Abstract
Effect of intensive insulin therapy on systemic nitric oxide levels and adenosine deaminase activity in secondary sulfonylurea failure
Highlights
Sulfonylurea stimulates insulin secretion by pancreatic β-cells and is generally used as a rst-line treatment for type 2 diabetes
In secondary sulfonylurea failure, baseline Adenosine deaminase (ADA) activity (17.0 [14.6-21.7] U/L) was signi cantly lower than ADA activity measured on day 3 (20.5 [16.2-23.4] U/L; P = 0.018) and at 6 months (21.2 [16.6-22.5] U/L; P = 0.010)
The role of Nitric oxide (NO) in amelioration of β cell function is not supported at the level of peripheral blood
Summary
Sulfonylurea stimulates insulin secretion by pancreatic β-cells and is generally used as a rst-line treatment for type 2 diabetes. Progressive decrease in β-cell mass, deterioration in β-cell secretory reserve, insulin resistance and dysfunction of the proinsulin conversion machinery have been suggested in the pathogenesis of secondary sulfonylurea failure [1,2]. Adenosine deaminase (ADA; EC 3.5.4.4) catalyzes irreversible hydrolytic deamination of adenosine and deoxyadenosine to yield inosine to deoxyinosine, respectively, as part of purine salvage pathway. Oxidative stress and apoptosis are suggested to take part in secondary sulfonylurea failure associated with β cell destruction and impaired β cell function. We aimed to investigate ADA activity and NO levels as potential mediators of intensive insulin treatment in patients with secondary sulfonylurea failure
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