From Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma: A Systems Understanding

Rozman, Damjana

doi:10.1007/s10620-013-2998-x

Cited by 22 publications

(22 citation statements)

References 10 publications

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“…NAFLD is a spectrum of chronic, progressive liver diseases characterized by hepatic steatosis and is closely related to obesity and metabolic syndrome [47,48] . NAFLD is globally prevalent now due to the obesity epidemic and has become a major public health problem because a significant portion of obese patients will progress to having nonalcoholic steatohepatitis (NASH), and no specific therapies are currently approved for NAFLD or NASH [47][48][49][50] .…”

Section: Fxr Nonalcoholic Fatty Liver Disease (Nafld) and Liver Cancermentioning

confidence: 99%

“…NAFLD is globally prevalent now due to the obesity epidemic and has become a major public health problem because a significant portion of obese patients will progress to having nonalcoholic steatohepatitis (NASH), and no specific therapies are currently approved for NAFLD or NASH [47][48][49][50] . NASH individuals demonstrate serious liver injuries including hepatocyte damage, inflammation and fibrosis [47][48][49][50] . Moreover, epidemiological evidence has proved that NASH and its two major comorbidities, obesity and diabetes mellitus (DM), increase the risk of HCC, especially when NASH-related cirrhosis has developed [47] .…”

Section: Fxr Nonalcoholic Fatty Liver Disease (Nafld) and Liver Cancermentioning

confidence: 99%

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FXR and liver carcinogenesis

2014

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Farnesoid X receptor (FXR) is a member of the nuclear receptor family and a ligand-modulated transcription factor. In the liver, FXR has been considered a multi-functional cell protector and a tumor suppressor. FXR can suppress liver carcinogenesis via different mechanisms: 1) FXR maintains the normal liver metabolism of bile acids, glucose and lipids; 2) FXR promotes liver regeneration and repair after injury; 3) FXR protects liver cells from death and enhances cell survival; 4) FXR suppresses hepatic inflammation, thereby preventing inflammatory damage; and 5) FXR can directly increase the expression of some tumor-suppressor genes and repress the transcription of several oncogenes. However, inflammation and epigenetic silencing are known to decrease FXR expression during tumorigenesis. The reactivation of FXR function in the liver may be a potential therapeutic approach for patients with liver cancer.

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Section: Fxr Nonalcoholic Fatty Liver Disease (Nafld) and Liver Cancermentioning

confidence: 99%

Section: Fxr Nonalcoholic Fatty Liver Disease (Nafld) and Liver Cancermentioning

confidence: 99%

FXR and liver carcinogenesis

2014

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“…Very similar as in ALD, NAFLD encompasses a wide range of pathological conditions from mild hepatic steatosis to steatohepatitis (a syndrome named non-alcoholic steatohepatitis (NASH)) with significant necroinflammation and progressive fibrosis. In its advanced form, NASH is believed to account for a large fraction, if not entirely for what was previously termed 'cryptogenic cirrhosis' and also progresses to HCC in a significant number of cases [5,6] . Also, hepatocellular fat accumulation is the first pathological step in NAFLD ( fig.…”

Section: Introductionmentioning

confidence: 99%

Alcohol and Obesity: A Dangerous Association for Fatty Liver Disease

Mahli

Hellerbrand²

2016

Dig Dis

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Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are the most frequent chronic liver disorders, and their advanced forms - alcoholic steatohepatitis and nonalcoholic steatohepatitis - are the most frequent conditions leading to liver cirrhosis and hepatocellular carcinoma worldwide. NAFLD is considered as the hepatic manifestation of the metabolic syndrome. With the pandemic rise of obesity, the incidence of NAFLD is also further increasing, and considering the life style in modern societies, there is a significant overlap of (risk factors causing) NAFLD and (alcohol consumption predisposing for) ALD at least in Western countries. Epidemiological studies propose a causative link between chronic alcohol consumption and progressive liver disease in obese individuals. Furthermore, experimental studies indicate combined pathological effects of alcohol and obesity or fatty acid levels, respectively, on hepatocellular lipid accumulation and injury as well as hepatic inflammation, fibrosis and cancerogenesis. Notably, these combined pathological effects are in part additive but partly even synergistic. And importantly, alcohol does already exhibit synergistic pathological effects with obesity at moderate doses. This indicates significant differences in the dose threshold for hepatotoxic alcohol effects in lean and obese subjects and herewith also has important implications for recommendations for ‘safe' alcohol consumption. The purpose of this brief review is to update the knowledge on the combined effects of alcohol and obesity on the development and progression of liver disease. Undoubtedly, alcohol and the metabolic syndrome appear as a dangerous mix, and there are important interactive effects of either condition with regard to crucial triggers of liver injury.

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“…NAFLD defines a spectrum of liver diseases that can progress from steatosis (nonalcoholic fat liver) to nonalcoholic steatohepatitis (NASH), hepatic fibrosis/cirrhosis, and also to hepatocellular carcinoma [2] . The prevalence of NAFLD is growing fast because of the increasing prevalence of obesity and diabetes [1,2] . It is expected, by this year, 2015, that the number of overweight subjects exceeds 2.3 billion.…”

Section: Introductionmentioning

confidence: 99%

“…More than 20%, 60% and 90% of the Western population, diabetic individuals, and morbidly obese patients, respectively, will present steatosis. Furthermore, up to 15% of the Western population, 25%-30% of subjects with either obesity or type-2 diabetes mellitus, and over 35% of the severely obese individuals will develop NASH [2] . NAFLD is strongly associated with insulin resistance (IR), visceral obesity, and dyslipidemia; therefore, it was early recognized as the hepatic manifestation of the metabolic syndrome (MS).…”

Section: Introductionmentioning

confidence: 99%

Dietary approach in the treatment of nonalcoholic fatty liver disease

Ferolla¹,

Silva²,

Ferrari³

et al. 2015

WJH

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Nonalcoholic fatty liver disease (NAFLD) has been identified as one of the most prevalent chronic liver disease in adults and children populations. NAFLD is usually associated with the metabolic syndrome (MS), which is chiefly related to insulin resistance and its consequences. Insulin resistance has a crucial role in the pathogenesis of hepatic steatosis and potentially nonalcoholic steatohepatitis (NASH). Because of the contemporary epidemics of MS and obesity, the burden of NAFLD is also expected to rise. Unhealthy diets, such as the so-called western diet, are enriched in fructose, trans-fatty acids and saturated fat and seem to be associated with the development of NAFLD. In human studies, certain dietary sugars, particularly fructose, are used as a substrate for lipogenesis leading to hepatic fatty infiltration, inflammation, and possibly fibrosis. Other investigations have shown that fat consumption especially cholesterol and trans/saturated fatty acids are also steatogenic and seem to increase visceral adiposity. The identification of specific dietary components that favor the development of NASH could be important for the management of this disorder. This review focuses on the effects of different dietary approaches to prevent and treat NAFLD emphasizing the macronutrients and energy composition.

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From Nonalcoholic Fatty Liver Disease to Hepatocellular Carcinoma: A Systems Understanding

Cited by 22 publications

References 10 publications

FXR and liver carcinogenesis

FXR and liver carcinogenesis

Alcohol and Obesity: A Dangerous Association for Fatty Liver Disease

Dietary approach in the treatment of nonalcoholic fatty liver disease

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