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Pioglitazone ameliorates endothelial dysfunction in obese rats with nephropathy
Tamehachi Namikoshi1, Minoru Satoh, Naruya Tomita
1Division of Nephrology, Department of Internal Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki 701-0192, Japan.
Biochemical and Biophysical Research Communications
|August 8, 2007
Summary
Metabolic syndrome causes kidney and blood vessel damage due to endothelial dysfunction. Pioglitazone treatment improved these conditions in obese rats by reducing nitrative stress and related molecular changes.
Area of Science:
- Nephrology
- Cardiovascular Research
- Metabolic Syndrome Research
Background:
- Endothelial dysfunction is a critical factor in renovascular complications associated with metabolic syndrome.
- The Zucker obese rat serves as a relevant model for studying metabolic syndrome-induced injuries.
Purpose of the Study:
- To investigate the mechanisms of renovascular injury in Zucker obese rats.
- To evaluate the therapeutic efficacy of pioglitazone in ameliorating these injuries.
Main Methods:
- Obese rats were fed a high-protein diet (OHP) for 12 weeks.
- Assessed nephropathy and endothelial dysfunction.
- Measured nitrotyrosine accumulation and mRNA expression of NADPH oxidase and inducible nitric oxide synthase in the aorta.
- Administered pioglitazone to assess therapeutic effects.
Main Results:
- OHP rats developed nephropathy and endothelial dysfunction.
- Increased nitrotyrosine and elevated mRNA expression of NADPH oxidase and inducible nitric oxide synthase were observed in OHP rats.
- Pioglitazone treatment improved nephropathy and endothelial dysfunction, reduced nitrotyrosine, and inhibited the augmented gene expression.
Conclusions:
- Nitrative stress plays a significant role in endothelial dysfunction and renovascular injury in this metabolic syndrome rat model.
- Pioglitazone demonstrates therapeutic potential by mitigating these injuries, likely through the reduction of nitrative stress.
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