Laurens Claire, Bergouignan Audrey, Moro Cedric
CNRS, IPHC, UMR 7178, Université de Strasbourg, Strasbourg, France.
Centre National d'Etudes Spatiales, Paris, France.
Front Physiol. 2020 Feb 13;11:91. doi: 10.3389/fphys.2020.00091. eCollection 2020.
Physical activity reduces cardiometabolic risk, while physical inactivity increases chronic diseases risk. This led to the idea that exercise-induced muscle contraction contributes to metabolic regulation and health. It is now well established that skeletal muscle, through the release of endocrine factors, i.e., so-called myokines, crosstalk with metabolic organs such as adipose tissue, liver and pancreas. Recent advances suggested that a number of myokines are able to modulate adipose tissue metabolism and thermogenic activity, liver endogenous glucose production and β-cell insulin secretion. This novel paradigm offers a compelling hypothesis and molecular basis to explain the link between physical inactivity and chronic diseases. Herein, we review major findings and recent advances linking exercise, myokines secretion and inter-organ crosstalk. Identifying the molecular mediators linking physical activity to metabolic health could open the path toward novel therapeutic targets in metabolic diseases.
身体活动可降低心血管代谢风险,而缺乏身体活动则会增加患慢性病的风险。这引发了一种观点,即运动诱导的肌肉收缩有助于代谢调节和健康。现在已经明确,骨骼肌通过释放内分泌因子,即所谓的肌动蛋白,与脂肪组织、肝脏和胰腺等代谢器官相互作用。最近的进展表明,一些肌动蛋白能够调节脂肪组织代谢和产热活性、肝脏内源性葡萄糖生成以及β细胞胰岛素分泌。这种新的范例为解释缺乏身体活动与慢性病之间的联系提供了一个令人信服的假设和分子基础。在此,我们综述了将运动、肌动蛋白分泌和器官间相互作用联系起来的主要发现和最新进展。确定将身体活动与代谢健康联系起来的分子介质可能为代谢疾病的新治疗靶点开辟道路。