Widjaja Sry Suryani, Rusdiana Rusdiana, Helvi Tengku Mardani, Simanullang Rostime Hermayeni, Jayalie Vito Filbert, Amelia Rina, Arisa Jessie
Department of Biochemistry, Medical Faculty, Universitas Sumatera Utara, Medan, Sumatera Utara, Indonesia.
Department of Nursing School, University of Murni Teguh, Medan, Sumatera Utara, Indonesia.
Iran J Public Health. 2024 Jan;53(1):12-22. doi: 10.18502/ijph.v53i1.14679.
Cell aging is associated with changes in telomeres due to DNA damage arising from chronic inflammation in obese patients. The aim of the systematic review and meta-analysis was to find the relationship between obesity and aging or senescence.
The systematic review was conducted through PRISMA guideline, beginning with literature search within 2012-2022 in several databases (PubMed, EBSCOHost, Science Direct, Scopus, and Cochrane) followed by screening process using predetermined PICO criteria. Original studies on the topic of obesity and senescence (aging), from preclinical studies to clinical research (cohort or cross-sectional studies) that were published within the last ten years. All studies were appraised using SYRCLE risk of bias tool for preclinical studies and Newcastle-Ottawa Scale (NOS) for cross-sectional and cohort studies. The data extraction on the studies' characteristic and outcome on aging or senescence were followed by quantitative analysis using MetaXL process on prevalence ratio and hazard ratio of obesity to comorbidities and mortality.
Fifteen studies were enrolled. Obesity and white adipose tissue cause increased levels of pro-inflammatory and pro-senescence cytokine and macrophage whilst the aging process lowers metabolism with increased insulin resistance and linked to increased risk of obesity. Obesity occurs in 22% (95% CI 18%-26%) of elderly population with higher prevalence rate in the women population. Obesity is associated with significant increased risk of multimorbidity by 56% (OR = 1.58 [95% CI 1.48-1.96]).
The obesity and aging or senescence has reciprocal relationship between each other.
由于肥胖患者的慢性炎症导致DNA损伤,细胞衰老与端粒变化有关。本系统评价和荟萃分析的目的是找出肥胖与衰老或衰老之间的关系。
本系统评价按照PRISMA指南进行,首先在2012年至2022年期间在多个数据库(PubMed、EBSCOHost、Science Direct、Scopus和Cochrane)中进行文献检索,然后使用预先确定的PICO标准进行筛选。关于肥胖和衰老(老化)主题的原始研究,涵盖过去十年内发表的从临床前研究到临床研究(队列或横断面研究)。所有研究均使用SYRCLE偏倚风险工具对临床前研究进行评估,并使用纽卡斯尔-渥太华量表(NOS)对横断面和队列研究进行评估。在对研究的特征以及衰老或衰老结果进行数据提取之后,使用MetaXL程序对肥胖与合并症和死亡率的患病率比和风险比进行定量分析。
纳入了15项研究。肥胖和白色脂肪组织会导致促炎和促衰老细胞因子以及巨噬细胞水平升高,而衰老过程会降低新陈代谢,增加胰岛素抵抗,并与肥胖风险增加有关。22%(95%CI 18%-26%)的老年人群患有肥胖症,女性人群的患病率更高。肥胖与多病症风险显著增加56%相关(OR = 1.58 [95%CI 1.48-1.96])。
肥胖与衰老或衰老之间存在相互关系。