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Published on: October 22, 2014
Oxidative stress is increased in sarcopenia and associated with cardiovascular disease risk in sarcopenic obesity
Francesco Bellanti1, Antonino D Romano1, Aurelio Lo Buglio1
1Department of Medical and Surgical Sciences, University of Foggia, Italy.
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) <7.25kg/m2 for men or <5.67kg/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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