Department of Radiology, University of Washington, Seattle, WA, 98109, USA.
Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Geroscience. 2021 Aug;43(4):1615-1625. doi: 10.1007/s11357-021-00390-6. Epub 2021 Jun 8.
Aging and poor nutrition are independent risk factors for the development of chronic disease. When young animals are given diets high in fat or sugar, they exhibit hallmarks of aging like mitochondrial dysfunction and inflammation, and also develop a greater risk for age-related disease. The same mitochondrial dysfunction and inflammation that progress with aging may also further predispose older individuals to dietary insults by fat and sugar. The purpose of this work is to review the most recent studies that address the impact of fat and sugar consumption on hallmarks of aging (mitochondrial dysfunction and inflammation). Findings from these studies show that obesogenic, high-fat diets can exacerbate age-related disease and hallmarks of aging in young animals, but high-fat diets that are non-obesogenic may play a beneficial role in old age. In contrast, high-sugar diets do not require an obesogenic effect to induce mitochondrial dysfunction or inflammation in young rodents. Currently, there is a lack of experimental studies addressing the impact of sugar in the context of aging, even though empirical evidence points to the detrimental effect of sugar in aging by contributing to a variety of age-related diseases. Fig. 1 Mitochondrial dysfunction and altered cellular communication (e.g. inflammation) progress with advancing age and increase the risk for age-related disease (ARD). Given the physiological changes that occur with age, the impact of high-fat (HFD) and high-sugar diets (HSD) may differ in later and earlier stages of life. HFD can promote the development of hallmarks of aging in young animals and can also exacerbate the risk for ARD when consumed at an old age. However, non-obesogenic high-fat diets may also reduce the risk for ARD in old age by acting on these hallmarks of aging. On the other hand, HSD promotes mitochondrial dysfunction and inflammation without necessarily inducing weight gain in young animals. Empirical evidence points to sugar as a major contributor to age-related disease and more experimental studies are needed to clarify whether aged individuals are more susceptible to its effects.
衰老和营养不良是慢性病发展的独立危险因素。当年轻动物摄入高脂肪或高糖饮食时，它们会表现出与衰老相关的特征，如线粒体功能障碍和炎症，并且也会增加与年龄相关的疾病的风险。随着衰老而进展的相同的线粒体功能障碍和炎症也可能使老年人更容易受到脂肪和糖的饮食损伤。这项工作的目的是综述最近研究，这些研究涉及脂肪和糖的消耗对衰老标志（线粒体功能障碍和炎症）的影响。这些研究的结果表明，致肥胖的高脂肪饮食可以加剧年轻动物的与年龄相关的疾病和衰老标志，但非致肥胖的高脂肪饮食可能对老年有益。相比之下，高糖饮食不需要致肥胖作用即可在年轻啮齿动物中诱导线粒体功能障碍或炎症。目前，尽管有经验证据表明糖会通过导致各种与年龄相关的疾病对衰老产生有害影响，但缺乏针对糖在衰老背景下影响的实验研究。图 1 线粒体功能障碍和细胞通讯改变（例如炎症）随着年龄的增长而进展，并增加与年龄相关的疾病（ARD）的风险。鉴于随着年龄的增长而发生的生理变化，高脂肪（HFD）和高糖饮食（HSD）的影响在生命的后期和早期可能会有所不同。HFD 可以促进年轻动物衰老标志的发展，并且在老年时食用时也会加剧 ARD 的风险。然而，非致肥胖的高脂肪饮食也可以通过作用于这些衰老标志来降低老年时 ARD 的风险。另一方面，HSD 促进线粒体功能障碍和炎症，而无需在年轻动物中引起体重增加。经验证据表明糖是与年龄相关的疾病的主要贡献者，需要更多的实验研究来阐明老年人是否更容易受到其影响。
