A high-sucrose diet does not enhance spontaneous metastasis of Lewis lung carcinoma in mice

Authors: Yan, Lin; Sundaram, Sneha

Submitted to: Nutrition Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/3/2018
Publication Date: 8/1/2018
Publication URL: https://handle.nal.usda.gov/10113/6119252
Citation: Yan, L., Sundaram, S. 2018. A high-sucrose diet does not enhance spontaneous metastasis of Lewis lung carcinoma in mice. Nutrition Research. https://doi.org/10.1016/j.nutres.2018.07.001.
DOI: https://doi.org/10.1016/j.nutres.2018.07.001

Interpretive Summary: Consumption of sweeteners has increased in recent decades. A high energy intake contributes to obesity, a leading risk factor for cancer. Being obese at the time of cancer diagnosis is associated with poor prognosis and greater risk of developing recurrent or metastatic cancer, which directly affects the quality life and survival of cancer patients. To study the role of high-sugar intake in cancer spread, we compared a high-sucrose diet with a high-fat diet, on an equal energy basis, in a mouse model of lung metastasis. Mice fed the high-sucrose diet had fewer numbers of cancer nodules formed in the lungs than mice fed the high-fat diet. Mice fed the high-sucrose diet exhibited body fat buildup, but to a less degree compared to the high-fat diet. These mice had lower blood concentrations of cancer promoting chemicals that are associated with body fat buildup. This study shows that the sucrose diet does not enhance cancer spread in a mouse model of obesity. This lack of effect on cancer spread may be due to the less capability of the sucrose diet in building up body fat mass and producing related cancer promoting chemicals in mice. This study indicates the importance of maintaining a healthy body weight by reducing body fat in order to reduce the risk of chronic diseases, such as cancer, and promote health.

Technical Abstract: A high energy intake contributes to obesity, a risk factor for cancer. We previously reported that an excessive intake of dietary fat enhances malignant spread in mice. This study tested the hypothesis that consumption of a diet with an excessive amount of sucrose enhances metastasis. In a spontaneous metastasis model of Lewis lung carcinoma (LLC), male C57BL/6 mice were maintained on an AIN93G, a high-fat, or a high-sucrose diet for the duration of the study. Pulmonary metastases from a primary tumor, established by a subcutaneous injection of LLC cells, were quantified. There were no differences in energy intake among the groups. The percent body fat of the high-sucrose group, while higher than that of the AIN93G control group, was lower than that of the high-fat group. The number and size of lung metastases were significantly higher in the high-fat group than in the AIN93G group; these measurements in the high-sucrose group remained similar to those in the AIN93G group. Hepatic concentrations of triacylglycerols and plasma concentrations of insulin, proinflammatory cytokines (leptin, plasminogen activator inhibitor-1, and monocyte chemotactic protein-1) and angiogenic factors (vascular endothelial growth factor and tissue inhibitor of metalloproteinase-1) in the high-sucrose group were significantly lower than those in the high-fat group. In conclusion, the high-sucrose diet does not enhance spontaneous metastasis of LLC. This null effect may be due to the inadequate production of tumorigenic proinflammatory cytokines and angiogenic factors by the high-sucrose diet compared to the high-fat diet.