Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
FEBS Lett. 2011 Jan 21;585(2):269-74. doi: 10.1016/j.febslet.2010.12.022. Epub 2010 Dec 19.
The role of protein kinase C (PKCs) isoforms in the regulation of glucose metabolism by insulin is complex, partly due to the large PKC family consisting of three sub-groups: conventional, novel and atypical. Activation of some conventional and novel PKCs in response to increased levels of diacylglycerol (DAG) have been shown to counteract insulin signalling. However, roles of atypical PKCs (aPKCs) remain poorly understood. aPKCs act as molecular switches by promoting or suppressing signalling pathways, in response to insulin or ceramides respectively. Understanding how DAG- and ceramide-activated PKCs impair insulin signalling would help to develop treatments to fight insulin resistance.
蛋白激酶 C(PKC)同工型在胰岛素调节葡萄糖代谢中的作用较为复杂,部分原因在于 PKC 家族庞大,包括三个亚群:经典型、新型和非典型型。已有研究表明,某些经典型和新型 PKC 在应对二酰基甘油(DAG)水平升高时被激活,从而拮抗胰岛素信号。然而,非典型型 PKC(aPKC)的作用仍知之甚少。aPKC 作为分子开关,分别通过促进或抑制胰岛素或神经酰胺信号通路来发挥作用。了解 DAG 和神经酰胺激活的 PKC 如何损害胰岛素信号,将有助于开发对抗胰岛素抵抗的治疗方法。