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本文引用的文献

1
Sirt1 improves healthy ageing and protects from metabolic syndrome-associated cancer.Sirt1 可改善健康衰老并预防代谢综合征相关癌症。
Nat Commun. 2010 Apr 12;1:3. doi: 10.1038/ncomms1001.
2
SIRT1 promotes the central adaptive response to diet restriction through activation of the dorsomedial and lateral nuclei of the hypothalamus.SIRT1 通过激活下丘脑的背内侧核和外侧核促进了饮食限制的中枢适应反应。
J Neurosci. 2010 Jul 28;30(30):10220-32. doi: 10.1523/JNEUROSCI.1385-10.2010.
3
Calorie restriction enhances cell adaptation to hypoxia through Sirt1-dependent mitochondrial autophagy in mouse aged kidney.热量限制通过 Sirt1 依赖性线粒体自噬增强老年小鼠肾脏细胞对缺氧的适应
J Clin Invest. 2010 Apr;120(4):1043-55. doi: 10.1172/JCI41376. Epub 2010 Mar 24.
4
Calories and carcinogenesis: lessons learned from 30 years of calorie restriction research.热量与癌症发生:限制热量摄入研究 30 年得到的启示。
Carcinogenesis. 2010 Jan;31(1):83-9. doi: 10.1093/carcin/bgp280. Epub 2009 Dec 7.
5
SIRT1 redistribution on chromatin promotes genomic stability but alters gene expression during aging.SIRT1在染色质上的重新分布促进基因组稳定性,但在衰老过程中会改变基因表达。
Cell. 2008 Nov 28;135(5):907-18. doi: 10.1016/j.cell.2008.10.025.
6
Impaired DNA damage response, genome instability, and tumorigenesis in SIRT1 mutant mice.SIRT1 突变小鼠的 DNA 损伤反应受损、基因组不稳定与肿瘤发生
Cancer Cell. 2008 Oct 7;14(4):312-23. doi: 10.1016/j.ccr.2008.09.001.
7
The role of calorie restriction and SIRT1 in prion-mediated neurodegeneration.热量限制和SIRT1在朊病毒介导的神经退行性变中的作用。
Exp Gerontol. 2008 Dec;43(12):1086-93. doi: 10.1016/j.exger.2008.08.050. Epub 2008 Aug 30.
8
Sirt1 protects against high-fat diet-induced metabolic damage.Sirt1可防止高脂饮食诱导的代谢损伤。
Proc Natl Acad Sci U S A. 2008 Jul 15;105(28):9793-8. doi: 10.1073/pnas.0802917105. Epub 2008 Jul 3.
9
SirT1 regulates energy metabolism and response to caloric restriction in mice.SirT1调节小鼠的能量代谢及对热量限制的反应。
PLoS One. 2008 Mar 12;3(3):e1759. doi: 10.1371/journal.pone.0001759.
10
Increase in activity during calorie restriction requires Sirt1.热量限制期间活动量的增加需要Sirt1。
Science. 2005 Dec 9;310(5754):1641. doi: 10.1126/science.1118357.

限制 Sirt1 的作用对饮食限制的癌症保护作用有限。

Limited role of Sirt1 in cancer protection by dietary restriction.

机构信息

Tumor Suppression Group, Spanish National Cancer Research Center, Madrid, Spain.

出版信息

Cell Cycle. 2011 Jul 1;10(13):2215-7. doi: 10.4161/cc.10.13.16185.

DOI:10.4161/cc.10.13.16185
PMID:21606675
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3578182/
Abstract

Dietary restriction (DR) has multiple beneficial effects, the two most prominently studied being an increased longevity and an increased cancer protection. Mammalian Sirt1 is a protein deacetylase that has been linked to DR. To explore the relation between Sirt1 and DR, we have examined here DR-induced cancer protection in mice overexpressing Sirt1 (2-3 fold) under its own regulatory elements (Sirt1-tg mice). In particular, we have subjected p53‑deficient mice, carrying or not the Sirt1-tg allele, to every-other-day fasting (EOD), which is a type of DR that significantly delays cancer onset. As expected, EOD extended the survival of p53-heterozygous (p53 (+/-) ) mice. However, the extension of survival of p53-heterozygous mice by EOD was the same in the presence or absence of the Sirt1-tg allele. These results suggest that Sirt1 has a limited role in mediating cancer protection by DR in mammals.

摘要

饮食限制(DR)具有多种有益作用,其中两个最受关注的作用是延长寿命和增强抗癌能力。哺乳动物 Sirt1 是一种去乙酰化酶,与 DR 有关。为了探讨 Sirt1 与 DR 的关系,我们在此研究了在自身调节元件(Sirt1-tg 小鼠)下过表达 Sirt1(2-3 倍)的小鼠中 DR 诱导的抗癌保护作用。具体而言,我们使携带或不携带 Sirt1-tg 等位基因的 p53 缺陷型小鼠进行隔日禁食(EOD),这是一种可显著延迟癌症发生的 DR 类型。正如预期的那样,EOD 延长了 p53 杂合子(p53( +/- ))小鼠的生存时间。然而,EOD 对 p53 杂合子小鼠的生存时间的延长在 Sirt1-tg 等位基因存在或不存在的情况下是相同的。这些结果表明,Sirt1 在介导哺乳动物 DR 的抗癌保护作用方面的作用有限。