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Submitted on March 13, 2006
Accepted on August 25, 2006
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892; Nutrition and Molecular Carcinogenesis Section, Laboratory of Biosystems and Cancer, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892-1758; Department of Medicine and Surgery, McGill University Health Center, Royal Victoria Hospital, Montreal, Quebec, Canada; Basic Research Program, SAIC-Frederick, Inc., NCI Frederick, Frederick, MD 21702-1201; Department of Carcinogenesis, University of Texas-MD Anderson Cancer Center, Smithville, TX 78957
* To whom correspondence should be addressed. E-mail: shoshana.yakar{at}mssm.edu.
Obesity increases the risk of many cancers in both males and females. This study describes a link between obesity, obesity-associated metabolic alterations and the risk of developing cancer in male and female mice. The goal of this study was to evaluate the relationship between gender and obesity and to determine the role of estrogen status in obese females and its effect on tumor growth. We examined the susceptibility of C57BL/6 mice to diet-induced obesity, insulin resistance/glucose intolerance and tumors. Mice were injected subcutaneously with one of two tumorigenic cell lines, Lewis lung carcinoma or mouse colon 38- adenocarcinoma. Results show that tumor growth rate was increased in obese mice vs. control mice irrespective of the tumor cell type. To investigate the effect of estrogen status on tumor development in obese females, we compared metabolic parameters and tumor growth in ovariectomized and intact obese female mice. Obese ovariectomized female mice developed insulin resistance and glucose intolerance similar to that observed in obese males. Our results demonstrate that body adiposity increased in ovariectomized females irrespective of the diet administered and that tumor growth correlated positively with body adiposity. Overall, these data point to more rapid tumor growth in obese mice and suggest that endogenous sex steroids, together with diet, affect adiposity, insulin sensitivity, and tumor growth in female mice.
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