Abstract:
BACKGROUND:Type 1 diabetes (T1D) mellitus and obesity are recognized risk factors for cardiovascular disease (CVD). A common mechanism underlying an increased risk for endothelial dysfunction in these two metabolic diseases is oxidative stress. OBJECTIVE:To evaluate and compare the oxidant/antioxidant defense systems in children affected with T1D or obesity in order to determine the importance of oxidative stress before the emergence of complications. SUBJECTS:Children with T1D (n = 20) or obesity (n = 22), without comorbidities, and age- and sex-matched controls (n = 16). METHODS:We assessed lipid peroxidation by circulating levels of lipoperoxides and malondialdehyde, as well as protein oxidation by the concentration of plasma carbonyl groups. The endogenous antioxidative defense system was evaluated by the red cell glutathione peroxidase and reduced glutathione. The serum levels of alpha-tocopherol and beta-carotene were determined to assess exogenous antioxidants. RESULTS:Lipid peroxidation was significantly higher in both T1D and obese children when compared with control children. However, T1D patients showed a more elevated level, because their malondialdehyde values were significantly increased with respect to obese children. Protein oxidation was present in both groups of children and did not differ between them. With respect to obese children, the glutathione peroxidase activity and exogenous antioxidants were decreased in T1D patients. CONCLUSION:Oxidative stress is present in both children with T1D and obesity, although it is more pronounced in the former. Obese children may suffer an additional oxidative stress in the case of developing impaired glucose metabolism.
journal_name
Pediatr Diabetesjournal_title
Pediatric diabetesauthors
Codoñer-Franch P,Pons-Morales S,Boix-García L,Valls-Bellés Vdoi
10.1111/j.1399-5448.2009.00565.xsubject
Has Abstractpub_date
2010-06-01 00:00:00pages
251-7issue
4eissn
1399-543Xissn
1399-5448pii
PDI565journal_volume
11pub_type
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更新日期:2010-12-01 00:00:00
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更新日期:2018-04-19 00:00:00
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