phosphorylation of PKA substrates, including HSL. This observation was supported in VA-13 cells, an EtOH-metabolizing human hepatoma cell line, which displayed marked defects in both PKA activation and isoproterenol-induced ATGL translocation to the LD periphery. In summary, these findings suggest that ß-AR stimulation mobilizes cytosolic lipases for LD breakdown in hepatocytes, and perturbation of this pathway could be a major consequence of chronic EtOH insult leading to fatty liver.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos beta/farmacologia
AMP Cíclico/agonistas
Fígado Gorduroso Alcoólico/metabolismo
Hepatócitos/efeitos dos fármacos
Lipólise/efeitos dos fármacos
Receptores Adrenérgicos beta/metabolismo
Sistemas do Segundo Mensageiro/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Células Cultivadas
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/química
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Ativação Enzimática/efeitos dos fármacos
Fígado Gorduroso Alcoólico/patologia
Feminino
Hepatócitos/citologia
Hepatócitos/metabolismo
Hepatócitos/patologia
Seres Humanos
Lipase/química
Lipase/metabolismo
Gotículas Lipídicas/efeitos dos fármacos
Gotículas Lipídicas/metabolismo
Gotículas Lipídicas/patologia
Masculino
Fosforilação/efeitos dos fármacos
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Ratos
Receptores Adrenérgicos beta/química
Esterol Esterase/química
Esterol Esterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Receptors, Adrenergic, beta); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.1.1.13 (Sterol Esterase); EC 3.1.1.3 (Lipase); EC 3.1.1.3 (PNPLA2 protein, rat)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.777748


  7 / 1302 MEDLINE  
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[PMID]:28476407
[Au] Autor:Guo C; Ma J; Zhong Q; Zhao M; Hu T; Chen T; Qiu L; Wen L
[Ad] Endereço:School of Life Sciences, Longyan University, Longyan 364012, People's Republic of China; Fujian Provincial Key Laboratory for the Prevention and Control of Animal Infectious Diseases and Biotechnology, Longyan 364012, People's Republic of China; Key Laboratory of Preventive Veterinary Medicine and B
[Ti] Título:Curcumin improves alcoholic fatty liver by inhibiting fatty acid biosynthesis.
[So] Source:Toxicol Appl Pharmacol;328:1-9, 2017 Aug 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcoholic fatty liver is a threat to human health. It has been long known that abstinence from alcohol is the most effective therapy, other effective therapies are not available for the treatment in humans. Curcumin has a great potential for anti-oxidation and anti-inflammation, but the effect on metabolic reconstruction remains little known. Here we performed metabolomic analysis by gas chromatography/mass spectrometry and explored ethanol pathogenic insight as well as curcumin action pattern. We identified seventy-one metabolites in mouse liver. Carbohydrates and lipids were characteristic categories. Pathway analysis results revealed that ethanol-induced pathways including biosynthesis of unsaturated fatty acids, fatty acid biosynthesis and pentose and glucuronate interconversions were suppressed by curcumin. Additionally, ethanol enhanced galactose metabolism and pentose phosphate pathway. Glyoxylate and dicarboxylate metabolism and pyruvate metabolism were inhibited in mice fed ethanol diet plus curcumin. Stearic acid, oleic acid and linoleic acid were disease biomarkers and therapical biomarkers. These results reflect the landscape of hepatic metabolism regulation. Our findings illustrate ethanol pathological pathway and metabolic mechanism of curcumin therapy.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Curcumina/uso terapêutico
Ácidos Graxos/antagonistas & inibidores
Ácidos Graxos/biossíntese
Fígado Gorduroso Alcoólico/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Depressores do Sistema Nervoso Central/toxicidade
Etanol/toxicidade
Fígado Gorduroso Alcoólico/metabolismo
Galactose/metabolismo
Ácido Glucurônico/metabolismo
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Metabolômica
Camundongos
Via de Pentose Fosfato/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Central Nervous System Depressants); 0 (Fatty Acids); 3K9958V90M (Ethanol); 8A5D83Q4RW (Glucuronic Acid); IT942ZTH98 (Curcumin); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170616
[Lr] Data última revisão:
170616
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170507
[St] Status:MEDLINE


