Oxidative stress and endothelium influenced by metformin in type 2 diabetes mellitus
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články, randomizované kontrolované studie, práce podpořená grantem
- MeSH
- cévní endotel účinky léků MeSH
- diabetes mellitus 2. typu farmakoterapie metabolismus MeSH
- dospělí MeSH
- hypoglykemika farmakologie terapeutické užití MeSH
- klinické křížové studie MeSH
- kůže krevní zásobení účinky léků MeSH
- lidé středního věku MeSH
- lidé MeSH
- malondialdehyd krev MeSH
- metformin farmakologie terapeutické užití MeSH
- mikrocirkulace účinky léků MeSH
- oxidační stres účinky léků MeSH
- pilotní projekty MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- randomizované kontrolované studie MeSH
- Názvy látek
- hypoglykemika MeSH
- malondialdehyd MeSH
- metformin MeSH
OBJECTIVE: Metformin may influence atherogenesis but the mechanisms are not well understood. A pilot study was undertaken to determine whether metformin administration is associated with changes in oxidative stress and endothelial function. METHODS: Fifteen type 2 diabetic patients were treated for 3 months with metformin (1,700 mg daily) or with a placebo in a crossover study. Laboratory parameters of oxidative stress, fibrinolysis and endothelial function were evaluated both prior to and following the respective treatments. In addition, laser Doppler was used to determine microcirculation changes in the skin. RESULTS: Increases in serum N-acetyl-beta-glucosaminidase activity (p < 0.05) and plasma malondialdehyde concentration were found following 1 month of metformin administration. Three months of treatment was accompanied by significantly increased plasma malondialdehyde (p < 0.001) and ascorbic acid (p < 0.01) concentrations as well as the alpha-tocopherol/(cholesterol + triglyceride) ratio (p < 0.001). The concentration of tissue plasminogen activator (tPA), vascular cell-adhesion molecules (VCAM) and intercellular cell-adhesion molecules (ICAM) were significantly decreased (p < 0.01) compared with placebo. Microcirculation measured by laser Doppler flowmetry was not significantly changed. CONCLUSIONS: We conclude that initiation of metformin treatment in type 2 diabetic patients is associated with improved diabetes control as well as with activation of oxidative stress together with antioxidant system. The atherogenic process measured by biochemical indicators is diminished in parallel. Our results show that in short-term metformin administration in type 2 diabetes promotes endothelium effects associated with a complex of metabolic changes.
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