Dehydroepiandrosterone Administration Counteracts Oxidative Imbalance and Advanced Glycation End Product Formation in Type 2 Diabetic Patients  

Oleh:

Runzo, Cristina ; Brignardello, Enrico ; Aragno, Manuela ; Catalano, Maria Graziella ; and Others

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 30 no. 11 (Nov. 2007), page 2922.
Topik: AGE; advanced glycation end product ; DHEA; dehydroepiandrosterone ; DHEAS; DHEA sulfate ; GSH; glutathione ; HNE; hydroxynonenal ; HOMA; homeostasis model assessment ; PBMC; peripheral blood mononuclear cell ; ROS; reactive oxygen species ; sTNF-R; soluble tumor necrosis factor receptor ; TNF; tumor necrosis factor

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2007.04 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

OBJECTIVE—Dehydroepiandrosterone (DHEA) has been shown to prevent oxidative stress in several in vivo and in vitro models. This study aimed to evaluate the effects of DHEA administration on oxidative stress, pentosidine concentration, and tumor necrosis factor (TNF)-/TNF- receptor system activity in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS—Twenty patients were enrolled in the study and randomly assigned to the DHEA (n = 10) or placebo (n = 10) group. Twenty healthy sex- and age-matched subjects with normal glucose levels served as control subjects. DHEA was given as a single daily dose of 50 mg for 12 weeks. RESULTS—Oxidative stress parameters were significantly higher in diabetic patients versus control subjects. Pentosidine levels, as well as soluble TNF receptor (sTNF-R)I and sTNF-RII, were also higher in diabetic patients. After DHEA, plasma levels of reactive oxygen species and hydroxynonenal dropped by 53 and 47%, respectively, whereas the nonenzymatic antioxidants glutathione and vitamin E increased (+38 and +76%, respectively). The same changes in oxidative parameters were detected in peripheral blood mononuclear cells (PBMCs). DHEA treatment also induced a marked decrease of pentosidine plasma concentration in diabetic patients (–50%). Moreover, the TNF-/TNF- receptor system was shown to be less activated after DHEA treatment, in both plasma and PBMCs. CONCLUSIONS—Data indicate that DHEA treatment ameliorates the oxidative imbalance induced by hyperglycemia, downregulates the TNF-/TNF- receptor system, and prevents advanced glycation end product formation, suggesting a beneficial effect on the onset and/or progression of chronic complications in type 2 diabetic patients.

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