Tetrahydrobiopterin Deficiency in Diabetic Rats
Vascular complications are major causes of morbidity and mortality in patients with insulin-dependent diabetes mellitus. Defects in the generation and release of nitric oxide (NO), the so-called endothelium-derived relaxing factor, have been implicated in the development of diabetic vasculopathy. Our previous data indicated that a deficiency in tetrahydrobiopterin (BH4), a cofactor essential for the activity of NO synthase, was responsible for reduced NO production in coronary endothelial cells of the spontaneously diabetic BB rat, an animal model of human type I diabetes mellitus (1). The BH4 deficiency was the result of decreased expression of GTP cyclohydrolase I (GTP-CH), the first and rate-limiting enzyme for the generation of BH4.
KeywordsDiabetic Animal Coronary Endothelial Cell Diabetic Vasculopathy Juvenile Diabetes Foundation Venular Endothelial Cell
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