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Effects of diet-induced obesity on colitis-associated colon tumor formation in A/J mice

Authors
Park, S-YKim, J-SSeo, Y-RSung, M-K
Issue Date
Feb-2012
Publisher
NATURE PUBLISHING GROUP
Keywords
colon cancer; high-fat diet; insulin; leptin
Citation
INTERNATIONAL JOURNAL OF OBESITY, v.36, no.2, pp.273 - 280
Journal Title
INTERNATIONAL JOURNAL OF OBESITY
Volume
36
Number
2
Start Page
273
End Page
280
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/11984
DOI
10.1038/ijo.2011.83
ISSN
0307-0565
Abstract
Objective: Studies have indicated that obesity is associated with a higher risk of colorectal cancer. This study was performed to determine the effect of diet-induced obesity on the formation of azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colon tumors and to identify adiposity-related mechanisms. Methods: Male A/J mice were placed on either a high-fat diet (HFD; 45% of total calories from fat) or a normal diet (ND; 15% of calories from fat) for 12 weeks. To induce colon tumors, AOM was administered at a dose of 10 mg/kg body weight, followed by two cycles of DSS supply. Results: Study results indicated that the HFD group had twofold higher numbers of colonic tumors, as compared with the ND group. The HFD group also had significantly increased body weight and epididymal fat weight, which were associated with increases of serum insulin, insulin-like growth factor-1, leptin, epididymal fat pad leptin mRNA and colonic leptin receptor (Ob-R) mRNA. Animals on HFD showed higher expressions of Ob-R, insulin receptor, phosphorylated Akt, phosphorylated extracellular signal-regulated kinases, Bcl-xL and Cyclin D1 proteins in the colon. Conclusion: The results suggest that HFD-induced obesity facilitates colon tumor formation, possibly by regulating downstream targets of circulating adiposity-related factors via receptor-mediated signaling of the phosphatidylinositol 3-kinase/Akt pathway. International Journal of Obesity (2012) 36, 273-280; doi:10.1038/ijo.2011.83; published online 19 April 2011
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