Sharma Ankit X, Holland William L
Touchstone Diabetes Center, Department of Internal Medicine, The University of Texas Southwestern Medical Center, Dallas, TX 75390-8549, USA.
J Nat Sci. 2017 Jun;3(6).
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.
在过去二十年中，脂联素与胰岛素敏感性之间的关联已得到阐明。作为神经酰胺降解的促进剂，它通过其同源受体AdipoR1和AdipoR2发挥作用，以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产物，可在肥胖诱导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，S1P是一种细胞保护分子，可增强脂联素的积极代谢作用。本综述重点关注近期的研究工作，这些工作巩固了对脂联素信号通路的认识，为脂联素受体的一些显著特征提供了新见解，最重要的是，确认脂联素受体激动剂是对抗升高的神经酰胺水平和改善II型糖尿病肥胖患者胰岛素敏感性的可行治疗工具。
