Int J Biol Sci 2019; 15(3):610-616. doi:10.7150/ijbs.29599 This issue
1. Department of Clinical Pathology Laboratory. IRCCS - Istituto Tumori Giovanni Paolo II, Viale Orazio Flacco 65, 70124 Bari, Italy
2. Interdisciplinary Department of Medicine, University of Bari School of Medicine, Piazza G. Cesare, 11, 70124 Bari, Italy
3. Experimental Medical Oncology, IRCCS - Istituto Tumori Giovanni Paolo II, Viale Orazio Flacco 65, 70124 Bari, Italy
Western populations are becoming increasingly sedentary and the incidence of nonalcoholic fatty liver disease (NAFLD) is increasing and becoming one of the most common causes of liver disease worldwide. Also, NAFLD is considered one the new emerging risk factors for development of tumors of the gastro-intestinal tract, particularly hepatocellular carcinoma (HCC). Visceral obesity is an important risk factor for the onset of NAFLD. An accumulation of ectopic fat, including visceral obesity and fatty liver leads to a dysfunction of the adipose tissue with impaired production of adipocytokines which, in turn, favor an increase in pro-inflammatory cytokines. In this review, we discuss how the obesity-related chronic state of low-grade inflammation and the presence of NAFLD lead to the emergence of a microenvironment favorable to the development of cancer.
Keywords: NAFLD, adipocytokines, inflammation, obesity, cancer