The epidemic of obesity/overweight induces a threatening spread of metabolic syndrome (MS). The existence of MS for 5–10 years induces the doubling of cardiovascular diseases and the type 2 diabetes mellitus (2TDM) will 5 times more frequent. More and more data sustain that MS and 2TDM promote the development of malignant tumors. Their risk in diabetics is double or more for liver, pancrea-tic and endometrial carcinomas, but the colon, rectum, breast and bladder cancers are also more frequent in DM. The increased frequency of tumors in MS and 2TDM may be attributed primarily to the central obesity and its metabolic consequences, and to their relationships with carcinogenesis. Important common etiological factors are the hyperglycaemia, the insulin resistance, the hyperinsulinism and the inflammation. We emphasize the role of insulin resistance and that of hyperinsulinaemia (hyperproinsulinaemia), because insulin exerts not only metabolic but also mitogenic (carcinogenic?) actions. The same time, the drugs reducing the insulin resistance (and hyperinsulinaemia), as thiazolidindiones, and especially metformin, exert anticancer effects in diabetics. Metformin has similar effects in non-diabetics, too; it reduces both the cancer risk and mortality, especially in colorectal and breast cancers. The mechanism of anticancer actions of metformin is complex: stimulates AMP-activated protein-kinase (AMPK) and so the catabolic processes, and reduces the insulin resistance. The first action results an inhibition of mTORC1 (mammalian TOR-complex 1), a signaling complex of mTOR. The same time metformin inhibits the IGF-I/AKT pathway and the cell cycle mediated by p53. Recently were described two other AMPK-independent anticancer mechanisms, too.
Keywords: metabolic syndrome, type 2 diabetes mellitus, anticancer effects of metformin.