节食“延长”寿命,又有新证据
2016/07/19
7月14日,发表在PLOS Genetics上的一项研究中,Sanford-Burnham Prebys医学发现研究所的科学家们证实,在很多物种中(包括人类),不造成营养不良的饮食限制对长寿有着有益的影响。


7月14日,发表在PLOS Genetics上的一项研究中,Sanford-Burnham Prebys医学发现研究所的科学家们证实,在很多物种中(包括人类),不造成营养不良的饮食限制对长寿有着有益的影响。

论文的通讯作者Malene Hansen博士说:“在这一研究中,我们使用秀丽隐杆线虫作为模型。结果发现,肠道中的自噬作用对延长寿命至关重要。饮食受到限制的线虫肠道中的自噬率(rate of autophagy)要高于正常水平。”

据悉,研究人员使用的是eat-2基因功能缺失的秀丽隐杆线虫突变体。从遗传学的角度,它们比普通的蠕虫吃得少,且活得更久。因此,它们为研究节食如何延长寿命提供了一个非常理想的模型。研究发现,阻断肠道中的自噬作用显著缩短了线虫的寿命。这揭示了eat-2长寿背后的关键机制。

Hansen说:“我们发现,尽管正常蠕虫的肠道屏障会随着它们变老出现漏洞,但eat-2并不会如此。这表明,没有漏洞(non-leaky)的肠道是长寿的关键因素。但肠道完整性是如何影响长寿的仍不清楚。一种可能性是,肠道屏障功能的下降会使有害物质或病原体进入体内。”

同时,研究小组还观察到,关闭肠道中的自噬作用会使线虫运动的更少。科学家们解释道,身体活动的减少表明,一个器官中自噬作用的变化对其它器官产生了重大的影响。想要找到运动性与肠道自噬作用之间关系还需要进一步的研究。但研究人员推测,抑制肠道中的自噬作用可能损害了肠道代谢营养物或者分泌对其它器官功能至关重要的激素的能力。

尽管蠕虫比人类简单的多,但许多相同的基本机制驱动着它们的生物学。Hansen说:“我们所获得的成果最终有望帮助人类活得更长、更健康。”但他也强调,在考虑通过调节自噬作用来管理疾病之前,科学家们还需要进行更多的研究。

其它进展:Cell Metabolism解析节食为何能使寿命延长

近年来,随着生物学知识的不断积累以及现代生物技术的快速发展,抗衰老、延长寿命等相关的研究得到了更多的重视。科学界探索节食延长寿命背后的机制也已有很长时间,并取得了一系列的成果。


3月8日,发表在Cell Metabolism上的一项研究中,中国科学院-马普学会计算生物学伙伴研究所韩敬东研究组揭示了节食导致线虫寿命延长的分子机制。

饮食限制是延长寿命最强大的自然手段。没有单一的基因干预能够复制饮食限制带来的全部影响。在这一研究中,科学家小组发现,节食的早期和晚期响应分别与代谢和细胞周期/DNA损伤有关。

研究者们构建了节食响应的网络模型,包含三个主要模块,与之相应的是不同的调控因子簇以及不同时期的节食响应。随后,科学家们通过遗传学干扰这些调控因子来调节对应的模块。结果发现,当越多的模块被调节时,对照组喂养下线虫的转录组越趋同于节食喂养下的情况。当三个模块均被遗传干扰时,线虫的寿命将会极大延长,平均寿命从不到20天延长到50余天,并且节食也不会再对该类线虫有效。

这项研究从系统生物学的角度揭示了节食调节衰老的分子机制,并为衰老干预策略提供了新概念,即节食依赖于轻微的多模块协同调节,且轻微的多模块协同调节远优于单模块靶向调节,只有通过多模块协同调节才能收获节食的长寿功效。

备注:本文内容部分编译自sciencedaily(Dietary restriction increases lifespan through effects on the gut),部分参考自中国科学院上海生命科学研究院官网。

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