Obesity and its related metabolic disorders, including
insulin resistance and chronic
inflammation, increase the risk of
colorectal cancer (CRC). This observation suggests that the metabolic abnormalities associated with
obesity can be effective targets for preventing the development of CRC in obese individuals. In recent years, many studies using obese and diabetic animal models have been conducted to investigate the
chemoprevention of CRC using
pharmaceutical or nutritional interventions.
Pitavastatin, a medicine used to treat
hyperlipidemia, prevents the development of
obesity-related colorectal
carcinogenesis by attenuating chronic
inflammation.
Anti-hypertensive medicines, such as
captopril and
telmisartan, also suppress the formation of colonic preneoplastic lesions in obese and diabetic mice. In addition, several
phytochemicals, including
green tea catechins, have been reported to improve metabolic disorders and prevent the development of various
cancers, including CRC. Moreover, the administration of
branched-chain amino acids, which improves
protein malnutrition and prevents the progression of
hepatic failure, is effective for suppressing
obesity-related colon
carcinogenesis, which is thought to be associated with improvements in
insulin resistance. In the present article, we summarize the detailed relationship between metabolic abnormalities and the development of CRC. This review also outlines recent evidence, in particular drawing from basic and clinical examinations using either
pharmaceutical or nutritional intervention that suggests that targeting metabolic alterations may be an effective strategy for preventing the development of CRC in obese individuals.