脂联素及其水解酶激活受体。

Journal of nature and science Pub Date : 2017-06-01
Ankit X Sharma, William L Holland
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摘要

在过去的二十年中,脂联素与胰岛素敏感性的相关性已经被阐明。作为神经酰胺降解的促进剂,它通过其同源受体AdipoR1和AdipoR2来改变生物活性鞘脂种类。脂联素减少神经酰胺的积累,神经酰胺是一种脂质代谢物,在肥胖引起的胰岛素抵抗中起因果作用。同时,脂联素刺激鞘氨醇-1-磷酸(S1P)的产生,鞘氨醇-1-磷酸是一种细胞保护分子,强化了脂联素的积极代谢作用。本文综述了最近的研究成果,巩固了对脂联素信号通路的认识,对脂联素受体的一些显著特征有了新的认识,最重要的是,肯定了脂联素受体激动作用作为一种可行的治疗工具,可以对抗神经酰胺水平升高,改善肥胖II型糖尿病患者的胰岛素敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Adiponectin and its Hydrolase-Activated Receptors.

The relevance of adiponectin to insulin sensitivity has been elucidated over the last two decades. As a promoter of ceramide degradation, it works through its cognate receptors, AdipoR1 and AdipoR2, to alter bioactive sphingolipid species. Adiponectin diminishes the accumulation of ceramide, a lipid metabolite which can play a causal role in obesity-induced insulin resistance. Concurrently, adiponectin stimulates the production of sphingosine-1-phosphate (S1P), a cyto-protective molecule that accentuates adiponectin's positive metabolic effects. This review focuses on recent work that solidifies knowledge of the adiponectin signaling pathway, gives new insight into some notable characteristics of adiponectin's receptors, and most importantly, affirms adiponectin receptor agonism as a viable therapeutic tool to combat elevated ceramide levels and improve insulin sensitivity in obese patients with type II diabetes.

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