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衰老对人成纤维细胞中果糖2,6-二磷酸代谢的胰岛素调节作用。

Effect of aging on insulin regulation of fructose 2,6-bisphosphate metabolism in human fibroblasts.

作者信息

Meacci E, Vannini F, Vasta V, Farnararo M, Bruni P

机构信息

Dipartimento di Scienze Biochimiche, Università di Firenze Viale G.B. Morgagni 50, Italy.

出版信息

Biochem Mol Biol Int. 1993 May;30(1):91-8.

PMID:8358339
Abstract

Fructose 2,6-bisphosphate (Fru-2,6-P2) content in human fibroblasts is under hormonal control and is strictly related to glycolytic flux. In the present study it has been examined whether aging process is accompanied with an impairment in the control exerted by insulin on the metabolite content. Upon insulin stimulation old fibroblasts show a reduced increase in Fru-2,6-P2 content and glycolytic flux. Similarly, 6-phosphofructo-2-kinase (PFK-2) activity in old fibroblasts is increased at a lesser extent by insulin treatment, suggesting that an impairment at post-receptor level in the signalling pathway of insulin might occur with aging. In addition in unstimulated senescent fibroblasts PFK-2 displays higher activity and reduced Km for substrate, suggesting either that during senescence PFK-2 undergoes a post-translational modification or that a different PFK-2 isoenzyme is expressed.

摘要

人成纤维细胞中果糖-2,6-二磷酸(Fru-2,6-P2)的含量受激素控制,且与糖酵解通量密切相关。在本研究中,已对衰老过程是否伴随着胰岛素对代谢物含量控制的损害进行了检测。胰岛素刺激后,老年成纤维细胞中Fru-2,6-P2含量和糖酵解通量的增加减少。同样,胰岛素处理对老年成纤维细胞中6-磷酸果糖-2-激酶(PFK-2)活性的增强作用较小,这表明随着衰老,胰岛素信号通路在受体后水平可能出现损害。此外,在未受刺激的衰老成纤维细胞中,PFK-2表现出较高的活性和较低的底物米氏常数(Km),这表明在衰老过程中,PFK-2可能经历了翻译后修饰,或者表达了不同的PFK-2同工酶。

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