氧化应激
代谢综合征
背景(考古学)
炎症
胰岛素抵抗
医学
生物信息学
人口
脂肪组织
糖尿病
内科学
内分泌学
生物
环境卫生
古生物学
作者
Sylwia Dzięgielewska-Gęsiak,Małgorzata Muc‐Wierzgoń
出处
期刊:Metabolites
[Multidisciplinary Digital Publishing Institute]
日期:2023-03-26
卷期号:13 (4): 475-475
被引量:26
标识
DOI:10.3390/metabo13040475
摘要
In developed countries, aging is often seen as typical, but it is made complicated by many disorders and co-morbidities. Insulin resistance seems to be an underlying pathomechanism in frailty and metabolic syndromes. The decline in insulin sensitivity leads to changes in the oxidant–antioxidant balance and an accelerated inflammatory response, especially by adipocytes and macrophages in adipose tissue, as well as muscle mass density. Thus, in the pathophysiology of syndemic disorders—the metabolic syndrome and frailty syndrome—an extremely important role may be played by increased oxidative stress and pro-inflammatory state. Papers included in this review explored available full texts and the reference lists of relevant studies from the last 20 years, before the end of 2022; we also investigated the PubMed and Google Scholar electronic databases. The online resources describing an elderly population (≥65 years old) published as full texts were searched for the following terms: “oxidative stress and/or inflammation”, “frailty and/or metabolic syndrome”. Then, all resources were analyzed and narratively described in the context of oxidative stress and/or inflammation markers which underlie pathomechanisms of frailty and/or metabolic syndromes in elderly patients. So far, different metabolic pathways discussed in this review show that a similar pathogenesis underlies the development of the metabolic as well as frailty syndromes in the context of increased oxidative stress and acceleration of inflammation. Thus, we argue that the syndemia of the syndromes represents two sides of the same coin.
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