Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 73
Filtrar
2.
Chin J Nat Med ; 18(3): 169-177, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32245586

RESUMO

The objective of this study was to verify the protective effect of Bifidobacterium longum (BL) and the synergistical effect of Selenium and BL on alcohol plus high fat diet (HFD) induced hepatic injury in mice. We also want to explore the mechanism of Selenium-enriched Bifidobacterium longum (SeBL). C57BL/6 mice were treated with alcohol plus HFD with or without different dosage of BL or SeBL for 4 weeks. Serum levels of ALT, AST, TC, TG, LDL-C, HDL-C, FFAs, TNF-α, IL-6 and IL-1ß, hepatic MDA level, SOD activity, the mRNA levels of AMPK, PPAR-α and SREBP1 were invested. SeBL inhibited lipid accumulation in hepatocytes; reduced serum AST and ALT levels; improved dyslipidemia; decreased serum FFAs, TC, TG and LDL-C levels. SeBL also inhibited alcohol plus HFD-induced hepatocyte oxidative stress through decrease in hepatic MDA levels and increase in SOD activity. SeBL also regulated lipid metabolism related genes such as AMPK, PPAR-α and SREBP1. Although BL had similar effect as SeBL, SeBL is more effective than BL. SeBL protected mice from alcohol plus HFD-induced hepatic injury in mice because of its inhibitory effect on hepatocellular oxidative stress, lipogenesis and inflammation. Selenium enhanced the protective effect of BL.


Assuntos
Bifidobacterium longum , Fígado Gorduroso Alcoólico/terapia , Hepatopatia Gordurosa não Alcoólica/terapia , Estresse Oxidativo , Probióticos/uso terapêutico , Selênio/química , Animais , Dieta Hiperlipídica/efeitos adversos , Suplementos Nutricionais , Etanol/efeitos adversos , Metabolismo dos Lipídeos , Fígado/efeitos dos fármacos , Fígado/fisiopatologia , Testes de Função Hepática , Masculino , Camundongos Endogâmicos C57BL
4.
Cell Host Microbe ; 27(1): 25-40.e6, 2020 01 08.
Artigo em Inglês | MEDLINE | ID: mdl-31866426

RESUMO

Although a link between the gut microbiota and alcohol-related liver diseases (ALDs) has previously been suggested, the causative effects of specific taxa and their functions have not been fully investigated to date. Here, we analyze the gut microbiota of 410 fecal samples from 212 Korean twins by using the Alcohol Use Disorders Identification Test (AUDIT) scales to adjust for host genetics. This analysis revealed a strong association between low AUDIT scores and the abundance of the butyrate-producing genus Roseburia. When Roseburia spp. are administered to ALD murine models, both hepatic steatosis and inflammation significantly improve regardless of bacterial viability. Specifically, the flagellin of R. intestinalis, possibly through Toll-like receptor 5 (TLR5) recognition, recovers gut barrier integrity through upregulation of the tight junction protein Occludin and helps to restore the gut microbiota through elevated expression of IL-22 and REG3γ. Our study demonstrates that Roseburia spp. improve the gut ecosystem and prevent leaky gut, leading to ameliorated ALDs.


Assuntos
Clostridiales/metabolismo , Fígado Gorduroso Alcoólico/terapia , Microbioma Gastrointestinal , Adulto , Consumo de Bebidas Alcoólicas/efeitos adversos , Transtornos Relacionados ao Uso de Álcool/patologia , Animais , Clostridiales/isolamento & purificação , Disbiose/microbiologia , Fígado Gorduroso Alcoólico/metabolismo , Fezes/microbiologia , Feminino , Flagelina/metabolismo , Humanos , Mucosa Intestinal/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Pessoa de Meia-Idade , Ocludina/metabolismo
7.
PLoS One ; 14(2): e0212523, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30794635

RESUMO

Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD)+ biosynthesis. Through its NAD+-biosynthetic activity, NAMPT influences the activity of NAD+-dependent enzymes, such as sirtuins. NAMPT is able to modulate processes involved in the pathogenesis of non-alcohol induced fatty liver disease (NAFLD), but the roles NAMPT plays in development of alcoholic liver disease (ALD) still remain unknown. Here, we show that ethanol treatment suppresses the expression of Nampt in hepatocytes. Consistently, chronic ethanol administration also reduces Nampt expression in the mouse liver. We next demonstrate that hepatocytes infected with Ad-NAMPT adenovirus exhibit significantly elevated intracellular NAD+ levels and decreased ethanol-induced triglyceride (TG) accumulation. Similarly, adenovirus-mediated overexpression of NAMPT in mice ameliorates ethanol induced hepatic steatosis. Moreover, we demonstrate that SIRT1 is required to mediate the effects of NAMPT on reduction of hepatic TG accumulation and serum ALT, AST levels in ethanol-fed mice. Our results provide important insights in targeting NAMPT for treating alcoholic fatty liver disease.


