Obesity has played a crucial role in the pathogenesis of various cancers, including colorectal cancer (CRC). Obesity has shown to increase the blood levels of insulin, insulin-like growth factor-1 (IGF-1), leptin, resistin, inflammatory cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1) which in turn acts via various signaling pathways to induce colonic cell proliferation and in turn CRC development. It has been shown that estrogen can prevent and cause CRC based on which receptor it acts. Obese patients have relatively low levels of ghrelin and adiponectin that inhibit cell proliferation which further adds to their risk of developing CRC. Obesity can alter the microbial flora of the gut in such a way as to favor carcinogenesis. Weight loss and good physical activity have been related to a reduced incidence of CRC; obese individuals should be screened for CRC and counseled about the importance of weight reduction, diet, and exercise. The best way of screening is using BMI and waist circumference (WC) to calculate the CRC risk in obese people. This study has reviewed the association between obesity and its pathophysiological association with CRC development.
Keywords: colorectal cancer (crc); estrogen and crc; ghrelin and crc; obesity and cancer; obesity and inflammatory markers; obesity and mutation; oxidative dna damage; resistin and cancer; role of gut microbiomes in cancer; role of obesity and diabetes.
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