作者: Joo Young Huh , Eun-Young Seo , Hi Bahl Lee , Hunjoo Ha
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摘要: Objective Accumulation of visceral fat is one the major risk factors for development cardiovascular disease in peritoneal dialysis (PD) patients. Adiponectin, an adipokine commonly regarded as a negative indicator metabolic disease, reported to be downregulated its gene level end-stage renal Since excessive deposit involved increased reactive oxygen species (ROS), PD solution (PDS) may contribute ROS production, resulting dysregulation adiponectin. In this study, we tested our hypothesis that oxidative stress induced by PDS play role regulation Methods Commercial containing 3.86% glucose (20 - 30 mL) was administered SD rats 12 weeks with and without N-acetylcysteine (NAC; 10 mmol/L). ELISA used quantify adiponectin plasma spent dialysate. For vitro studies, fully differentiated 3T3-L1 adipocytes isolated from abdominal were treated high solution, PDS, H(2)O(2). Adiponectin levels conditioned media measured immunoblot assays. The mRNA mature examined using real-time RT-PCR. Results dialysate significantly effect suppressed NAC. adipocytes, secretion inhibited 50 mmol/L glucose, diluted 2-fold, H(2)O(2) (200 μmol/L). addition, expression oligomer complexes. Conclusions Our data suggest conventional glucose-based pathophysiological changes downregulate secreted during long-term PD.