Abstract
The objective of this study was to determine whether a reduction in energy intake ameliorated the high-fat diet-enhanced spontaneous metastasis of Lewis lung carcinoma in mice. Male C57BL/6 mice were fed the AIN93G diet, a high-fat diet or a high-fat diet with a 5% restriction of the intake. Energy restriction reduced body adiposity and body weight, but maintained growth similar to mice fed the AIN93G diet. The high-fat diet significantly increased the number and size (cross-sectional area and volume) of metastases formed in lungs. Restricted feeding reduced the number of metastases by 23%, metastatic cross-sectional area by 32% and volume by 45% compared to the high-fat diet. The high-fat diet elevated plasma concentrations of proinflammatory cytokines (monocyte chemotactic protein-1, plasminogen activator inhibitor-1, leptin), angiogenic factors (vascular endothelial growth factor, tissue inhibitor of metalloproteinase-1) and insulin. Restricted feeding significantly reduced the high-fat diet-induced elevations in plasma concentrations of proinflammatory cytokines, angiogenic factors and insulin. These results demonstrated that a reduction in diet intake by 5% reduced high-fat diet-enhanced metastasis, which may be associated with the mitigation of adiposity and down-regulation of cancer-promoting proinflammatory cytokines and angiogenic factors.
Highlights
Overweight and obesity affect cancer survival and are associated with increased mortality caused by cancer in the U.S [1]
We reported that feeding mice a high-fat diet enhances spontaneous metastasis of Lewis lung carcinoma (LLC) in lungs [17, 18]
Consistent with our previous reports [9, 17], the present study showed that feeding mice an obesogenic, high-fat diet enhances spontaneous metastasis of LLC in the lungs
Summary
Overweight and obesity affect cancer survival and are associated with increased mortality caused by cancer in the U.S [1]. Obesity at the time of cancer diagnosis can be predictive of increased risk of early recurrence and metastasis [2,3,4,5]. Animal studies support the clinical observation that consumption of an obesogenic, high-fat diet increases primary tumorigenesis [6,7,8] and metastasis [6, 9]. Weight reduction through energy restriction is considered useful in alleviating obesity and obesityassociated cancer risk. Animal studies show that energy restriction is effective in reducing primary tumorigenesis in various models [14,15,16]. Few studies have investigated the efficacy of energy restriction on metastasis
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