Exercise suppresses tumor growth independent of high fat food intake and associated immune dysfunction
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Exercise suppresses tumor growth independent of high fat food intake and associated immune dysfunction. / Hojman, Pernille; Stagaard, Rikke; Adachi-Fernandez, Emi; Deshmukh, Atul S.; Mund, Andreas; Olsen, Caroline H.; Keller, Lena; Pedersen, Bente K.; Gehl, Julie.
In: Scientific Reports, Vol. 12, No. 1, 5476, 2022.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Exercise suppresses tumor growth independent of high fat food intake and associated immune dysfunction
AU - Hojman, Pernille
AU - Stagaard, Rikke
AU - Adachi-Fernandez, Emi
AU - Deshmukh, Atul S.
AU - Mund, Andreas
AU - Olsen, Caroline H.
AU - Keller, Lena
AU - Pedersen, Bente K.
AU - Gehl, Julie
N1 - Publisher Copyright: © 2022, The Author(s).
PY - 2022
Y1 - 2022
N2 - 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.
AB - 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.
U2 - 10.1038/s41598-022-08850-5
DO - 10.1038/s41598-022-08850-5
M3 - Journal article
C2 - 35361802
AN - SCOPUS:85127431150
VL - 12
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
IS - 1
M1 - 5476
ER -
ID: 305184681