Chu Dinh-Toi, Tao Yang, Taskén Kjetil
Centre for Molecular Medicine Norway, Nordic European Molecular Biology Laboratory Partnership, University of Oslo and Oslo University Hospital, Oslo, Norway.
College of Food Science and Technology, Nanjing Agricultural University, Nanjing, China.
Horm Metab Res. 2017 Apr;49(4):276-285. doi: 10.1055/s-0043-100384. Epub 2017 Apr 20.
OPA1 (Optic Atrophy 1) is a mitochondrial GTPase known to regulate fission of mitochondria. It was recently also shown to locate on lipid droplets in adipocytes where it functions as an A-kinase anchoring protein (AKAP) that mediates adrenergic control of lipolysis by facilitating PKA phosphorylation of perilipin (Plin1). In brown adipocytes indirect evidence support the notion that OPA1 regulation of fission serves to increase thermogenesis, which thereby contributes to dissipation of energy. In white adipocytes, OPA1 located on lipid droplets serves as a gatekeeper to control lipolysis induced by adrenergic agonists. However, the function of OPA1 in lipolysis and thermogenesis in inducible brown adipocytes (brite/beige cells) remains elusive. Here we discuss the role of OPA1 in lipid metabolism.
OPA1(视神经萎缩蛋白1)是一种线粒体GTP酶,已知其可调节线粒体的分裂。最近还发现它定位于脂肪细胞的脂滴上,在那里它作为一种A激酶锚定蛋白(AKAP)发挥作用,通过促进PKA对 perilipin(Plin1)的磷酸化来介导肾上腺素能对脂解的控制。在棕色脂肪细胞中,间接证据支持OPA1对分裂的调节有助于增加产热,从而促进能量消耗的观点。在白色脂肪细胞中,位于脂滴上的OPA1作为守门人控制肾上腺素能激动剂诱导的脂解。然而,OPA1在诱导型棕色脂肪细胞(米色细胞)的脂解和产热中的功能仍不清楚。在此我们讨论OPA1在脂质代谢中的作用。