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神经节苷脂GM3作为肥胖相关胰岛素抵抗的守门人:证据与机制

Ganglioside GM3 as a gatekeeper of obesity-associated insulin resistance: Evidence and mechanisms.

作者信息

Lipina Christopher, Hundal Harinder S

机构信息

Division of Cell Signalling and Immunology, Sir James Black Centre, School of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, United Kingdom.

Division of Cell Signalling and Immunology, Sir James Black Centre, School of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, United Kingdom.

出版信息

FEBS Lett. 2015 Oct 24;589(21):3221-7. doi: 10.1016/j.febslet.2015.09.018. Epub 2015 Oct 8.

DOI:10.1016/j.febslet.2015.09.018
PMID:26434718
Abstract

Gangliosides constitute a large family of sialic acid-containing glycosphingolipids which play a key regulatory role in a diverse array of cellular processes, including receptor-associated signalling. Accordingly, the aberrant production of the ganglioside GM3 has been linked to pathophysiological changes associated with obesity, which in turn can lead to metabolic disorders such as insulin resistance and type 2 diabetes mellitus. This review examines the role of GM3 in mediating obesity-induced perturbations in metabolic function, including impaired insulin action. By doing so, we highlight the potential use of therapies targeting GM3 biosynthesis in order to counteract obesity-related metabolic disorders.

摘要

神经节苷脂构成了一个含有唾液酸的糖鞘脂大家族,它们在包括受体相关信号传导在内的一系列细胞过程中发挥关键的调节作用。因此,神经节苷脂GM3的异常产生与肥胖相关的病理生理变化有关,而肥胖又可能导致代谢紊乱,如胰岛素抵抗和2型糖尿病。本综述探讨了GM3在介导肥胖引起的代谢功能紊乱(包括胰岛素作用受损)中的作用。通过这样做,我们强调了靶向GM3生物合成的疗法在对抗肥胖相关代谢紊乱方面的潜在用途。

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