β细胞去分化：2型糖尿病β细胞功能衰竭机制新解——能“去”…还能“回”？

βcell dedifferentiation： new insight into the pathogenesis of cell failure in type 2 diabetes Gone backward already. and Coming back again？

胰岛β细胞功能衰退是2型糖尿病的重要发病机制之一，保护和逆转β细胞功能是糖尿病治疗的重要环节。通常认为β细胞功能衰竭是细胞凋亡的结果，但最新研究结果提示高血糖时体内叉头转录因子Fox01活性丧失，β细胞发生去分化改变，成为具有多向分化潜能的内分泌祖细胞样细胞，部分细胞甚至可以分泌胰升糖素。这一发现对阐明2型糖尿病B细胞功能耗竭的机制、调整糖尿病早期治疗策略，保护而非刺激β细胞、研发促进已去分化的β细胞再次分化回归至功能性β细胞的全新降糖药物，将会有重大的理论意义和临床价值。

β cell failure is one of the important components in the pathogenesis of type 2 diabetes. Protecting and reversing β cell function is a critical part in diabetes treatments. It has been recently discovered that rather than apoptosis, β cell dedifferentiation into an endocrine progenitor-like stage is the main mechanism of β cell failure, which is closely related with the loss of FoxO1 on β cells. Some of these dedifferentiated β cells even have the potency to convert into β-cells. These great discoveries expand our understanding for the β cell exhaustion during the progression of hyperglycemia. It is worthwhile to reconsider our current treatment strategy for type 2 diabetes, especially during the beginning period, to protect rather than stimulate β cells. It also paves the way to develop a brand-new class of hypoglycemic agent to re-differentiate the already dedifferentiated β cells back into insulinsecreting cells.