It the insulin-like growth factor 1 and 2)

It has been suggested by several
studies that in patients with metabolic syndrome there is a greater risk of
developing CRC and IR is associated with an increased risk of developing CRC.
Metabolic syndrome occurs as a result of modern life style. This hypothesis is
supported by studies showing that some of the IR factors (insulin and the
insulin-like growth factor 1 and 2) promote the progression of CRC precursors
(colon polyps) in invasive adenocarcinoma.In recent years, numerous studies
have shown the importance of MS, IR and chronic inflammation in the
pathogenesis of CRC. As previously mentioned, patients with NAFLD have reduced
levels of protective adipokines like adiponectin, in fact decreased levels of
adiponectin leads to the promotion of malignant alterations of the colon cells.
Therefore IR, chronic inflammation, oxidative stress and low adiponectin levels
are common factors between NAFLD, polyposis of the colon and CRC. However, at
present it is not yet clear what is the pathophysiological mechanism underlying
the link between NAFLD, CRC and adenomatous colorectal polyps. It is thought
that this mechanism is derived from the bidirectional relationship between
NAFLD and MetS. It is plausible that the base of the promotion of neoplastic
growth there is an increase of insulin and pro-inflammatory cytokines (for
example, the insulin-like growth factor (IGF) -1). In patients with NAFLD has
been demonstrated an increased cardiovascular risk, as a prolonged accumulation
of lipids make the liver tissue as a source of factors that would increase the
pro-inflammatory systemic state. In a similar way, the dysfunction of adipose
tissue in obese subjects is associated with an increased risk of cancer due to
the secretion of various pro-inflammatory factors-promoting carcinogenesis such
as IL-6 and TNF-? and to a decrease of protective factors such as’ adiponectin
(figure 2). A similar relationship may exist between fatty liver disease and
development of pre-neoplastic lesions that would promote colon cancer. The
exact nature of these soluble mediators derived from fatty liver is not yet