Abstract
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.
Highlights
Published: 23 October 2021Nonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases [1]
NAFLD comprises a spectrum of histological conditions ranging from simple steatosis which is considered a benign as well as a reversible condition to nonalcoholic steatohepatitis (NASH) in which triglyceride accumulation in the hepatic parenchyma is associated with inflammation and ballooning [3]
NASH-hepatocellular carcinoma (HCC) showed a unique tumor signature characterized by bile and fatty acid signaling, oxidative stress, inflammation, and mitochondrial dysfunction and in patients who carried the PNPLA3 I148M variant it was enriched in defective pathways of DNA repair and reduced TP53 signaling, reinforcing the role of this polymorphism in
Summary
Nonalcoholic fatty liver disease (NAFLD) is the leading contributor to the global burden of chronic liver diseases [1]. NASH may progress to fibrosis, cirrhosis and hepatocellular carcinoma (HCC) and it represents the second most common indication for liver transplantation in the United States [4]. NASH-HCC usually occurs in older patients, it is diagnosed at later stages and is associated with poorer survival compared to viral hepatitis-related HCC [2]. It may develop in the absence of cirrhosis most commonly in patients with advanced fibrosis and the lack of HCC screening in these patients partly explains the late diagnosis [5,6]. The present review aims to discuss the metabolic, genetic, dietary, and immunity-related factors which predispose to liver cancer in NAFLD patients, emphasizing the potential effect of nutritional therapy in HCC
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