Lloyd Jesse W, Zerfass Kristy M, Heckstall Ebony M, Evans Kristin A
Department of Exercise Science, Syracuse University, 820 Comstock Avenue, Women's Building Room 201 Syracuse, NY 13244, USA.
Department of Exercise Science, Syracuse University, Syracuse, NY 13244, USA.
Ther Adv Endocrinol Metab. 2015 Oct;6(5):189-98. doi: 10.1177/2042018815589088.
Chemerin concentrations are elevated in obesity and associated with inflammation and insulin resistance. Exercise improves insulin sensitivity, which may be facilitated by changes in chemerin. We explored the effects of chronic exercise on chemerin levels in diet-induced obese mice.
We divided 40 mice into 4 groups: high-fat diet/exercise, high-fat diet/sedentary, normal diet/exercise, and normal diet/sedentary. A 9-week dietary intervention was followed by a 12-week exercise intervention (treadmill run: 11 m/min for 30 min, 3×/week). We analyzed blood samples before and after the exercise intervention. We used t-tests and linear regression to examine changes in chemerin, insulin resistance, and inflammatory markers, and associations between changes in chemerin and all other biomarkers.
Chemerin increased significantly across all mice over the 12-week intervention (mean ± SD = 40.7 ± 77.8%, p = 0.01), and this increase was smaller in the exercise versus sedentary mice (27.2 ± 83.9% versus 54.9 ± 70.5%, p = 0.29). The increase among the high-fat diet/exercise mice was ~44% lower than the increase among the high-fat diet/sedentary mice (55.7 ± 54.9% versus 99.8 ± 57.7%, p = 0.12). The high-fat diet mice showed significant increases in insulin (773.5 ± 1286.6%, p < 0.0001) and homeostatic model assessment of insulin resistance (HOMA-IR; 846.5 ± 1723.3%, p < 0.01). Mediation analyses showed that increases in chemerin explained a substantial amount of the diet-induced increases in insulin and HOMA-IR.
Chronic exercise may attenuate diet-driven increases in circulating chemerin, and the insulin resistance associated with a high-fat diet may be mediated by diet-induced increases in chemerin.
肥胖人群中凯莫瑞蛋白(chemerin)浓度升高,且与炎症和胰岛素抵抗相关。运动可改善胰岛素敏感性,这可能通过凯莫瑞蛋白的变化来促进。我们探讨了长期运动对饮食诱导肥胖小鼠凯莫瑞蛋白水平的影响。
我们将40只小鼠分为4组:高脂饮食/运动组、高脂饮食/久坐组、正常饮食/运动组和正常饮食/久坐组。先进行为期9周的饮食干预,随后进行为期12周的运动干预(跑步机跑步:11米/分钟,持续30分钟,每周3次)。我们分析了运动干预前后的血样。我们使用t检验和线性回归来检查凯莫瑞蛋白、胰岛素抵抗和炎症标志物的变化,以及凯莫瑞蛋白变化与所有其他生物标志物之间的关联。
在为期12周的干预中,所有小鼠的凯莫瑞蛋白均显著增加(平均值±标准差=40.7±77.8%,p = 0.01),且运动小鼠的增加幅度小于久坐小鼠(27.2±83.9%对54.9±70.5%,p = 0.29)。高脂饮食/运动组小鼠的增加幅度比高脂饮食/久坐组小鼠低约44%(55.7±54.9%对99.8±57.7%,p = 0.12)。高脂饮食小鼠的胰岛素(773.5±1286.6%,p < 0.0001)和胰岛素抵抗稳态模型评估(HOMA-IR;846.5±1723.3%,p < 0.01)显著增加。中介分析表明,凯莫瑞蛋白的增加解释了饮食诱导的胰岛素和HOMA-IR增加的很大一部分。
长期运动可能会减弱饮食驱动的循环凯莫瑞蛋白增加,与高脂饮食相关的胰岛素抵抗可能由饮食诱导的凯莫瑞蛋白增加介导。