Abstract
A large number of epidemiological studies have demonstrated that obesity is a risk factor for several human cancers. Several animal studies using rodents with diet-induced or genetic obesity have also demonstrated that obesity can promote tumor development. However, the effects of obesity on the early stages of carcinogenesis, and especially on the spontaneous occurrence of somatic gene mutations, remain unclear. To investigate the effects of obesity on the rate of spontaneous gene mutations, we performed reporter gene mutation assays in liver, kidney, and colon, organs in which obesity appears to be associated with cancer development on the basis of epidemiological or animal studies, in mice with high fat diet (HFD)-induced obesity. Six-week-old male and female C57BL/6 gpt delta mice were fed HFD or standard diet (STD) for 13 or 26 weeks. At the end of the experiments, reporter gene mutation assays of liver, kidney, and colon were performed. Final body weights and serum leptin levels of male and female mice fed HFD for 13 or 26 weeks were significantly increased compared with corresponding STD-fed groups. Reporter gene mutation assays of liver, kidney, and colon revealed that there were no significant differences in gpt or Spi- mutant frequencies between STD- and HFD-fed mice in either the 13-week or 26-week groups. These results indicate that HFD treatment and consequent obesity does not appear to influence the spontaneous occurrence of somatic gene mutations.
Highlights
A large number of epidemiological studies have demonstrated that obesity is a risk factor for several human cancers
These results indicate that high fat diet (HFD) treatment and consequent obesity does not appear to influence the spontaneous occurrence of somatic gene mutations
Final body weights of male mice fed standard diet (STD) or HFD for 13 weeks were 30.6±1.9 g and 36.2±3.2 g, and those of mice fed the diets for 26 weeks were 35.5±3.7 g and 45.2±3.4 g, respectively
Summary
A large number of epidemiological studies have demonstrated that obesity is a risk factor for several human cancers. A greater BMI is a modifiable risk factor for colon cancer for Asia population (Morrison et al, 2013). On the basis of epidemiological studies, the World Cancer Research Fund and the American Institute for Cancer Research suggested that greater body fat is associated with increased risk for several cancers, including colorectal, kidney, pancreas, breast (postmenopausal) and endometrial cancer, and has been suspected as a causative factor for gallbladder cancer. There is limited evidence suggesting that greater body fatness increases the risk of liver cancer (World Cancer Research Fund, 2007). The effects of obesity on the promotion of tumor development and the associated cancer cell biology
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