Copyright ©The Author(s) 2016.
World J Gastroenterol. Jan 7, 2016; 22(1): 394-406
Published online Jan 7, 2016. doi: 10.3748/wjg.v22.i1.394
Figure 1
Figure 1 Proposed mechanisms linking obesity and its related metabolic abnormalities to the development of hepatocellular carcinoma. HCC: Hepatocellular carcinoma; HSCs: Hepatic stellate cells; TNF-α: Tumor necrosis factor-α; IL-6: Interleukin-6; IGF-1: Insulin-like growth factor-1; IGFBP-3: IGF-binding protein-3; NAFLD: Nonalcoholic fatty liver disease; NASH: Nonalcoholic steatohepatitis; Jak: Janus kinase; Stat: Signal transducer and activator of transcription; SASP: Senescence-associated secretory phenotype; PI3K: Phosphatidylinositol 3-kinase.
Figure 2
Figure 2 Mechanisms of action of green tea catechins, branched-chain amino acids, and acyclic retinoid in the inhibition of obesity-related liver carcinogenesis. HCC: Hepatocellular carcinoma; GTCs: Green tea catechins; BCAA: Branched-chain amino acid; ACR: Acyclic retinoid; TNF-α: Tumor necrosis factor-α; IL-6: Interleukin-6; IL-1β: Interleukin-1β; IGF-1: Insulin-like growth factor-1; IGF-1R: Insulin-like growth factor-1 receptor; IGFBP-3: IGF-binding protein-3; Stat3: Signal transducer and activator of transcription-3; Erk-1/2: Extracellular signal-regulated kinase-1/2; GSK-3β: Glycogen synthase kinase-3β; AMPK: AMP-activated kinase.