小柯机器人

加拿大麦吉尔大学Lawrence Kazak研究组发现，肌酸激酶B控制产热脂肪中的无意义肌酸循环。2021年2月17日，《自然》杂志发表了这项成果。

研究人员发现，肌酸激酶B（CKB）对于无意义肌酸循环所产生的生热是必不可少的，在此期间，肌酸激酶B使用内部线粒体靶向序列运输至线粒体。CKB在小鼠和人的脂肪细胞中均由产热刺激强烈诱导。小鼠Ckb的脂肪细胞选择性失活减少了产热能力，增加了肥胖的易感性，并破坏了葡萄糖的体内稳态。因此，CKB是无意义肌酸循环的关键效应因子。 

据了解，肥胖会增加新陈代谢后遗症（例如2型糖尿病和心血管疾病）的死亡风险。脂肪细胞的生热作用可以抵消肥胖和代谢性疾病。在生热脂肪中，肌酸释放出过量的线粒体ADP（据称是通过磷酸化循环）来驱动生热性呼吸。但是，控制这种无意义肌酸循环的蛋白质尚不清楚。

附：英文原文

Title: Creatine kinase B controls futile creatine cycling in thermogenic fat

Author: Janane F. Rahbani, Anna Roesler, Mohammed F. Hussain, Bozena Samborska, Christien B. Dykstra, Linus Tsai, Mark P. Jedrychowski, Laurent Vergnes, Karen Reue, Bruce M. Spiegelman, Lawrence Kazak

Issue&Volume: 2021-02-17

Abstract: Obesity increases the risk of mortality because of metabolic sequelae such as type 2 diabetes and cardiovascular disease1. Thermogenesis by adipocytes can counteract obesity and metabolic diseases2,3. In thermogenic fat, creatine liberates a molar excess of mitochondrial ADP—purportedly via a phosphorylation cycle4—to drive thermogenic respiration. However, the proteins that control this futile creatine cycle are unknown. Here we show that creatine kinase B (CKB) is indispensable for thermogenesis resulting from the futile creatine cycle, during which it traffics to mitochondria using an internal mitochondrial targeting sequence. CKB is powerfully induced by thermogenic stimuli in both mouse and human adipocytes. Adipocyte-selective inactivation of Ckb in mice diminishes thermogenic capacity, increases predisposition to obesity, and disrupts glucose homeostasis. CKB is therefore a key effector of the futile creatine cycle.

DOI: 10.1038/s41586-021-03221-y

Source: https://www.nature.com/articles/s41586-021-03221-y

Nature：《自然》，创刊于1869年。隶属于施普林格·自然出版集团，最新IF：69.504
官方网址：http://www.nature.com/
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