Assuntos
Citocinas/metabolismo , Fígado Gorduroso Alcoólico/metabolismo , Fígado Gorduroso Alcoólico/terapia , Nicotinamida Fosforribosiltransferase/metabolismo , Adenoviridae/genética , Animais , Células Cultivadas , Citocinas/genética , Citocinas/uso terapêutico , Modelos Animais de Doenças , Regulação para Baixo/efeitos dos fármacos , Etanol/toxicidade , Fígado Gorduroso Alcoólico/genética , Técnicas de Silenciamento de Genes , Terapia Genética , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , NAD/metabolismo , Nicotinamida Fosforribosiltransferase/genética , Nicotinamida Fosforribosiltransferase/uso terapêutico , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Proteínas Recombinantes de Fusão/uso terapêutico , Sirtuína 1/antagonistas & inibidores , Sirtuína 1/genética , Sirtuína 1/metabolismo , Sirtuínas/deficiência , Sirtuínas/genética , Sirtuínas/metabolismo , Triglicerídeos/metabolismo , Regulação para Cima
9.
J Hepatol ; 68(5): 1025-1032, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29343427

RESUMO

BACKGROUND & AIMS: Controlled attenuation parameter (CAP) is a novel non-invasive measure of hepatic steatosis, but it has not been evaluated in alcoholic liver disease. Therefore, we aimed to validate CAP for the assessment of biopsy-verified alcoholic steatosis and to study the effect of alcohol detoxification on CAP. METHODS: This was a cross-sectional biopsy-controlled diagnostic study in four European liver centres. Consecutive alcohol-overusing patients underwent concomitant CAP, regular ultrasound, and liver biopsy. In addition, we measured CAP before and after admission for detoxification in a separate single-centre cohort. RESULTS: A total of 562 patients were included in the study: 269 patients in the diagnostic cohort with steatosis scores S0, S1, S2, and S3 = 77 (28%), 94 (35%), 64 (24%), and 34 (13%), respectively. CAP diagnosed any steatosis and moderate steatosis with fair accuracy (area under the receiver operating characteristic curve [AUC] ≥S1 = 0.77; 0.71-0.83 and AUC ≥S2 = 0.78; 0.72-0.83), and severe steatosis with good accuracy (AUC S3 = 0.82; 0.75-0.88). CAP was superior to bright liver echo pattern by regular ultrasound. CAP above 290 dB/m ruled in any steatosis with 88% specificity and 92% positive predictive value, while CAP below 220 dB/m ruled out steatosis with 90% sensitivity, but 62% negative predictive value. In the 293 patients who were admitted 6.3 days (interquartile range 4-6) for detoxification, CAP decreased by 32 ±â€¯47 dB/m (p <0.001). Body mass index predicted higher CAP in both cohorts, irrespective of drinking pattern. Obese patients with body mass index ≥30 kg/m2 had a significantly higher CAP, which did not decrease significantly during detoxification. CONCLUSIONS: CAP has a good diagnostic accuracy for diagnosing severe alcoholic liver steatosis and can be used to rule in any steatosis. In non-obese but not in obese, patients, CAP rapidly declines after alcohol withdrawal. LAY SUMMARY: CAP is a new ultrasound-based technique for measuring fat content in the liver, but has never been tested for fatty liver caused by alcohol. Herein, we examined 562 patients in a multicentre setting. We show that CAP highly correlates with liver fat, and patients with a CAP value above 290 dB/m were highly likely to have more than 5% fat in their livers, determined by liver biopsy. CAP was also better than regular ultrasound for determining the severity of alcoholic fatty-liver disease. Finally, we show that three in four (non-obese) patients rapidly decrease in CAP after short-term alcohol withdrawal. In contrast, obese alcohol-overusing patients were more likely to have higher CAP values than lean patients, irrespective of drinking.


