The Cellular and Molecular Pharmacology Department, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
Trends Mol Med. 2013 Mar;19(3):176-86. doi: 10.1016/j.molmed.2013.01.002. Epub 2013 Jan 31.
Recent evidence indicates that Parkinson's disease and diabetes, both age-related chronic diseases, share remarkably similar dysregulated pathways. Exposure to environmental factors and genetic susceptibility play a role in the etiology and progression of both diseases. In light of recent findings, an intriguing hypothesis has emerged that suggests that mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and alterations in metabolism may lead to insulin resistance and, ultimately, to diabetes and/or neurodegeneration. In this article, we summarize the studies that have addressed the relationship between Parkinson's disease and diabetes and propose that disruptions in these shared molecular networks lead to both chronic diseases.
最近的证据表明，帕金森病和糖尿病这两种与年龄相关的慢性疾病，有着显著相似的失调途径。环境因素暴露和遗传易感性在这两种疾病的病因和进展中都起着作用。鉴于最近的发现，出现了一个有趣的假设，即线粒体功能障碍、内质网应激、炎症和代谢改变可能导致胰岛素抵抗，最终导致糖尿病和/或神经退行性变。在本文中，我们总结了探讨帕金森病和糖尿病之间关系的研究，并提出这些共同的分子网络的破坏导致了这两种慢性疾病。