  8 / 1302 MEDLINE  
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[PMID]:28426073
[Au] Autor:Lin YL; Tai SY; Chen JW; Chou CH; Fu SG; Chen YC
[Ad] Endereço:Department of Animal Science and Technology, National Taiwan University, Taipei City 106, Taiwan. ycpchen@ntu.edu.tw.
[Ti] Título:Ameliorative effects of pepsin-digested chicken liver hydrolysates on development of alcoholic fatty livers in mice.
[So] Source:Food Funct;8(5):1763-1774, 2017 May 24.
[Is] ISSN:2042-650X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:With developments in economics and increasing work loads, alcohol abuse becomes more and more severe, leading to occurrences of alcoholic liver disease (ALD). Pepsin-digested chicken liver hydrolysates (CLHs) contain high amounts of glutamic acid, leucine, lysine, and alanine while the contents of taurine, anserine, and carnosine are also elevated after pepsin hydrolyzation. The objectives of this study were to evaluate the protective effects of CLHs against chronic alcohol consumption. The results indicated that the enlarged (p < 0.05) sizes of liver and spleen, and serum AST, ALT, and ALKP levels of mice fed with an alcoholic diet were ameliorated by supplementing with CLHs. Moreover, increased hepatic immunocyte infiltration shown on the H&E staining and higher (p < 0.05) hepatic triglyceride contents, TBARS values, and proinflammatory cytokine levels in alcoholic diet fed mice were also reduced (p < 0.05) by supplementing with CLHs. Those benefits were attributed to up-regulated fatty acid ß-oxidation and down-regulated fatty acid synthesis, as well as increased (p < 0.05) SOD, CAT, and GPx activities, TEAC levels, and elevated alcohol metabolic enzymatic activities (ALDH).
[Mh] Termos MeSH primário: Fígado Gorduroso Alcoólico/dietoterapia
Fígado/química
Pepsina A/química
Hidrolisados de Proteína/metabolismo
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Galinhas
Fígado Gorduroso Alcoólico/sangue
Fígado Gorduroso Alcoólico/metabolismo
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Hidrolisados de Proteína/química
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Hydrolysates); 0 (Triglycerides); EC 2.6.1.2 (Alanine Transaminase); EC 3.4.23.1 (Pepsin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1039/c7fo00123a


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[PMID]:28424943
[Au] Autor:Hamarneh SR; Kim BM; Kaliannan K; Morrison SA; Tantillo TJ; Tao Q; Mohamed MMR; Ramirez JM; Karas A; Liu W; Hu D; Teshager A; Gul SS; Economopoulos KP; Bhan AK; Malo MS; Choi MY; Hodin RA
[Ad] Endereço:Department of Surgery, Harvard Medical School, Massachusetts General Hospital, 15 Parkman Street, Boston, MA, 02114, USA.
[Ti] Título:Intestinal Alkaline Phosphatase Attenuates Alcohol-Induced Hepatosteatosis in Mice.
[So] Source:Dig Dis Sci;62(8):2021-2034, 2017 Aug.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIMS: Bacterially derived factors from the gut play a major role in the activation of inflammatory pathways in the liver and in the pathogenesis of alcoholic liver disease. The intestinal brush-border enzyme intestinal alkaline phosphatase (IAP) detoxifies a variety of bacterial pro-inflammatory factors and also functions to preserve gut barrier function. The aim of this study was to investigate whether oral IAP supplementation could protect against alcohol-induced liver disease. METHODS: Mice underwent acute binge or chronic ethanol exposure to induce alcoholic liver injury and steatosis ± IAP supplementation. Liver tissue was assessed for biochemical, inflammatory, and histopathological changes. An ex vivo co-culture system was used to examine the effects of alcohol and IAP treatment in regard to the activation of hepatic stellate cells and their role in the development of alcoholic liver disease. RESULTS: Pretreatment with IAP resulted in significantly lower serum alanine aminotransferase compared to the ethanol alone group in the acute binge model. IAP treatment attenuated the development of alcohol-induced fatty liver, lowered hepatic pro-inflammatory cytokine and serum LPS levels, and prevented alcohol-induced gut barrier dysfunction. Finally, IAP ameliorated the activation of hepatic stellate cells and prevented their lipogenic effect on hepatocytes. CONCLUSIONS: IAP treatment protected mice from alcohol-induced hepatotoxicity and steatosis. Oral IAP supplementation could represent a novel therapy to prevent alcoholic-related liver disease in humans.
[Mh] Termos MeSH primário: Fosfatase Alcalina/administração & dosagem
Suplementos Nutricionais
Fígado Gorduroso Alcoólico/prevenção & controle
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Animais
Técnicas de Cocultura
Citocinas/análise
Citocinas/sangue
Etanol
Fígado Gorduroso Alcoólico/sangue
Fígado Gorduroso Alcoólico/enzimologia
Feminino
Células Estreladas do Fígado/enzimologia
Hepatócitos/enzimologia
Intestinos/enzimologia
Lipogênese
Lipopolissacarídeos/sangue
Fígado/química
Camundongos
Camundongos Endogâmicos C57BL
Permeabilidade
Ativador de Plasminogênio Tecidual
Triglicerídeos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Lipopolysaccharides); 0 (Triglycerides); 3K9958V90M (Ethanol); EC 2.6.1.2 (Alanine Transaminase); EC 3.1.3.1 (Alkaline Phosphatase); EC 3.4.21.68 (Tissue Plasminogen Activator)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4576-0


