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本文引用的文献

1
Neuronal SIRT1 regulates endocrine and behavioral responses to calorie restriction.神经元SIRT1调节对卡路里限制的内分泌和行为反应。
Genes Dev. 2009 Dec 15;23(24):2812-7. doi: 10.1101/gad.1839209.
2
Perturbation of mitochondrial complex V alters the response to dietary restriction in Drosophila.线粒体复合物 V 的扰动改变了果蝇对饮食限制的反应。
Aging Cell. 2010 Feb;9(1):100-3. doi: 10.1111/j.1474-9726.2009.00537.x. Epub 2009 Nov 25.
3
Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila.氨基酸失衡解释了饮食限制延长果蝇寿命的机制。
Nature. 2009 Dec 24;462(7276):1061-4. doi: 10.1038/nature08619. Epub 2009 Dec 2.
4
mTOR regulation and therapeutic rejuvenation of aging hematopoietic stem cells.mTOR 调控与衰老造血干细胞的治疗性重编程
Sci Signal. 2009 Nov 24;2(98):ra75. doi: 10.1126/scisignal.2000559.
5
Effects of long-term calorie restriction and endurance exercise on glucose tolerance, insulin action, and adipokine production.长期热量限制和耐力运动对葡萄糖耐量、胰岛素作用及脂肪因子产生的影响。
Age (Dordr). 2010 Mar;32(1):97-108. doi: 10.1007/s11357-009-9118-z. Epub 2009 Nov 11.
6
Glucose shortens the life span of C. elegans by downregulating DAF-16/FOXO activity and aquaporin gene expression.葡萄糖通过下调 DAF-16/FOXO 活性和水通道蛋白基因表达来缩短秀丽隐杆线虫的寿命。
Cell Metab. 2009 Nov;10(5):379-91. doi: 10.1016/j.cmet.2009.10.003.
7
4E-BP extends lifespan upon dietary restriction by enhancing mitochondrial activity in Drosophila.4E-BP通过增强果蝇的线粒体活性,在饮食限制条件下延长寿命。
Cell. 2009 Oct 2;139(1):149-60. doi: 10.1016/j.cell.2009.07.034.
8
Ribosomal protein S6 kinase 1 signaling regulates mammalian life span.核糖体蛋白S6激酶1信号通路调节哺乳动物寿命。
Science. 2009 Oct 2;326(5949):140-4. doi: 10.1126/science.1177221.
9
Cell signaling. Aging is RSKy business.细胞信号传导。衰老与核糖体S6激酶(RSK)相关。 (注:原句“RSKy business”表述有误,推测可能是“RSK-related business”,这里按纠正后的意思翻译,若不是此意思,请根据正确信息调整)
Science. 2009 Oct 2;326(5949):55-6. doi: 10.1126/science.1181034.
10
Caloric restriction delays disease onset and mortality in rhesus monkeys.热量限制可延缓恒河猴疾病的发作和死亡。
Science. 2009 Jul 10;325(5937):201-4. doi: 10.1126/science.1173635.

饮食限制与衰老,2009 年。

Dietary restriction and aging, 2009.

机构信息

Buck Institute for Age Research, Novato, CA 94945, USA.

出版信息

Aging Cell. 2010 Apr;9(2):105-12. doi: 10.1111/j.1474-9726.2010.00552.x. Epub 2010 Jan 20.

DOI:10.1111/j.1474-9726.2010.00552.x
PMID:20096035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2958258/
Abstract

Dietary restriction (DR) is a robust nongenetic, nonpharmacological intervention that is known to increase active and healthy lifespan in a variety of species. Despite a variety of differences in the protocols and the way DR is carried out in different species, conserved relationships are emerging among multiple species. 2009 saw the field of DR mature with important mechanistic insights from multiple species. A report of lifespan extension in rapamycin-treated mice suggested that the TOR pathway, a conserved mediator of DR in invertebrates, may also be critical to DR effects in mammals. 2009 also saw exciting discoveries related to DR in various organisms including yeast, worms, flies, mice, monkeys and humans. These studies complement each other and together aim to deliver the promise of postponing aging and age-related diseases by revealing the underlying mechanisms of the protective effects of DR. Here, we summarize a few of the reports published in 2009 that we believe provide novel directions and an improved understanding of dietary restriction.

摘要

饮食限制(DR)是一种强大的非遗传、非药物干预措施,已知它可以延长多种物种的活跃和健康寿命。尽管不同物种的方案和实施 DR 的方式存在多种差异,但在多个物种之间出现了保守的关系。2009 年,DR 领域取得了重要的进展,来自多个物种的机制见解也更加成熟。一项关于雷帕霉素处理的老鼠寿命延长的报告表明,TOR 途径,一种无脊椎动物中 DR 的保守介质,可能对哺乳动物的 DR 效应也很关键。2009 年还在各种生物体中包括酵母、蠕虫、苍蝇、老鼠、猴子和人类中发现了与 DR 相关的令人兴奋的发现。这些研究相互补充,共同旨在通过揭示 DR 的保护作用的潜在机制,实现推迟衰老和与年龄相关的疾病的承诺。在这里,我们总结了 2009 年发表的一些我们认为提供了新方向和对饮食限制的更好理解的报告。