VANADIUM AND DIABETES

We demonstrated in 1985 that vanadium administered in the drinking wat er to streptozotocin (STZ) diabetic rats restored elevated blood gluco se to normal. Subsequent studies have shown that vanadyl sulfate can l ower elevated blood glucose, cholesterol and triglycerides in a variet y of diabetic models including the STZ diabetic rat, the Zucker fatty rat and the Zucker diabetic fatty rat. Long-term studies of up to one year did not show toxicity in control or STZ rats administered vanadyl sulfate in doses that lowered elevated blood glucose. In the BE diabe tic rat, a model of insulin-dependent diabetes, vanadyl sulfate lowere d the insulin requirement by up to 75%. Vanadyl sulfate is effective o rally when administered by either single dose or chronic doses. It is also effective by the intraperitoneal route. We have also been able to demonstrate marked long-term effects of vanadyl sulfate in diabetic a nimals following treatment and withdrawal of vanadyl sulfate. Because vanadyl sulfate is not well absorbed we have synthesized and tested a number of organic vanadium compounds. One of these, bismaltolato-oxova nadium IV (BMOV), has shown promise as a therapeutic agent. BMOV is 2- 3x more potent than vanadyl sulfate and has shown less toxicity. Recen t studies from our laboratory have shown that the effects of vanadium are not due to a decrease in food intake and that while vanadium is de posited in bone it does not appear to affect bone strength or architec ture. The mechanism of action of vanadium is currently under investiga tion. Several studies indicate that vanadium is a phosphatase inhibito r and that vanadium can activate serine/threonine kinases distal to th e insulin receptor presumably by preventing dephosphorylation due to i nhibition of phosphatases Short-term clinical trials using inorganic v anadium compounds in diabetic patients have been promising.