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[PMID]:28411170
[Au] Autor:van der Veen JN; Kennelly JP; Wan S; Vance JE; Vance DE; Jacobs RL
[Ad] Endereço:Group on the Molecular and Cell Biology of Lipids, Canada; Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2S2, Canada.
[Ti] Título:The critical role of phosphatidylcholine and phosphatidylethanolamine metabolism in health and disease.
[So] Source:Biochim Biophys Acta;1859(9 Pt B):1558-1572, 2017 09.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) are the most abundant phospholipids in all mammalian cell membranes. In the 1950s, Eugene Kennedy and co-workers performed groundbreaking research that established the general outline of many of the pathways of phospholipid biosynthesis. In recent years, the importance of phospholipid metabolism in regulating lipid, lipoprotein and whole-body energy metabolism has been demonstrated in numerous dietary studies and knockout animal models. The purpose of this review is to highlight the unappreciated impact of phospholipid metabolism on health and disease. Abnormally high, and abnormally low, cellular PC/PE molar ratios in various tissues can influence energy metabolism and have been linked to disease progression. For example, inhibition of hepatic PC synthesis impairs very low density lipoprotein secretion and changes in hepatic phospholipid composition have been linked to fatty liver disease and impaired liver regeneration after surgery. The relative abundance of PC and PE regulates the size and dynamics of lipid droplets. In mitochondria, changes in the PC/PE molar ratio affect energy production. We highlight data showing that changes in the PC and/or PE content of various tissues are implicated in metabolic disorders such as atherosclerosis, insulin resistance and obesity. This article is part of a Special Issue entitled: Membrane Lipid Therapy: Drugs Targeting Biomembranes edited by Pablo V. Escribá.
[Mh] Termos MeSH primário: Fosfatidilcolinas/metabolismo
Fosfatidiletanolaminas/metabolismo
[Mh] Termos MeSH secundário: Animais
Fígado Gorduroso Alcoólico/metabolismo
Seres Humanos
Intestinos/metabolismo
Lipoproteínas VLDL/metabolismo
Fígado/metabolismo
Regeneração Hepática
Doenças Metabólicas/metabolismo
Mitocôndrias/metabolismo
Músculo Esquelético/metabolismo
Hepatopatia Gordurosa não Alcoólica/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Lipoproteins, VLDL); 0 (Phosphatidylcholines); 0 (Phosphatidylethanolamines); 39382-08-6 (phosphatidylethanolamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170416
[St] Status:MEDLINE



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