Assuntos
Abstinência de Álcool , Fígado Gorduroso Alcoólico/diagnóstico por imagem , Fígado Gorduroso Alcoólico/terapia , Ultrassonografia/métodos , Adulto , Alcoolismo/diagnóstico por imagem , Biópsia , Estudos de Coortes , Estudos Transversais , Técnicas de Imagem por Elasticidade , Feminino , Humanos , Fígado/diagnóstico por imagem , Masculino , Síndrome Metabólica/diagnóstico por imagem , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Fatores de Risco
10.
JCI Insight ; 2(17)2017 09 07.
Artigo em Inglês | MEDLINE | ID: mdl-28878132

RESUMO

Alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH) are among the most frequent causes of chronic liver disease in the United States. Although the two entities are triggered by different etiologies - chronic alcohol consumption (ASH) and obesity-associated lipotoxicity (NASH) - they share overlapping histological and clinical features owing to common pathogenic mechanisms. These pathogenic processes include altered hepatocyte lipid metabolism, organelle dysfunction (i.e., ER stress), hepatocyte apoptosis, innate immune system activation, and hepatic stellate cell activation. Nonetheless, there are several disease-specific molecular signaling pathways, such as differential pathway activation downstream of TLR4 (MyD88-dependence in NASH versus MyD88-independence in ASH), inflammasome activation and IL-1ß signaling in ASH, insulin resistance and lipotoxicity in NASH, and dysregulation of different microRNAs, which clearly highlight that ASH and NASH are two distinct biological entities. Both pathogenic similarities and differences have therapeutic implications. In this Review, we discuss these pathogenic mechanisms and their therapeutic implications for each disease, focusing on both shared and distinct targets.


Assuntos
Fígado Gorduroso Alcoólico/patologia , Fígado Gorduroso Alcoólico/terapia , Hepatopatia Gordurosa não Alcoólica/patologia , Hepatopatia Gordurosa não Alcoólica/terapia , Fígado Gorduroso Alcoólico/metabolismo , Humanos , Hepatopatia Gordurosa não Alcoólica/metabolismo
12.
Am J Physiol Gastrointest Liver Physiol ; 311(6): G1018-G1036, 2016 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-27686615

RESUMO

Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) represent a major health burden in industrialized countries. Although alcohol abuse and nutrition play a central role in disease pathogenesis, preclinical models support a contribution of the gut microbiota to ALD and NAFLD. This review describes changes in the intestinal microbiota compositions related to ALD and NAFLD. Findings from in vitro, animal, and human studies are used to explain how intestinal pathology contributes to disease progression. This review summarizes the effects of untargeted microbiome modifications using antibiotics and probiotics on liver disease in animals and humans. While both affect humoral inflammation, regression of advanced liver disease or mortality has not been demonstrated. This review further describes products secreted by Lactobacillus- and microbiota-derived metabolites, such as fatty acids and antioxidants, that could be used for precision medicine in the treatment of liver disease. A better understanding of host-microbial interactions is allowing discovery of novel therapeutic targets in the gut microbiota, enabling new treatment options that restore the intestinal ecosystem precisely and influence liver disease. The modulation options of the gut microbiota and precision medicine employing the gut microbiota presented in this review have excellent prospects to improve treatment of liver disease.


Assuntos
Fígado Gorduroso Alcoólico/terapia , Microbioma Gastrointestinal , Hepatopatia Gordurosa não Alcoólica/terapia , Medicina de Precisão/métodos , Animais , Fígado Gorduroso Alcoólico/metabolismo , Fígado Gorduroso Alcoólico/microbiologia , Humanos , Hepatopatia Gordurosa não Alcoólica/metabolismo , Hepatopatia Gordurosa não Alcoólica/microbiologia , Probióticos/uso terapêutico
13.
Sci Rep ; 6: 29352, 2016 07 11.
Artigo em Inglês | MEDLINE | ID: mdl-27404390

RESUMO

Alcohol consumption is one of the major causes of hepatic steatosis, fibrosis, cirrhosis, and superimposed hepatocellular carcinoma. Ethanol metabolism alters the NAD(+)/NADH ratio, thereby suppressing the activity of sirtuin family proteins, which may affect lipid metabolism in liver cells. However, it is not clear how long-term ingestion of ethanol eventually causes lipid accumulation in liver. Here, we demonstrate that chronic ethanol ingestion activates peroxisome proliferator-activated receptor γ (PPARγ) and its target gene, monoacylglycerol O-acyltransferase 1 (MGAT1). During ethanol metabolism, a low NAD(+)/NADH ratio repressed NAD-dependent deacetylase sirtuin 1 (SIRT1) activity, concomitantly resulting in increased acetylated PPARγ with high transcriptional activity. Accordingly, SIRT1 transgenic mice exhibited a low level of acetylated PPARγ and were protected from hepatic steatosis driven by alcohol or PPARγ2 overexpression, suggesting that ethanol metabolism causes lipid accumulation through activation of PPARγ through acetylation. Among the genes induced by PPARγ upon alcohol consumption, MGAT1 has been shown to be involved in triglyceride synthesis. Thus, we tested the effect of MGAT1 knockdown in mice following ethanol consumption, and found a significant reduction in alcohol-induced hepatic lipid accumulation. These results suggest that MGAT1 may afford a promising approach to the treatment of fatty liver disease.


