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Several epidemiological
studies have shown that obesity and related metabolic abnormalities are
associated with an increase in incidence and mortality rates for a number of
tumors. It has been shown that obesity and type 2 diabetes are risk factors
associated with the onset of malignant tumors such as colon cancer. Recently,
it is increasingly fueling that NAFLD may be added and a new risk factor for
the extra-hepatic tumors, in particular in the gastro intestinal tract. It is
seen that NAFLD is strongly associated with features of the metabolic syndrome,
including obesity, insulin resistance, type 2 diabetes mellitus (DM2) and
dyslipidemia. Certainly, poor eating habits associated with a sedentary life
style represent risk factors for the onset of NAFLD, in this case a combination
of dietary restrictions associated with physical activity is commonly
recommended for people with NAFLD. However, a significant percentage of
patients develop NAFLD despite having a body mass index (BMI) normal and
certain features of metabolic syndrome. As lifestyles have become increasingly
sedentary, NAFLD has quickly become one of the most common causes of liver
disease worldwide. The non-alcoholic hepatic steatosis of the liver (NAFLD) is
a condition closely related to obesity, diabetes and metabolic syndrome. It is
often discovered after an occasional ultrasound assessment during ultrasound of
the abdomen, but in reality many cases are associated with other metabolic
disorders (hypertriglyceridemia, hypercholesterolemia, hypertension), configuring
the framework of the so-called “metabolic syndrome”. With increasing
body mass index (BMI) increases the prevalence of NAFLD, and visceral obesity
is a major factor responsible for NAFLD. An ectopic fat accumulation, including
visceral obesity and fatty liver, can lead to a dysfunction of adipose tissue
with consequent alteration of adipocytokines levels. Insulin resistance (IR)
seems to be a key factor in the pathogenesis of NAFLD (Figure 1), so that NAFLD
is considered the hepatic component of the IR or metabolic syndrome (MS)
11.NAFLD is traditionally considered to be the hepatic manifestation of the
metabolic syndrome (MS) and numerous studies indicate an increased risk of
cancer onset in subjects with metabolic syndrome, particularly in the gastrointestinal
tract. In this context, NAFLD may share common risk factors (i.e. obesity and
diabetes type 2) or actively mediate some pathogenic mechanism, as in the case
of liver cancer (hepatocellular carcinoma, HCC). Excluding the latter,
colorectal cancer (CRC) has so far been consistently associated with NAFLD
10,11. To date the mechanisms that underlie the relationship between NAFLD
and the risk of cancer are not completely explained, but probably derived from
the two-way relationship
between NAFLD and metabolic syndrome. NAFLD and visceral adipose tissue
are the main parts of the axis of central obesity. In this state of chronic
low-grade inflammation and insulin resistance (IR), it creates a
micro-environment favorable for the development of cancer by stimulation of
insulin growth factor-factor 1 (IGF-1) axis hyperinsulinemia 9,69 -71.
Through its proliferative and anti-apoptotic effects, this process can increase
mutations that promote carcinogenesis. It is assumed that a state of insulin
resistance associated with the metabolic syndrome and the consequent
inflammatory cascade associated with the development of NAFLD appears to play
an important role in the development of colon cancer. Colorectal cancer (CRC)
is one of the most common cancers worldwide. It is known that the inflammatory
bowel diseases and genetic factors are well-known risk factors for the
development of CRC. Recent studies have shown that 75% -95% of all the
carcinomas of the colon-rectum are not caused by genetic factors, but are
related to factors associated with the lifestyle. Recently, it was demonstrated
a connection between NAFLD and CRC. Insulin resistance and the metabolic
syndrome are common risk factors shared in NAFLD and in colorectal cancer. 

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