Diabetes increases the risk of developing kidney disease, but some patients may be protected. Having noted higher pyruvate kinase M2 (PKM2) in protected patients (patients with diabetes but without kidney disease), Fu et al. induced diabetes in mice overexpressing Pkm2 in podocytes. Compared with wildtype controls, transgenic mice had less diabetesinduced glomerular pathology and metabolic impairment, despite comparable hyperglycaemia. PKM2 seems to provide protection by regulating vascular endothelial growth factor, which was higher in transgenic mice and in protected patients compared with their respective controls.

中文翻译：

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PKM2 诱导的高血糖保护

糖尿病会增加患肾病的风险，但一些患者可能会受到保护。Fu 等人注意到受保护患者（患有糖尿病但没有肾脏疾病的患者）中丙酮酸激酶 M2 (PKM2) 较高。在足细胞中过表达 Pkm2 的小鼠中诱发糖尿病。与野生型对照相比，转基因小鼠具有较少的糖尿病引起的肾小球病理和代谢障碍，尽管有相当的高血糖。PKM2 似乎通过调节血管内皮生长因子来提供保护，与各自的对照相比，转基因小鼠和受保护患者的血管内皮生长因子更高。