Background: Colorectal cancer (CRC) is one of the major causes of morbidity and mortality. According to National Cancer Registry, the incidence of colorectal cancer in Peninsular Malaysia increases with age. The incidence is highest among Chinese population but lower among Indians and Malays. Many reviews have suggested that obesity may be associated with a higher risk (>50%) of colorectal cancer. Methods: This study collects a comprehensive data from the literature review available from respective journals on dietary intervention and the chemo-protective mechanisms of a few natural resources in obesity -associated colon cancer based on previous and current studies. Results: In obesity-associated colon cancer, the genes of interest and pathways that are mainly involved include NFκB, P13K/Akt, and MAPK pathways, and FTO, leptin, Cyclin D, MMPs, and STAT3 genes. Dietary modification is one of the alternative steps in early prevention of colon cancer. It has been proposed that the components present in certain foods may have the ability to protect against many diseases including the prevention of cancer. Conclusion: There are many factors that lead to obesity-associated colon cancer and the mechanisms behind it is still undergoing intensive research. This review aims to scrutinize research as well as reviews that have been previously reported on obesity associated colorectal cancer and the beneficial effects of including antioxidants-rich foods such as vegetables and fruits in the diet to reduce the risk of obesity associated colorectal cancer.
A high-fat diet could lead to obesity, increasing colorectal cancer risk due to dyslipidemia and chronic inflammation, while Piper betle (PB) exhibits anti-tumor, anti-inflammation, and anti-oxidant benefits. This study aimed to determine whether PB possesses chemopreventive effects on high-fat diet (HFD)-induced and azoxymethane (AOM)-induced colon cancer. Male Sprague-Dawley rats receiving either a normal diet or HFD were divided into control, PB, AOM, and AOM+PB subgroups which were then sacrificed after 24 weeks. The lipid profile, leptin, and inflammatory markers were measured from serum, and aberrant crypt foci (ACF) in the colon were detected by methylene blue staining. Cellular proliferation was identified through immunohistochemical staining of antigen Kiel 67 (Ki67) and beta-catenin. There were significant differences in serum total cholesterol, low-density lipoprotein, triglycerides, and high-density lipoprotein in the HFD compared to the normal diet group. The AOM group for normal diet and HFD exhibited significantly increased serum leptin, interleukin-6, IL-12p70, tumor necrosis factor-α, and nuclear factor-κB, with overexpression of Ki67 and beta-catenin. These changes were reversed by PB supplementation. In conclusion, PB demonstrated lipid-modifying and chemopreventive effects against HFD and AOM-induced colon cancer in rats.