Starvation response in mouse liver shows strong correlation with life-span-prolonging processes
Starvation response in mouse liver shows strong correlation with life-span-prolonging processes
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DOI：
10.1152/physiolgenomics.00203.2003
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发表时间：
2004-04-13
影响因子：
4.6
通讯作者：
Katzenberger, JD
中科院分区：
文献类型：
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作者：
Bauer, M;Hamm, AC;Katzenberger, JD
我们利用高密度微阵列监测了小鼠肝脏中基因表达在禁食和喂糖条件下的整体变化。从相似的20，000个不同的基因中，显著调节的基因被分组为特定的信号传导和代谢途径。观察到脂质信号级联、胰岛素和脱氢表雄酮（DHEA）激素途径、尿素循环和基于S-腺苷甲硫氨酸的甲基转移系统以及细胞凋亡调节剂的显著变化。由于这些途径已被牵连到衰老过程中发挥作用，因为我们观察到的基因在饥饿时与热量限制后的调节显着重叠，我们的分析表明，饥饿可能会引起应激反应，也引起热量限制。因此，禁食期间调节的许多信号和代谢组分可能与介导热量限制依赖性寿命延长的那些相同。
We have monitored global changes in gene expression in mouse liver in response to fasting and sugar- fed conditions using high- density microarrays. From similar to 20,000 different genes, the significantly regulated ones were grouped into specific signaling and metabolic pathways. Striking changes in lipid signaling cascade, insulin and dehydroepiandrosterone ( DHEA) hormonal pathways, urea cycle and S- adenosylmethionine- based methyl transfer systems, and cell apoptosis regulators were observed. Since these pathways have been implicated to play a role in the aging process, and since we observe significant overlap of genes regulated upon starvation with those regulated upon caloric restriction, our analysis suggests that starvation may elicit a stress response that is also elicited during caloric restriction. Therefore, many of the signaling and metabolic components regulated during fasting may be the same as those which mediate caloric restriction- dependent life- span extension.