Kazumi Fujioka
It is known that Non-Alcoholic Fatty Liver Disease (NAFLD) causes NAFLD-associated Hepatocellular Carcinoma (HCC) and obesity, Type 2 Diabetes Mellitus (T2DM), and Cardiovascular Disease (CVD) as co-morbidities of NAFLD also promote the development and progression of HCC. Previous study indicated that dysregulated metabolites, low grade inflammation, immunity, and autophagy in the tumor microenvironment play a crucial role of HCC progression in obesity status. In this article, the author reviewed the current knowledge of association between obesity and hepatocellular carcinoma along with nitroglycerin-mediated vasodilation study. In result, with respect to the association between obesity and atherosclerosis, obesity is low grade inflammatory status, suggesting that inflammation and/or oxidative stress as a causal factor may induce decreased Flow-Mediated Dilatation (FMD) and impaired Nitroglycerin-Mediated Vasodilation (NMD). The clinical and experimental studies suggested that steatosisrelated lipotoxicity may cause hepatocarcinogenesis. It is putative that adipocytes serve as a critical role in the tumor microenvironment through the dysregulated adipokine secretion, leading to the effect of carcinogenesis, metastasis, and chemoresistance. Obesity-associated hepatocarcinogenesis may be associated with the remodeled adipose tissue, genetic factors, inflammation, oxidative stress, and immunity alteration.