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在多组学时代整合脂肪细胞胰岛素信号和代谢。

Integrating adipocyte insulin signaling and metabolism in the multi-omics era.

机构信息

Program in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA; Facultad de Medicina, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Endocrinología Molecular (LEM), Universidad de Buenos Aires, Buenos Aires, Argentina.

Program in Molecular Medicine, University of Massachusetts Chan Medical School, Worcester, MA, 01605, USA.

出版信息

Trends Biochem Sci. 2022 Jun;47(6):531-546. doi: 10.1016/j.tibs.2022.02.009. Epub 2022 Mar 15.

Abstract

Insulin stimulates glucose uptake into adipocytes via mTORC2/AKT signaling and GLUT4 translocation and directs glucose carbons into glycolysis, glycerol for TAG synthesis, and de novo lipogenesis. Adipocyte insulin resistance is an early indicator of type 2 diabetes in obesity, a worldwide health crisis. Thus, understanding the interplay between insulin signaling and central carbon metabolism pathways that maintains adipocyte function, blood glucose levels, and metabolic homeostasis is critical. While classically viewed through the lens of individual enzyme-substrate interactions, advances in mass spectrometry are beginning to illuminate adipocyte signaling and metabolic networks on an unprecedented scale, yet this is just the tip of the iceberg. Here, we review how 'omics approaches help to elucidate adipocyte insulin action in cellular time and space.

摘要

胰岛素通过 mTORC2/AKT 信号和 GLUT4 易位刺激脂肪细胞摄取葡萄糖,并将葡萄糖碳引导进入糖酵解、甘油用于 TAG 合成和从头脂肪生成。肥胖是全球健康危机,脂肪细胞胰岛素抵抗是 2 型糖尿病的早期指标。因此,了解维持脂肪细胞功能、血糖水平和代谢平衡的胰岛素信号和中心碳代谢途径之间的相互作用至关重要。虽然传统上通过单个酶-底物相互作用的视角来看待,但质谱技术的进步开始以前所未有的规模揭示脂肪细胞信号和代谢网络,但这只是冰山一角。在这里,我们回顾了“组学”方法如何帮助阐明脂肪细胞胰岛素在细胞时间和空间中的作用。

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