Assuntos
Aciltransferases/metabolismo , Fígado Gorduroso Alcoólico/terapia , PPAR gama/metabolismo , Aciltransferases/genética , Animais , Etanol/metabolismo , Fígado Gorduroso Alcoólico/etiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , NAD/metabolismo , Reação em Cadeia da Polimerase em Tempo Real , Sirtuína 1/genética , Sirtuína 1/metabolismo
15.
Ann Hepatol ; 15(4): 463-73, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27236145

RESUMO

 The burden of alcoholic liver disease continues to be a major public health problem worldwide. The spectrum of disease ranges from fatty liver to cirrhosis and hepatocellular carcinoma. Alcoholic hepatitis (AH) is a type of acute-on-chronic liver failure and the most severe form of alcoholic liver disease. Severe AH carries a poor short-term prognosis and its management is still challenging, with scarce advances in the last decades. Corticosteroids are still the first line of therapy in severe cases. Unfortunately, many patients do not respond and novel targeted therapies are urgently needed. Liver transplantation has shown extraordinary results in non-responders to corticosteroids however; its applicability is very low. This review summarizes the epidemiology, natural history, risk factors and pathogenesis of alcoholic liver disease with special focus on the latest advances in prognostic stratification and therapy of patients with alcoholic hepatitis.


Assuntos
Insuficiência Hepática Crônica Agudizada/fisiopatologia , Fígado Gorduroso Alcoólico/fisiopatologia , Hepatite Alcoólica/fisiopatologia , Insuficiência Hepática Crônica Agudizada/epidemiologia , Insuficiência Hepática Crônica Agudizada/terapia , Corticosteroides/uso terapêutico , Fígado Gorduroso Alcoólico/epidemiologia , Fígado Gorduroso Alcoólico/terapia , Hepatite Alcoólica/epidemiologia , Hepatite Alcoólica/terapia , Humanos , Cirrose Hepática Alcoólica/epidemiologia , Cirrose Hepática Alcoólica/fisiopatologia , Cirrose Hepática Alcoólica/terapia , Transplante de Fígado , Prognóstico , Fatores de Risco
16.
J Microbiol ; 53(12): 856-63, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26626356

RESUMO

Lactobacillus rhamnosus CCFM1107 was screened for high antioxidative activity from 55 lactobacilli. The present study attempted to explore the protective properties of L. rhamnosus CCFM1107 in alcoholic liver injury. A mouse model was induced by orally feeding alcohol when simultaneously treated with L. rhamnosus CCFM1107, the drug Hu-Gan- Pian (HGP), L. rhamnosus GG (LGG), and L. plantarum CCFM1112 for 3 months. Biochemical analysis was performed for both serum and liver homogenate. Detailed intestinal flora and histological analyses were also carried out. Our results indicated that the administration of L. rhamnosus CCFM1107 significantly inhibited the increase in the levels of serum aminotransferase and endotoxin, as well as the levels of triglyceride (TG) and cholesterol (CHO) in the serum and in the liver. Glutathione (GSH), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were elevated while the levels of malondialdehyde (MDA) were decreased. The enteric dysbiosis caused by alcohol was restored by increasing the numbers of both lactobacilli and bifidobacteria and decreasing the numbers of both enterococci and enterobacter. Histological analysis confirmed the protective effect of L. rhamnosus CCFM1107. Compared with the other lactobacilli and to the drug Hu-Gan-Pian, there is a high chance that L. rhamnosus CCFM1107 provides protective effects on alcoholic liver injury by reducing oxidative stress and restoring the intestinal flora.


