Nature:科学家证实吃七分饱,会延长早衰小鼠的寿命!
2016/08/28
《Nature》期刊近期发表一篇文章揭示,减少食物的摄取量,能够显著延长患早衰症小鼠的寿命。更重要的是,相比于正常饮食的小鼠,限制饮食的小鼠会更健康。这一最新发现有望用于治疗早衰症儿童,并对阿尔兹海默症、帕金森症等老龄化疾病防治有指示意义。


来自于鹿特丹大学、国家公共卫生与环境研究所(RIVM)的研究团队近期在《Nature》期刊发表文章证实,如果患有严重衰老疾病的小鼠减少30%的食量,它们的寿命将会延迟3倍。更重要的是,相比于正常饮食的小鼠,控制饮食结构的小鼠会更健康。

这一发现对于患有早衰疾病的儿童有着重要意义,它有望帮助揭示老龄化疾病的病因,例如阿尔兹海默症、帕金森症。

减少30%的食量,延迟3倍寿命

最初,通过修改基因,研究团队构建出患有类似于人类老龄化疾病的小鼠。这类患病小鼠的DNA修复系统存在故障。对于人类而言,这一缺陷会导致早衰症,例如Cockayne综合征和毛发硫营养不良,患病儿童平均只能存活12岁。伴随着衰老,他们的父母通常会满足他们的需求,包括饮食。

然而,当以食物为变量时,他们却发现:患病小鼠正常饮食时,它们仅仅只能够存活4—6个月;当患病小鼠每顿都减少30%的食量后,它们能够存活超1年时间。

以限制食量的患病小鼠为研究模型发现,它们的神经系统、视网膜、运动机能快速退化过程会停止,肝脏、肾脏、骨骼、免疫系统和心血管系统都能够维持更为健康的状态。这一特殊模型有望用于研究早衰症引发的并发症。

为什么简单化食谱能够产生神奇的效果?

鹿特丹大学的研究人员Wilbert Vermeij解释,修复系统是复原受损DNA的关键体系,一旦该体系出现故障,就会导致DNA损伤累积,最终造成机体严重衰弱和老化。

然而,严格控制饮食能够让身体进入防御状态,重新配置能量、增强机体免疫能力。更重要的是,限制食量会降低DNA损伤,从而减缓衰老。”

研究人员强调,这种饮食控制模式同样适用于患早衰症的儿童。

之前的研究已经表明,老鼠的修复系统与人类的工作机制类似,小鼠和人类的DNA修复基因只有5%的差异,且与酵母的修复基因也类似。如果基因在十亿年的进化历程中几乎没有改变,这意味着它们对于健康意义非凡。

此外,限制饮食会减缓很多生物的衰老,包括酵母。所以,这一最新结果同样适用于人类。研究团队表示,现有的数据对于预防阿尔兹海默症、帕金森症也有重要指示意义。

备注:文章参考自“Strict diet combats rare progeria aging disorders”。

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  • Restricted diet delays accelerated ageing and genomic stress in DNA-repair-deficient mice

    Mice deficient in the DNA excision-repair gene Ercc1 (Ercc1∆/−) show numerous accelerated ageing features that limit their lifespan to 4-6 months1, 2, 3, 4. They also exhibit a ‘survival response’, which suppresses growth and enhances cellular maintenance. Such a response resembles the anti-ageing response induced by dietary restriction (also known as caloric restriction)1, 5. Here we report that a dietary restriction of 30% tripled the median and maximal remaining lifespans of these progeroid mice, strongly retarding numerous aspects of accelerated ageing. Mice undergoing dietary restriction retained 50% more neurons and maintained full motor function far beyond the lifespan of mice fed ad libitum. Other DNA-repair-deficient, progeroid Xpg−/− (also known as Ercc5−/−) mice, a model of Cockayne syndrome6, responded similarly. The dietary restriction response in Ercc1∆/− mice closely resembled the effects of dietary restriction in wild-type animals. Notably, liver tissue from Ercc1∆/− mice fed ad libitum showed preferential extinction of the expression of long genes, a phenomenon we also observed in several tissues ageing normally. This is consistent with the accumulation of stochastic, transcription-blocking lesions that affect long genes more than short ones. Dietary restriction largely prevented this declining transcriptional output and reduced the number of γH2AX DNA damage foci, indicating that dietary restriction preserves genome function by alleviating DNA damage. Our findings establish the Ercc1∆/− mouse as a powerful model organism for health-sustaining interventions, reveal potential for reducing endogenous DNA damage, facilitate a better understanding of the molecular mechanism of dietary restriction and suggest a role for counterintuitive dietary-restriction-like therapy for human progeroid genome instability syndromes and possibly neurodegeneration in general.

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