The Epidemiology of Nonalcoholic Fatty Liver Disease: A Global Perspective

Lazo, Mariana; Clark, Jeanne M.

doi:10.1055/s-0028-1091978

Cited by 652 publications

(517 citation statements)

References 106 publications

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“…The mechanisms by which diet may play a role include modulation of hepatic triglyceride accumulation and regulation of the antioxidant activity, as well as changes in insulin sensitivity and postprandial triglyceride metabolism (1,24,25). Both excessive carbohydrate intake (26) and excessive fat intake could play a role in increasing blood glucose, free fat acids, and insulin concentrations, independently or together (1,6). The diet containing 25% soybean oil and 1% cholesterol promoted hypercholesterolemia in rats and simple steatosis.…”

Section: Discussionmentioning

confidence: 99%

Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers

Abreu

Guerra

Pereira

et al. 2014

Arq Bras Endocrinol Metab

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Objective: This study aimed to determine whether a hypercholesterolemic diet induces hepatic steatosis, alterations in mRNA expression of NADPH oxidase subunits, and antioxidant defenses. Materials and methods: Fischer rats were divided into two groups of eight animals according to the treatment, control (C) and hypercholesterolemic diet (H). Those in group C were fed a standard diet (AIN-93M), and those of the group H were fed a hypercholesterolemic diet (25% soybean oil and 1% cholesterol). Results: The hypercholesterolemic diet did not affect body weight, but resulted in the accumulation of lipids in the liver, increased serum activities of aminotransferases and cholesterol levels. Biomarker of lipid peroxidation (TBARS) and mRNA expression of NADPH oxidase subunits p22 phox and p47 phox were increased in the liver of animals in group H. Besides, the activity and expression of antioxidant enzymes were altered. Conclusion:The results show increased mRNA expression of NADPH oxidase subunits and changes in antioxidant enzyme activities in diet-induced hepatic steatosis. Arq Bras Endocrinol Metab. 2014;58(3):251-9 Keywords Antioxidant enzymes; hepatic steatosis; hypercholesterolemic diet; NADPH oxidase; non-alcoholic fatty liver disease; oxidative stress RESUMO Objetivo: Determinar se uma dieta hipercolesterolemiante induz esteatose hepática, alterações na expressão de mRNA da NADPH oxidase e nas defesas antioxidantes. Materiais e métodos: Ratas Fischer foram divididas em dois grupos de oito animais de acordo com o tratamento recebido, controle (C) e hipercolesterolêmico (H). Aquelas do grupo C foram alimentadas com dieta padrão (AIN-93M) e as do grupo H foram alimentadas com dieta hipercolesterolemiante (25% de óleo de soja e 1% de colesterol). As dietas foram oferecidas por oito semanas. Resultados: O grupo H apresentou acúmulo de lipídios no fígado, aumento das atividades de ALT e AST e da concentração de colesterol no soro comparado ao grupo C. O marcador da peroxidação lipídica (TBARS) e os níveis de mRNA das subunidades p47 phox da NADPH-oxidase e p22 phox foram aumentados no fígado de animais do grupo H, além de alteração da atividade e expressão de enzimas antioxidantes. Conclusão: Os resultados mostram um aumento na expressão de subunidades da NADPH oxidase e alterações na atividade das enzimas antioxidantes na esteatose hepática induzida por dieta hipercolesterolemiante. Arq Bras Endocrinol Metab. 2014;58(3):251-9 Descritores Enzimas antioxidantes; esteatose hepática; dieta hipercolesterolemiante; NADPH oxidase; doença hepática gordurosa não alcoólica; estresse oxidativo

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Section: Discussionmentioning

confidence: 99%

Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers

Abreu

Guerra

Pereira

et al. 2014

Arq Bras Endocrinol Metab

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“…It is the most common cause of cirrhosis worldwide (Lazo & Clark, 2008) and is strongly associated with the development of diabetes, obesity, hypertension, and dyslipidemia (Browning et al ., 2004a,b). The impact of NAFLD as a cause of liver cancer is projected to expand in coming years as the rate of obesity (Riordan & Nadeau, 2014) and the aging segment of the population increase (2008).…”

Section: Introductionmentioning

confidence: 99%

Ghrelin deletion protects against age‐associated hepatic steatosis by downregulating the C/EBPα‐p300/DGAT1 pathway

et al. 2017

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SummaryNonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. NAFLD usually begins as low‐grade hepatic steatosis which further progresses in an age‐dependent manner to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma in some patients. Ghrelin is a hormone known to promote adiposity in rodents and humans, but its potential role in hepatic steatosis is unknown. We hypothesized that genetic ghrelin deletion will protect against the development of age‐related hepatic steatosis. To examine this hypothesis, we utilized ghrelin knockout (KO) mice. Although no different in young animals (3 months old), we found that at 20 months of age, ghrelin KO mice have significantly reduced hepatic steatosis compared to aged‐matched wild‐type (WT) mice. Examination of molecular pathways by which deletion of ghrelin reduces steatosis showed that the increase in expression of diacylglycerol O‐acyltransferase‐1 (DGAT1), one of the key enzymes of triglyceride (TG) synthesis, seen with age in WT mice, is not present in KO mice. This was due to the lack of activation of CCAAT/enhancer binding protein‐alpha (C/EBPα) protein and subsequent reduction of C/EBPα‐p300 complexes. These complexes were abundant in livers of old WT mice and were bound to and activated the DGAT1 promoter. However, the C/EBPα‐p300 complexes were not detected on the DGAT1 promoter in livers of old KO mice resulting in lower levels of the enzyme. In conclusion, these studies demonstrate the mechanism by which ghrelin deletion prevents age‐associated hepatic steatosis and suggest that targeting this pathway may offer therapeutic benefit for NAFLD.

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“…It is also associated with a large amount of heath care cost [4] . NAFLD represents the most frequent chronic liver disease in the general population and is anticipated to become even more prevalent with time, due to the elevating proportion of people of both younger and older age, obesity and diabetes [5][6][7][8][9] . Putting together, NAFLD is emerging as a serious and global health problem which needs to be more precisely and critically addressed.…”

Section: Introductionmentioning

confidence: 99%

Elevated alanine aminotransferase activity is not associated with dyslipidemias, but related to insulin resistance and higher disease grades in non-diabetic non-alcoholic fatty liver disease

Ghamar-Chehreh

Amini

Khedmat

et al. 2012

Asian Pacific Journal of Tropical Biomedicine

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The Epidemiology of Nonalcoholic Fatty Liver Disease: A Global Perspective

Cited by 652 publications

References 106 publications

Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers

Hypercholesterolemic diet induces hepatic steatosis and alterations in mRNA expression of NADPH oxidase in rat livers

Ghrelin deletion protects against age‐associated hepatic steatosis by downregulating the C/EBPα‐p300/DGAT1 pathway

Elevated alanine aminotransferase activity is not associated with dyslipidemias, but related to insulin resistance and higher disease grades in non-diabetic non-alcoholic fatty liver disease

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