Assuntos
Terapia Biológica/métodos , Etanol/efeitos adversos , Fígado Gorduroso Alcoólico/terapia , Lactobacillus rhamnosus , Fígado/efeitos dos fármacos , Probióticos/uso terapêutico , Alanina Transaminase/sangue , Animais , Colesterol/sangue , Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/uso terapêutico , Disbiose/induzido quimicamente , Endotoxinas/sangue , Fígado Gorduroso Alcoólico/prevenção & controle , Microbioma Gastrointestinal/efeitos dos fármacos , Glutationa/sangue , Glutationa Peroxidase/sangue , Fígado/patologia , Masculino , Malondialdeído/sangue , Camundongos , Estresse Oxidativo/efeitos dos fármacos , Superóxido Dismutase/sangue , Triglicerídeos/sangue
17.
J Nutr Biochem ; 26(4): 337-44, 2015 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-25622859

RESUMO

BACKGROUND: We have previously demonstrated that Lactobacillus rhamnosus GG culture supernatant (LGGs) prevents acute-alcohol-exposure-induced hepatic steatosis and injury. The protective effects of LGGs were attributed to the improved intestinal barrier function leading to decreased endotoxemia. The purpose of this study was to determine whether LGGs was effective in protecting against chronic-alcohol-induced hepatic steatosis and injury and to evaluate the underlying mechanisms of LGGs on hepatic lipid metabolism. METHODS: C57BL/6N mice were fed liquid diet containing 5% alcohol or pair-fed isocaloric maltose dextrin for 4 weeks. LGGs at a dose equivalent to 10(9) CFU/day/mouse was given in the liquid diet. Hepatic steatosis, liver enzymes and hepatic apoptosis were analyzed. RESULTS: LGGs prevented alcohol-mediated increase in hepatic expression of lipogenic genes, sterol regulatory element binding protein-1 and stearoyl-CoA desaturase-1 and increased the expression of peroxisome proliferator activated receptor-α, peroxisome proliferator-activated receptor gamma coactivator protein-1α and carnitine palmitoyltransferase-1, leading to increased fatty acid ß-oxidation. Importantly, chronic alcohol exposure decreased adenosine-monophosphate-activated protein kinase (AMPK) phosphorylation and increased acetyl-CoA carboxylase activity, which were attenuated by LGGs administration. LGGs also decreased Bax expression and increased Bcl-2 expression, which attenuated alcohol-induced hepatic apoptosis. These LGGs-regulated molecular changes resulted in the attenuation of chronic-alcohol-exposure-mediated increase in hepatic fat accumulation and liver injury. CONCLUSIONS: Probiotic LGG culture supernatant is effective in the prevention of chronic-alcohol-exposure-induced hepatic steatosis and injury. LGGs likely exerts its beneficial effects, at least in part, through modulation of hepatic AMPK activation and Bax/Bcl-2-mediated apoptosis.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Consumo de Bebidas Alcoólicas/efeitos adversos , Meios de Cultivo Condicionados/farmacologia , Fígado Gorduroso Alcoólico/microbiologia , Fígado Gorduroso Alcoólico/terapia , Lactobacillus rhamnosus/química , Proteínas Quinases Ativadas por AMP/genética , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Carnitina O-Palmitoiltransferase/genética , Carnitina O-Palmitoiltransferase/metabolismo , Linhagem Celular Tumoral , Regulação para Baixo , Metabolismo dos Lipídeos/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , PPAR alfa/genética , PPAR alfa/metabolismo , PPAR gama/genética , PPAR gama/metabolismo , Fosforilação , Probióticos/administração & dosagem , Estearoil-CoA Dessaturase/genética , Estearoil-CoA Dessaturase/metabolismo , Proteína de Ligação a Elemento Regulador de Esterol 1/genética , Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo , Regulação para Cima , Proteína X Associada a bcl-2/genética , Proteína X Associada a bcl-2/metabolismo
18.
Gastroenterology ; 147(4): 754-64, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25109884

RESUMO

Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are significant causes of chronic liver disease worldwide. Both are characterized by histological lesions that can include steatosis, and each can lead to cirrhosis. It might be possible for pathologists to identify lesions and patterns of ALD and NAFLD; we review these lesions and propose methods to distinguish between the disorders. Any form of ALD can lead to end-stage liver disease, according to long-term studies of biopsy specimens and patient outcomes. Although steatosis can be a significant cofactor in progression of established chronic liver disease, or even development of hepatocellular carcinoma, only steatohepatitis indicates the presence of progressive liver disease in patients with NAFLD. Pediatric and adolescent NAFLD differ from adult nonalcoholic steatohepatitis and should be recognized as distinct conditions. Benign and malignant liver tumors have been more frequently reported with the increasing prevalence of obesity and diabetes. Histological scoring systems for ALD and NAFLD have been proposed to monitor efficacy in clinical trials and serve as prognostic factors. We review what we have learned from pathological analyses about the development of these disorders and how this information might be used to detect and treat them.


