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Does Nitric Oxide (NO) and/or Superoxide (.O2-) Cause Type 2 Diabetes and can it be Prevented?

Knox Van Dyke, Erica Ghareeb, Mark Van Dyke, Chris Van Dyke, Michael Gunther and David H Van Thie

Diabetes 2 is caused by metabolic effects on the pancreatic ß cells with loss of insulin sensitivity or effectiveness and control of its secretion. Some damage to the Beta cells probably occurs continuously once the disease process starts and oxidative and nitrosative stresses likely play a role as well caused by the proper lack of glucose control. Recent work indicates that excessive glucagon from alpha cells which replace Beta cells have an important role raising glucose levels. If this scenario is correct, specific antioxidant substances might have an important potential to quench, degrade or react with the key substances causing oxidative stress via oxidation/nitration processes causing chemically induced diabetes namely, superoxide (.O2 )-, nitric oxide (NO. ), peroxynitrite (OONO- ), etc. This pre-exposure may be able to prevent type 2 diabetes mellitus and/or its clinical consequences. Previously we found that correct doses of carboxy-PTIO (sodium salt) prevented diabetes mellitus I caused by Streptozotocin (STZ) in rats. Carboxy -PTIO oxidizes excessive nitric oxide from STZ occurring in the Beta cell. An intermediate dose of (STZ) in rats should partially mimic a type 2 diabetic state (glucose levels approx 300 mg/dl vs. 100 mg/dl in normal animals. We added effective antioxidants tempol and acetaminophen to prevent any excessive oxidative damage from STZ