In nature, vanadium is a group V transition metal found mainly in its pentavalent state as vanadate (VO3-) and its trivalent state as the vanadyl ion (VO2+). The different oxidation states of vanadium produces a range of colours in solution from which it derived its early name, panchromium, given by its discoverer del Rio in 1813. Some evidence from animal studies involving rats suggests that vanadium may have an essential role in some animals, however this viewpoint is controversial as no distinct deficiency disease has been established. In humans, total body stores of vanadium are around 100mg, but little in known about the exact role of vanadium. Vanadium shows pharmacological actions in humans that have been well documented, and vanadium salts are increasingly being reported to be able to mimic or potentiate the effects of insulin in both humans and animal.
In humans the total body pool of vanadium is roughly 100 to 200µg with approximately 90% bound to proteins such as transferin. Vanadium ingested in the diet in converted to VO2+ in the stomach and absorbed in this form where it is found mainly in the bone, liver and kidney. In rat studies vanadium as sodium orthovanadate was able to stabilise hyperglycaemia when administered at 100mg/kg body weight. From these studies it was reported that insulin levels do not increase with administration of vanadium, suggesting that its primary action is to increase insulin sensitivity. Subsequent rat experiments using vanadyl sulphate supported the finding using sodium orthovanadate in that diabetic rats could become euglycaemic upon administration. In addition, the use of vanadium in organic complexes such as bis(maltolato)oxovanadium(VI) also proved effective at lowering blood glucose levels in rats with similar results to other vanadium compounds.
The mechanisms of action of vanadium in potentiating or mimicking insulin are not fully understood. Vanadium is known to affect several aspects of the insulin signal pathway, with some speculative interest that vanadium behaves as a phosphate analogue that stimulates phosphorylation by inhibiting phosphatases. However, the intracellular form of vanadium is vanadyl, which is not a potent phosphatise inhibitor, and so other mechanisms may explain the action of vanadium on insulin. Vanadium may act further down the insulin signal cascade or may influence intracellular calcium influx. Some evidence suggests that the signal cascades that rely on reversible protein phosphorylation and dephosporylation may become defective in insulin resistance and that this can in some way be rectified by vanadium. The fact that the anti-diabetic effects remain for up to 20 weeks upon withdrawal of vanadium may suggest that tissue stores are released over time.
Vanadium is also able to lower the hyperphagia associated with experimental diabetes in animal studies. This has lead to suggestions that it is the dietary restriction that is responsible for the euglycaemic effect seen in animal models. However more recent studies have disproved this theory and shown that vanadium has specific insulin mimetic effects separate from dietary restriction. Human studies using both sodium orthovanadate and vanadyl sulphate have reported similar findings to those seen in animal studies. Particularly, reductions in fasting glucose levels and improved insulin sensitivity which persisted for up to 2 weeks after withdrawal of the vanadium salt. The daily intake is <50mg/day. However, the amount required for the pharmacological effect on blood glucose is around 500 to 1000mg/kg of vanadium salt in animals and around 100 to 125mg of vanadium salt in man.
Verma, S., Cam, M. C. and McNeill, J. H. 1998. Nutritional factors that can favourably influence the glucose/insulin system: vanadium. Journal of the American College of Nutrition. 17: 11-18
