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Effects of diet‐induced obesity on secondary tumor development and plasma cytokine expression in mice
Author(s) -
Yan Lin,
DeMars Lana
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.977.11
Subject(s) - endocrinology , medicine , adiponectin , lewis lung carcinoma , obesity , leptin , cytokine , lung , biology , cancer , metastasis , insulin resistance
We studied the effects of diet‐induced obesity on secondary tumor development and growth in mice. Three‐wk old male C57BL/6 mice were fed the AIN‐93G or a 45% fat diet (n=25) for 7 wks before they were subcutaneously injected with 2.5×10 5 Lewis lung carcinoma cells. The primary tumor was resected 2 wks later, and mice were maintained on their respective diets for an additional 2 wks. There was a 2‐fold increase in the number of lung metastases in the high‐fat diet‐fed mice compared to the AIN‐93G‐fed mice ( P <0.05). Feeding tumor‐bearing mice the high‐fat diet resulted in ≥50% increases in expression of 16 plasma cytokines (including leptin, IL‐1β, MCP‐1, TIMP‐1 and VEGF), and an approximately 50% decrease in adiponectin, compared to the AIN‐93G‐fed tumor‐bearing mice. Results of ELISA assays showed that were no differences in plasma concentrations of IL‐1β, MCP‐1, TIMP‐1 and VEGF in non‐tumor‐bearing mice fed the AIN‐93G or the high‐fat diet, but significant increases in these cytokines in tumor‐bearing mice fed the AIN‐93G diet compared to the non‐tumor‐bearing mice fed the same diet, and further significant increases in these cytokines were observed in tumor‐bearing mice fed the 45% fat diet. The present study demonstrated that diet‐induced obesity enhanced secondary tumor development and growth in tumor‐bearing mice and that this aggressiveness was accompanied with increases in angiogenic cytokines in plasma.

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