运动刺激的脂肪组织中的溶解素生物合成被高脂肪饮食诱导的上腺素缺乏症所废除
Ernesto Pena Calderin1,2, Jing-Juan Zheng1, Nolan L Boyd1
1Division of Environmental Medicine, Center for Cardiometabolic Science, Christina Lee Brown Envirome Institute, University of Louisville School of Medicine, KY. (E.P.C., J.-J.Z., N.L.B., W.L., B.S., B.G.H., J.H.).
概括
运动促进脂肪组织中的抗炎途径,但高脂肪饮食通过减少catecholamine产量来阻止这些益处. 这凸显了饮食对运动的影响.
科学领域:
- 代谢健康 代谢健康
- 免疫学 免疫学 免疫学
- 运动生理学 运动生理学
背景情况:
- 白色脂肪组织的饮食引起的炎症与胰岛素抵抗有关.
- 运动可以对抗饮食引起的炎症和胰岛素抵抗,但机制尚不清楚.
- 运动可以通过通过上腺体信号传递来增强专门的前溶解脂质介质 (SPMs) 来缓解炎症.
研究的目的:
- 为了研究运动是否刺激脂肪组织中的前溶解通路.
- 为了确定饮食是否会改变运动的预解决效果.
- 为了测试运动诱导的上腺体信号是否被高脂肪饮食抑制.
主要方法:
- 给小鼠食控制或高脂肪饮食,并进行跑步机炼.
- 评估葡萄糖处理,身体组成和运动表现.
- 在脂肪组织中测量了catecholamines,SPM水平和巨细胞表型.
主要成果:
- 运动增加了脂肪组织SPM生物合成和抗炎M2巨细胞.
- 高脂肪饮食取消了运动的前期解决效果.
- 高脂肪饮食抑制了运动诱导的上腺素的产生和PNMT的表达.
结论:
- 运动刺激脂肪组织前溶解通路.
- 高脂肪饮食会损害运动在脂肪组织中的抗炎作用.
- 饮食中的脂肪摄入干扰了运动诱导的甲醇胺生物合成,阻碍了炎症的解决.
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