Assuntos
Fígado Gorduroso Alcoólico/patologia , Fígado/patologia , Hepatopatia Gordurosa não Alcoólica/patologia , Animais , Diagnóstico Diferencial , Progressão da Doença , Fígado Gorduroso Alcoólico/complicações , Fígado Gorduroso Alcoólico/terapia , Humanos , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/terapia , Valor Preditivo dos Testes , Prognóstico , Índice de Gravidade de Doença
19.
Mitochondrion ; 15: 40-51, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-24727595

RESUMO

Exercise is considered a non-pharmacological tool against several lifestyle disorders in which mitochondrial dysfunction is involved. The present study aimed to analyze the preventive (voluntary physical activity-VPA) and therapeutic (endurance training-ET) role of exercise against non-alcoholic steatohepatitis (NASH)-induced liver mitochondrial dysfunction. Sixty male Sprague-Dawley rats were divided into standard-diet sedentary (SS, n=20), standard-diet VPA (SVPA, n=10), high-fat diet sedentary (HS, n=20) and high-fat diet VPA (HVPA, n=10). After 9weeks of diet-treatment, half of SS and HS animals were engaged in an ET program (SET and HET) for 8weeks, 5days/week and 60min/day. Liver mitochondrial oxygen consumption and transmembrane-electric potential (ΔΨ) were evaluated in the presence of glutamate-malate (G/M), palmitoyl-malate (P/M) and succinate (S/R). Mitochondrial enzymes activity, lipid and protein oxidation, oxidative phosphorylation (OXPHOS) subunits, cytochrome c, adenine nucleotide translocator (ANT) and uncoupling protein-2 (UCP2) content were assessed. HS groups show the histological features of NASH in parallel with decreased ΔΨ and respiratory control (RCR) and ADP/O ratios (G/M and P/M). A state 3 decrease (G/M and S/R), FCCP-induced uncoupling respiration (S/R) and ANT content were also observed. Both exercise types counteracted oxygen consumption (RCR, ADP/O and FCCP-uncoupling state) impairments and improved ΔΨ (lag-phase). In conclusion, exercise prevented or reverted (VPA and ET, respectively) the bioenergetic impairment induced by NASH, but only ET positively remodeled NASH-induced liver structural damage and abnormal mitochondria. It is possible that alterations in inner membrane integrity and fatty acid oxidation may be related to the observed phenotypes induced by exercise.


Assuntos
Metabolismo Energético , Fígado Gorduroso Alcoólico/fisiopatologia , Fígado/patologia , Fígado/fisiopatologia , Mitocôndrias/patologia , Mitocôndrias/fisiologia , Condicionamento Físico Animal , Animais , Modelos Animais de Doenças , Fígado Gorduroso Alcoólico/terapia , Mitocôndrias/ultraestrutura , Ratos Sprague-Dawley
20.
Anim Sci J ; 85(1): 75-80, 2014 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-23841884

RESUMO

The purposes of this study were to assess the improvement of fatty liver induced by ethanol with animal liver and bile extracts. This research aimed to increase the economic values of animal liver and bile extracts and used these to reduce damage of ethanol-induced fatty liver. Extracts came from animal liver and bile, including pig bile powder, pig liver extract, a mixture of pig bile powder and pig liver extract, chicken bile powder, chicken liver extract, and a mixture of chicken bile powder and chicken liver extract, and these were fed to Long-Evans rats. The results showed that rats fed ethanol for long terms could increase values of aspartate transaminase, cholesterol, γ-glutamy-transferase and alkaline phosphatase. Pig bile powder could decrease the values of aspartate transaminase, cholesterol and γ-glutamy-transferase. The significances also decreased on aspartate transaminase, γ-glutamy-transferase and aspartate transaminase, which were carried out with the pig liver extract treatment. These results suggest pig bile and liver extracts have high potential to improve rats' ethanol-induced fatty liver with serum biochemical parameters.


Assuntos
Bile/química , Fígado Gorduroso Alcoólico/terapia , Fígado/química , Extratos de Tecidos/uso terapêutico , Fosfatase Alcalina/sangue , Animais , Aspartato Aminotransferases/sangue , Galinhas , Colesterol/sangue , Fígado Gorduroso Alcoólico/sangue , Masculino , Ratos Long-Evans , Suínos , Extratos de Tecidos/farmacologia , gama-Glutamiltransferase/sangue
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA