Epidemiology of non-alcoholic fatty liver disease and hepatocellular carcinoma

Younossi, Zobair M.; Henry, Linda

doi:10.1016/j.jhepr.2021.100305

Cited by 92 publications

(86 citation statements)

References 126 publications

(287 reference statements)

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“…Depending on the world region, the main risk factors of HCC are viral hepatitis (HCV, HBV), aflatoxin-B1 exposure [83], alcoholic-related liver disease (ARLD), and NAFLD [45,82,84]. Importantly, NAFLD is becoming the leading HCC cause in both obese patients and non-obese individuals with metabolic disorders [85]. In addition, NAFLD has become a major cause of HCC-related mortality [86].…”

Section: Hepatocellular Carcinoma and Lipid Alterationsmentioning

confidence: 99%

The Role of Fatty Acids in Non-Alcoholic Fatty Liver Disease Progression: An Update

Hliwa

Ramos‐Molina

Łaski

et al. 2021

IJMS

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Non-alcoholic fatty liver disease (NAFLD) is a major public health problem worldwide. NAFLD (both simple steatosis and steatohepatitis) is characterized by alterations in hepatic lipid metabolism, which may lead to the development of severe liver complications including cirrhosis and hepatocellular carcinoma. Thus, an exhaustive examination of lipid disorders in the liver of NAFLD patients is much needed. Mass spectrometry-based lipidomics platforms allow for in-depth analysis of lipid alterations in a number of human diseases, including NAFLD. This review summarizes the current research on lipid alterations associated with NAFLD and related complications, with special emphasis on the changes in long-chain and short-chain fatty acids levels in both serum and liver tissue, as well as in the hepatic expression of genes encoding the enzymes catalyzing lipid interconversions.

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Section: Hepatocellular Carcinoma and Lipid Alterationsmentioning

confidence: 99%

The Role of Fatty Acids in Non-Alcoholic Fatty Liver Disease Progression: An Update

Hliwa

Ramos‐Molina

Łaski

et al. 2021

IJMS

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“…Non-alcoholic fatty liver disease (NAFLD) is the liver manifestation of metabolic syndrome and encompasses a large spectrum of clinic-pathological entities including steatosis, nonalcoholic steatohepatitis (NASH), and cirrhosis and its complications [1] . Recently, the term metabolic dysfunction-associated fatty liver disease (MAFLD) has been proposed to better define the liver manifestations of metabolic disorder [2] . As opposed to NAFLD, which is a diagnosis of exclusion, MAFLD is defined by positive diagnostic criteria and do not exclude chronic alcohol intake [2] .…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of liver carcinogenesis related to metabolic syndrome

Campani¹,

Nault²

2022

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Global prevalence of non-alcoholic fatty liver disease (NAFLD) and of NAFLD-hepatocellular carcinoma (HCC) is estimated to grow in the next years. The burden of NAFLD and the evidence that NAFLD-HCC arises also in non-cirrhotic patients, explain the urgent need of a better characterization of the molecular mechanisms involved in NAFLD progression. Obesity and diabetes cause a chronic inflammatory state which favors changes in serum cytokines and adipokines, an increase in oxidative stress, DNA damage, and the activation of multiple signaling pathways involved in cell proliferation. Moreover, a role in promoting NAFLD-HCC has been highlighted in the innate and adaptive immune system, dysbiosis, and alterations in bile acids metabolism. Several dietary, genetic, or combined mouse models have been used to study nonalcoholic steatohepatitis (NASH) development and its progression to HCC, but models that fully recapitulate the biological and prognostic features of human NASH are still lacking. In humans, four single nucleotide polymorphisms (PNPLA3, TM6SF2, GCKR, and MBOAT7) have been linked to the development of both NASH and HCC in cirrhotic and non-cirrhotic patients, whereas HSD17B13 polymorphism has a protective effect. In addition, higher rates of somatic ACVR2A mutations and a novel mutational signature have been recently discovered in NASH-HCC patients. The knowledge of the molecular pathogenesis of NAFLD-HCC will be helpful to personalized screening programs and allow for primary and secondary chemopreventive treatments for NAFLD patients who are more likely to progress to HCC.

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“…Nonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases [ 1 ]. Its prevalence is approximately 25% ranging from 13% in Africa and 42% in southeast Asia and the hallmark of the disease is excessive fat deposition in hepatocytes [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC

2021

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Nonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases. The phenotypic umbrella of NAFLD spans from simple and reversible steatosis to nonalcoholic steatohepatitis (NASH), which may worsen into cirrhosis and hepatocellular carcinoma (HCC). Notwithstanding, HCC may develop also in the absence of advanced fibrosis, causing a delayed time in diagnosis as a consequence of the lack of HCC screening in these patients. The precise event cascade that may precipitate NASH into HCC is intricate and it entails diverse triggers, encompassing exaggerated immune response, endoplasmic reticulum (ER) and oxidative stress, organelle derangement and DNA aberrancies. All these events may be accelerated by both genetic and environmental factors. On one side, common and rare inherited variations that affect hepatic lipid remodeling, immune microenvironment and cell survival may boost the switching from steatohepatitis to liver cancer, on the other, diet-induced dysbiosis as well as nutritional and behavioral habits may furtherly precipitate tumor onset. Therefore, dietary and lifestyle interventions aimed to restore patients’ health contribute to counteract NASH progression towards HCC. Even more, the combination of therapeutic strategies with dietary advice may maximize benefits, with the pursuit to improve liver function and prolong survival.

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Epidemiology of non-alcoholic fatty liver disease and hepatocellular carcinoma

Cited by 92 publications

References 126 publications

The Role of Fatty Acids in Non-Alcoholic Fatty Liver Disease Progression: An Update

The Role of Fatty Acids in Non-Alcoholic Fatty Liver Disease Progression: An Update

Molecular mechanisms of liver carcinogenesis related to metabolic syndrome

Genetics, Immunity and Nutrition Boost the Switching from NASH to HCC

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