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Figure 3 Hypothetical scheme illustrating the possible mechanism of impaired endothelial function in the insulin-resistant state. Increased quinonoid dihydrobiopterin (qBH2) synthesis in the insulin-resistant state is closely associated with a decrement in the activity of dihydropteridine reductase (DHPR), the recycling enzyme that converts BH2 to tetrahydrobiopterin (BH4). As a result, both BH4/BH2 ratio and BH4 to total biopterin (BH2 + BH4) were significantly decreased in the insulin-resistant subjects. These results indicate that decreased nitric oxide (NO)-dependent vasodilation in the insulin-resistant state may be related to abnormal pteridine metabolism and vascular oxidative stress. GTP = guanosine triphosphate; eNOS = endothelial nitric oxide synthase; O2– = superoxide anion; PTPS = 6-pyruvoyltetrahydropterine synthase; SR = sepiapterin reductase.
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