新证据!热量限制+低脂肪饮食=抵抗衰老
2018/04/03
如何通过控制饮食来抵抗衰老是很多科学家正在积极研究的问题。近日,来自格罗宁根大学的研究小组发现了一种阻止衰老诱导的相关变化的“吃法”!


图片来源:Frontiers in Molecular Neuroscience(https://doi.org/10.3389/fnmol.2018.00065)

3月12日,发表在Frontiers in Molecular Neuroscience上题为“Low-Fat Diet With Caloric Restriction Reduces White Matter Microglia Activation During Aging”的这项研究证实,“低脂肪饮食”结合“热量限制”阻止了老龄小鼠中大脑免疫细胞——小胶质细胞——的激活。

论文的通讯作者Bart Eggen说:“在世界范围内,肥胖和衰老都是普遍存在的,并且在不断增加,但它们对中枢神经系统的影响却不是很清楚。在这一研究中,我们决定调查高脂肪饮食或低脂肪饮食,结合运动和食物限制,是否会在小鼠衰老期间影响小胶质细胞。”

作为脑细胞的一种,小胶质细胞有助于维持大脑组织的完整性和正常功能。这类细胞的功能障碍与神经发育障碍和神经退行性疾病有关。同时,在大脑特定的区域中,由小胶质细胞驱动的炎症反应也被证实与衰老有关。


图片来源:16sucai

研究中,Eggen及其同事调查了高脂肪饮食和低脂肪饮食对6月龄小鼠下丘脑中炎症和小胶质细胞标志物的影响。同时,他们还进一步研究了这两类饮食对两岁大小鼠小胶质细胞的影响。值得一提的是,这些两岁大的小鼠经历了终身运动(lifelong exercise regime)或终身饮食限制(热量减少40%)。

结果显示,只有当小鼠被喂以低脂肪饮食,并结合了热量限制才能阻止衰老诱导的小胶质细胞的炎症激活(Aging-induced inflammatory activation of microglia)。仅靠低脂肪饮食不足以发挥相同的作用。

Eggen等还发现,尽管其他研究显示,运动与患某些疾病的风险降低有关,但该研究表明,在预防与衰老相关的变化方面,运动明显不如热量限制有效。

科学家们谨慎地指出,要理解这些发现的意义还需要做更多的工作。在他们的研究中,小鼠一生只接受一种饮食,目前还不清楚饮食变化会如何改变这些结果,如,是否改用低脂肪饮食能够消除高脂肪饮食以及不受限制的饮食带来的负面影响。此外,他们还需要进一步确定,这些变化是如何与小鼠的认知能力相对应的。

“尽管如此,这些数据确实已经证明,对小鼠而言,饮食中的脂肪含量和热量摄入是影响大脑衰老的一个重要参数。只有当脂肪含量和热量摄入同时被限制,小胶质细胞中衰老诱导的变化才能被预防。”Eggen总结道。

责编:风铃

参考资料:

Caloric restriction in combination with low-fat diet helps protect aging mouse brains

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  • Low-Fat Diet With Caloric Restriction Reduces White Matter Microglia Activation During Aging

    Rodent models of both aging and obesity are characterized by inflammation in specific brain regions, notably the corpus callosum, fornix, and hypothalamus. Microglia, the resident macrophages of the central nervous system, are important for brain development, neural support, and homeostasis. However, the effects of diet and lifestyle on microglia during aging are only partly understood. Here, we report alterations in microglia phenotype and functions in different brain regions of mice on a high-fat diet (HFD) or low-fat diet (LFD) during aging and in response to voluntary running wheel exercise. We compared the expression levels of genes involved in immune response, phagocytosis, and metabolism in the hypothalamus of 6-month-old HFD and LFD mice. We also compared the immune response of microglia from HFD or LFD mice to peripheral inflammation induced by intraperitoneal injection of lipopolysaccharide (LPS). Finally, we investigated the effect of diet, physical exercise, and caloric restriction (40% reduction compared to ad libitum intake) on microglia in 24-month-old HFD and LFD mice. Changes in diet caused morphological changes in microglia, but did not change the microglia response to LPS-induced systemic inflammation. Expression of phagocytic markers (i.e., Mac-2/Lgals3, Dectin-1/Clec7a, and CD16/CD32) in the white matter microglia of 24-month-old brain was markedly decreased in calorically restricted LFD mice. In conclusion, LFD resulted in reduced activation of microglia, which might be an underlying mechanism for the protective role of caloric restriction during aging-associated decline.

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