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脂肪组织和β细胞中的自噬:对肥胖和糖尿病的影响。

Autophagy in adipose tissue and the beta cell: implications for obesity and diabetes.

机构信息

Department of General Medicine, Radboud University Medical Centre, Nijmegen, the Netherlands.

出版信息

Diabetologia. 2014 Aug;57(8):1505-16. doi: 10.1007/s00125-014-3255-3. Epub 2014 May 5.

Abstract

Autophagy is a lysosomal degradation pathway recycling intracellular long-lived proteins and damaged organelles, thereby maintaining cellular homeostasis. In addition to inflammatory processes, autophagy has been implicated in the regulation of adipose tissue and beta cell functions. In obesity and type 2 diabetes autophagic activity is modulated in a tissue-dependent manner. In this review we discuss the regulation of autophagy in adipose tissue and beta cells, exemplifying tissue-specific dysregulation of autophagy and its implications for the pathophysiology of obesity and type 2 diabetes. We will highlight common themes and outstanding gaps in our understanding, which need to be addressed before autophagy could be envisioned as a therapeutic target for the treatment of obesity and diabetes.

摘要

自噬是溶酶体降解途径,可回收细胞内的长寿命蛋白质和受损的细胞器,从而维持细胞内的稳态。除了炎症过程,自噬还参与调节脂肪组织和β细胞的功能。在肥胖和 2 型糖尿病中,自噬活性以组织依赖的方式进行调节。在这篇综述中,我们讨论了自噬在脂肪组织和β细胞中的调节,举例说明了自噬的组织特异性失调及其对肥胖和 2 型糖尿病病理生理学的影响。我们将强调我们理解中的共同主题和突出的差距,在自噬被设想为肥胖和糖尿病治疗的治疗靶点之前,需要解决这些问题。

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