Division of Biokinesiology and Physical Therapy, Ostrow School of Dentistry, University of Southern California (USC), 1540 E. Alcazar St., CHP 155, Los Angeles, CA, 90089, USA.
Diabetes & Obesity Program and Department of Pediatrics, Children's Hospital Los Angeles, Keck School of Medicine (KSOM), Los Angeles, USA.
Breast Cancer Res Treat. 2018 Feb;168(1):147-157. doi: 10.1007/s10549-017-4576-y. Epub 2017 Nov 22.
Obesity is a leading modifiable contributor to breast cancer mortality due to its association with increased recurrence and decreased overall survival rate. Obesity stimulates cancer progression through chronic, low-grade inflammation in white adipose tissue, leading to accumulation of adipose tissue macrophages (ATMs), in particular, the pro-inflammatory M1 phenotype macrophage. Exercise has been shown to reduce M1 ATMs and increase the more anti-inflammatory M2 ATMs in obese adults. The purpose of this study was to determine whether a 16-week exercise intervention would positively alter ATM phenotype in obese postmenopausal breast cancer survivors.
Twenty obese postmenopausal breast cancer survivors were randomized to a 16-week aerobic and resistance exercise (EX) intervention or delayed intervention control (CON). The EX group participated in 16 weeks of supervised exercise sessions 3 times/week. Participants provided fasting blood, dual-energy X-ray absorptiometry (DXA), and superficial subcutaneous abdominal adipose tissue biopsies at baseline and following the 16-week study period.
EX participants experienced significant improvements in body composition, cardiometabolic biomarkers, and systemic inflammation (all p < 0.03 vs. CON). Adipose tissue from EX participants showed a significant decrease in ATM M1 (p < 0.001), an increase in ATM M2 (p < 0.001), increased adipose tissue secretion of anti-inflammatory cytokines such as adiponectin, and decreased secretion of the pro-inflammatory cytokines IL-6 and TNF- α (all p < 0.055).
A 16-week aerobic and resistance exercise intervention attenuates adipose tissue inflammation in obese postmenopausal breast cancer survivors. Future large randomized trials are warranted to investigate the impact of exercise-induced reductions in adipose tissue inflammation and breast cancer recurrence.
肥胖是导致乳腺癌死亡率的主要可改变因素,因为它与复发增加和总生存率降低有关。肥胖通过白色脂肪组织中的慢性、低水平炎症刺激癌症进展,导致脂肪组织巨噬细胞(ATMs)的积累,特别是促炎 M1 表型巨噬细胞。运动已被证明可减少肥胖成年人中的 M1 ATM 并增加更抗炎的 M2 ATM。本研究的目的是确定 16 周的运动干预是否会对肥胖绝经后乳腺癌幸存者的 ATM 表型产生积极影响。
20 名肥胖绝经后乳腺癌幸存者被随机分为 16 周有氧运动和抗阻运动(EX)干预组或延迟干预对照组(CON)。EX 组参加了 16 周的监督运动课程,每周 3 次。参与者在基线和 16 周研究期后提供空腹血液、双能 X 射线吸收法(DXA)和浅表皮下腹部脂肪组织活检。
EX 参与者的身体成分、心脏代谢生物标志物和全身炎症均有显著改善(均 p<0.03 与 CON 相比)。EX 参与者的脂肪组织中 ATM M1 显著减少(p<0.001),ATM M2 增加(p<0.001),抗炎细胞因子如脂联素的脂肪组织分泌增加,促炎细胞因子 IL-6 和 TNF-α 的分泌减少(均 p<0.055)。
16 周有氧运动和抗阻运动干预可减轻肥胖绝经后乳腺癌幸存者的脂肪组织炎症。未来需要进行大型随机试验,以研究运动引起的脂肪组织炎症减少和乳腺癌复发的影响。