肌萎缩
医学
肌萎缩性肥胖
内科学
氧化应激
内分泌学
谷胱甘肽
逻辑回归
体质指数
胃肠病学
生物化学
生物
酶
作者
Francesco Bellanti,Antonino Davide Romano,Aurelio Lo Buglio,Valeria Castriotta,Giuseppe Guglielmi,Antonio Greco,Gaetano Serviddio,Gianluigi Vendemiale
出处
期刊:Maturitas
[Elsevier BV]
日期:2017-12-05
卷期号:109: 6-12
被引量:115
标识
DOI:10.1016/j.maturitas.2017.12.002
摘要
Objectives To define whether circulating markers of oxidative stress correlate with sarcopenia in terms of glutathione balance and oxidative protein damage, and whether these biomarkers are associated with risk of cardiovascular disease (CVD). Study design Population-based cross-sectional study. 115 out of 347 elderly subjects were classified as non-sarcopenic non-obese (NS-NO), sarcopenic non-obese (S-NO), non-sarcopenic obese (NS-O), and sarcopenic obese (S-O). Main outcome measurements Sarcopenia was defined as a relative skeletal muscle mass index (RASM) <7.25 kg/m2 for men or <5.67 kg/m2 for women, while obesity was diagnosed in those presenting with% fat >27 for men or >38 for women. The CVD risk was estimated by the carotid intima-media thickness (IMT) and the Framingham score. Blood reduced glutathione (GSH), oxidized glutathione (GSSG), plasma malondialdehyde-(MDA) and 4-hydroxy-2,3-nonenal-(HNE) protein adducts were analyzed. Results Significantly greater blood GSSG/GSH ratio and plasma MDA/HNE protein adducts were observed in sarcopenic than in non-sarcopenic patients. A logistic regression model showed a close relationship between serum HNE and MDA adducts and sarcopenia (OR = 1.133, 95% CI 1.057–1.215, and OR = 1.592, 95% CI 1.015–1.991, respectively). Linear and logistic regression analysis evidenced strong associations between the IMT or the Framingham CVD risk category and blood GSSG/GSH or serum HNE protein adducts in the S-O group. Conclusion Circulating markers of oxidative stress are increased in sarcopenia and related to CVD risk in sarcopenic obesity, suggesting that redox balance analysis would be a useful part of a multidimensional evaluation in aging. Further research is encouraged to support interventional strategies to correct redox imbalance, which might contribute to the prevention or at least limitation of sarcopenia and its co-morbidities.
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