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Exercise suppresses tumor growth independent of high fat food intake and associated immune dysfunction

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Epidemiological data suggest that exercise training protects from cancer independent of BMI. Here, we aimed to elucidate mechanisms involved in voluntary wheel running-dependent control of tumor growth across chow and high-fat diets. Access to running wheels decreased tumor growth in B16F10 tumor-bearing on chow (− 50%) or high-fat diets (− 75%, p < 0.001), however, tumor growth was augmented in high-fat fed mice (+ 53%, p < 0.001). Tumor growth correlated with serum glucose (p < 0.01), leptin (p < 0.01), and ghrelin levels (p < 0.01), but not with serum insulin levels. Voluntary wheel running increased immune recognition of tumors as determined by microarray analysis and gene expression analysis of markers of macrophages, NK and T cells, but the induction of markers of macrophages and NK cells was attenuated with high-fat feeding. Moreover, we found that the regulator of innate immunity, ZBP1, was induced by wheel running, attenuated by high-fat feeding and associated with innate immune recognition in the B16F10 tumors. We observed no effects of ZBP1 on cell cycle arrest, or exercise-regulated necrosis in the tumors of running mice. Taken together, our data support epidemiological findings showing that exercise suppresses tumor growth independent of BMI, however, our data suggest that high-fat feeding attenuates exercise-mediated immune recognition of tumors.

OriginalsprogEngelsk
Artikelnummer5476
TidsskriftScientific Reports
Vol/bind12
Udgave nummer1
ISSN2045-2322
DOI
StatusUdgivet - dec. 2022

Bibliografisk note

Funding Information:
The Centre for Physical Activity Research (CFAS) is supported by TrygFonden (grants ID 101390, ID 20045, and ID 125132). During the study period, the Centre of Inflammation and Metabolism (CIM) was supported by a Grant from the Danish National Research Foundation (DNRF55). The study was further supported by Grants from Lundbeck Foundation, the Danish Cancer Society and the Research fund of the Capital Region of Copenhagen. We also like to acknowledge support from Novo Nordisk Foundation Center for Protein Research (NNF14CC001).

Publisher Copyright:
© 2022, The Author(s).

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