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饮食限制可改善小鼠脂肪组织中与年龄相关的 DNA 损伤、衰老和炎症的增加。

Dietary Restriction Ameliorates Age-Related Increase in DNA Damage, Senescence and Inflammation in Mouse Adipose Tissuey.

机构信息

Dr. Gabriele Saretzki, The Ageing Biology Centre and Institute for Cell and Molecular Biosciences, Campus for Ageing and Vitality, Edwardson Building, Newcastle upon Tyne, NE4 5PL, United Kingdom, Phone: 0044 191 208 1214, Fax: 0044 191 208 1101, Email:

出版信息

J Nutr Health Aging. 2018;22(4):555-561. doi: 10.1007/s12603-017-0968-2.

DOI:10.1007/s12603-017-0968-2
PMID:29582897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5866821/
Abstract

UNLABELLED

Ageing is associated with redistribution of fat around the body and saturation of visceral adipose depots. Likewise, the presence of excess fat in obesity or during ageing places extra stress on visceral depots, resulting in chronic inflammation and increased senescence. This process can contribute to the establishment of the metabolic syndrome and accelerated ageing. Dietary restriction (DR) is known to alleviate physiological signs of inflammation, ageing and senescence in various tissues including adipose tissue.

OBJECTIVES

Our pilot study aimed to analyse senescence and inflammation parameters in mouse visceral fat tissue during ageing and by short term, late-onset dietary restriction as a nutritional intervention. Design, measurements: In this study we used visceral adipose tissue from mice between 5 and 30 months of age and analysed markers of senescence (adipocyte size, γH2A.X, p16, p21) and inflammation (e.g. IL-6, TNFα, IL-1β, macrophage infiltration) using immuno-staining, as well as qPCR for gene expression analysis. Fat tissues from 3 mice per group were analysed.

RESULTS

We found that the amount of γH2A.X foci as well as the expression of senescence and inflammation markers increased during ageing but decreased with short term DR. In contrast, the increase in amounts of single or aggregated macrophages in fat depots occurred only at higher ages. Surprisingly, we also found that adipocyte size as well as some senescence parameters decreased at very high age (30 months).

CONCLUSIONS

Our results demonstrate increased senescence and inflammation during ageing in mouse visceral fat while DR was able to ameliorate several of these parameters as well as increased adipocyte size at 17.5 months of age. This highlights the health benefits of a decreased nutritional intake over a relatively short period of time at middle age.

摘要

未加标签

衰老与身体脂肪的再分布以及内脏脂肪沉积的饱和有关。同样,肥胖或衰老时体内脂肪过多会给内脏脂肪沉积带来额外的压力,导致慢性炎症和衰老增加。这一过程可能导致代谢综合征和加速衰老的建立。饮食限制(DR)已知可减轻包括脂肪组织在内的各种组织的炎症、衰老和衰老迹象。

目的

我们的初步研究旨在分析衰老和短期、晚期饮食限制(作为一种营养干预)对小鼠内脏脂肪组织衰老和炎症参数的影响。设计、测量:在这项研究中,我们使用了 5 至 30 个月大的小鼠的内脏脂肪组织,并使用免疫染色分析衰老(脂肪细胞大小、γH2A.X、p16、p21)和炎症标志物(如 IL-6、TNFα、IL-1β、巨噬细胞浸润),以及 qPCR 进行基因表达分析。每组 3 只小鼠的脂肪组织进行了分析。

结果

我们发现,γH2A.X 焦点的数量以及衰老和炎症标志物的表达随着年龄的增长而增加,但随着短期 DR 的增加而减少。相反,脂肪组织中单个或聚集的巨噬细胞数量的增加仅在较高年龄时发生。令人惊讶的是,我们还发现脂肪细胞大小以及一些衰老参数在非常高的年龄(30 个月)时降低。

结论

我们的结果表明,在小鼠内脏脂肪中,衰老过程中会出现更多的衰老和炎症,而 DR 能够改善其中的一些参数,以及在 17.5 个月时增加脂肪细胞的大小。这突出表明,在中年期间相对较短的时间内减少营养摄入具有健康益处。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/539887a3b68c/12603_2017_968_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/197bd6d9819b/12603_2017_968_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/10f58fe7e48f/12603_2017_968_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/aa41132432e5/12603_2017_968_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/841cd98264ce/12603_2017_968_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/539887a3b68c/12603_2017_968_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/197bd6d9819b/12603_2017_968_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/10f58fe7e48f/12603_2017_968_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/aa41132432e5/12603_2017_968_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/841cd98264ce/12603_2017_968_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9f2f/5866821/539887a3b68c/12603_2017_968_Fig6_HTML.jpg

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