胰岛素缺乏与成脂细胞去分化的关联
首发时间:2014-02-10
摘要:目前关于成熟脂肪细胞去分化的研究工作,多限于对其现象的描述以及少量涉及其发生机制的初步研究。在体外诱导动物前脂肪细胞成脂分化过程中,胰岛素是必要的诱导剂。近期我们发现在小鼠原代前脂肪细胞成脂分化诱导中期,一旦撤除胰岛素,可令成脂分化终止,转而启动去分化程序;数天后若再次添加胰岛素,则可使该群细胞重新进入成脂分化-成脂再分化程序。目前尚未发现国内外有类似现象的研究报道。本文从形态学的角度描述了这一新发现的时序性变化特征,检测了成脂关键基因的表达变化,并对成脂细胞发生去分化的机制进行了初步探讨。结果提示:胰岛素信号对于维持成熟脂肪细胞表型是重要的,由于其缺乏导致的脂肪细胞去分化与成脂基因表达受到抑制以及脂解基因功能增强有关,也不排除有其他主动启动脂肪细胞去分化调控分子的参与。本研究对于进一步理解脂肪细胞生物学特性以及为肥胖研究,提供了新的线索和思路。目前相关实验工作正在进一步展开。
关键词: 细胞生物学 脂肪细胞去分化 胰岛素信号通路 脂肪分解
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The relationship of adipogenic cells dedifferentiation and absence of insulin
Abstract:There is a limited data on mechanism of dedifferentiation of mature adipocyte, especially about absence of insulin signaling on adipocytes dedifferentiation. Insulin is a key regulator for induces adipogenesis in vitro. We found recently that absent of insulin induced dedifferentiation of preadipocytes, which isolated from both obese and lean mice, in vitro. In this primary study, we described characteristics of morphology changes of adipogenic cells dedifferentiation during period of insulin deficiency, and discussed a mechanism of this event. Our data indicated that insulin signaling is essential for keeping phenotype of mature adipocyte, and the dedifferentiation of the adipocytes observed in our study may due to inhibition of adipogenic factor and promotion function of lipolytic factor, caused by absence of insulin signaling. Our data will provide a possibility for further understand biologic feature of adipocyte and a new idea for obese study.
Keywords: cell biology adipocyte dedifferentiation insulin signaling lipolysis
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No.4584309743163139****
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