The potential molecular mechanism of carcinogenesis is as follows: the metabolically active visceral adipose tissues promote the production of inflammatory mediators and cytokines (e.g., TNF-α and leptin), inhibit the secretion of adiponectin, and facilitate the development of insulin resistance (99, 100) and subsequent hyperinsulinemia to partially promote carcinogenesis by stimulating the increase in the expression of insulin-like growth factor (IGF-1) (101). This evidence concerns the gene LEP and hyperinsulinism.