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《有计划的体重减轻对氧化应激、DNA 修复和端粒长度标志物的影响——系统综述》。

Effects of Intentional Weight Loss on Markers of Oxidative Stress, DNA Repair and Telomere Length - a Systematic Review.

机构信息

Department of Population Sciences, Huntsman Cancer Institute, Salt Lake City, UT, USA.

出版信息

Obes Facts. 2017;10(6):648-665. doi: 10.1159/000479972. Epub 2017 Dec 14.

Abstract

BACKGROUND

Altered levels of markers of oxidative stress, DNA repair, and telomere integrity have been detected in obese individuals and may underlie the pathogenesis of obesity-related diseases. However, whether or not such effects are reversed by intentional weight loss has not been systematically reviewed.

METHODS

A literature search in PubMed/Medline identified 2,388 articles of which 21 studies (randomized controlled trial (RCT) (n = 10) and non-randomized intervention studies (n = 11)) were classified as testing the effects of intentional weight loss on i) oxidative stress (n = 15), ii) DNA repair (n = 2), and iii) telomere length (n = 4).

RESULTS

Across a broad range of intervention designs, diet-, exercise-, surgery-, balloon-induced weight loss regimens decreased oxidative stress measures. Studies investigating DNA repair capacity or telomere length as endpoints after weight loss were less common in number and yielded null or inconsistent results, respectively.

CONCLUSION

While this systematic review supports a role for intentional weight loss in reducing obesity-associated oxidative stress, it is not clear whether the effects are primary outcomes or secondary to improvement in obesity-associated insulin resistance and/or chronic inflammation. Although the lack of effect of intentional weight loss on DNA repair capacity might be anticipated given that oxidative stress is reduced, additional studies are needed. The inconsistent effects of weight loss on telomere length or DNA repair suggest the need for a re-assessment of intervention designs and assay methodology to definitively address this topic.

摘要

背景

在肥胖个体中检测到氧化应激、DNA 修复和端粒完整性标志物水平的改变,这些改变可能是肥胖相关疾病发病机制的基础。然而,通过有意减肥是否可以逆转这些影响尚未得到系统评价。

方法

在 PubMed/Medline 中进行文献检索,共检索到 2388 篇文章,其中 21 项研究(随机对照试验(RCT)(n=10)和非随机干预研究(n=11))被归类为测试有意减肥对 i)氧化应激(n=15)、ii)DNA 修复(n=2)和 iii)端粒长度(n=4)的影响。

结果

在广泛的干预设计中,饮食、运动、手术、气球诱导的减肥方案降低了氧化应激指标。研究减肥后 DNA 修复能力或端粒长度作为终点的研究数量较少,结果分别为阴性或不一致。

结论

虽然这项系统评价支持有意减肥在降低肥胖相关氧化应激中的作用,但尚不清楚这些影响是主要结果还是继发于肥胖相关胰岛素抵抗和/或慢性炎症的改善。尽管考虑到氧化应激的减少,有意减肥对 DNA 修复能力的影响可能是可以预期的,但仍需要更多的研究。减肥对端粒长度或 DNA 修复的影响不一致,这表明需要重新评估干预设计和检测方法,以明确解决这一问题。

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