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VANADIUM Rough file: "When Dr. John McNeill, dean of pharmaceutical sciences at UBC, and his
colleagues Clayton Heilinger and Arun Tahiliani were testing vanadium - a common
trace element found in seaweed - on diabetes induced female rats to see if it
would prevent the development of cardiac problems, they made a startling
discovery. Vanadium not only improved the rats' cardiovascular performance, it
also regulated the levels of glucose in their blood and prevented the formation
of cataracts. In fact, the rats that were fed vanadium in their drinking water
appeared normal in all respects. ... Adds McNeill: 'The fact that vanadium
appears to fix the whole system is a very nice discovery. It was not something
we originally intended to look for.' A two-factor, two-by-three factorially arranged experiment was performed to ascertain whether iodine affects the response of rats to vanadium deprivation. Male weanling Wistar-Kyoto rats were fed a 16% casein 68% acid-washed ground corn diet for 8 weeks. The variables were supplemental vanadium at 0 or 1 microgram/g and supplemental iodine at 0, 0.33 or 25 micrograms/g. Vanadium deprivation increased thyroid weight and thyroid weight/body weight ratio and decreased the concentration of vanadium in liver. Vanadium and iodine interacted such that, as dietary iodine was increased, plasma glucose increased in the vanadium-deficient rats but decreased in the vanadium-supplemented rats. Also, as dietary iodine was increased, thyroid peroxidase activity decreased; the decrease was more marked in the vanadium-supplemented than the vanadium-deprived rats. The findings suggest that vanadium may have a physiological role affecting iodine metabolism and thyroid function. vanadium and iodine interaction effects on thyroid.doc
Vanadium and ascorbate effects on 3-hydroxy-3-methylglutaryl coenzyme A reductase, cholesterol and tissue minerals in guinea pigs fed low-chromium diets. Seaborn CD, Mitchell ED, Stoecker BJ Department of Nutritional Sciences, Oklahoma State University, Stillwater. Vanadium has been reported to affect numerous physiological processes; however, a demonstration that vanadium deficiency consistently impairs biological function is lacking. The purpose of this study was to determine if the activity of hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme in cholesterol synthesis, is affected by dietary supplementation of vanadate and/or chronic ascorbic acid deficiency. To determine if vanadium and/or ascorbic acid affected mineral metabolism, tissue minerals also were analyzed. Weanling male guinea pigs were assigned randomly to groups of 10 in a 2 x 2 factorial design. The dietary variables were ascorbate, 0.5 or 10 mg/day, and vanadium < 0.01 microgram or 0.5 microgram/g diet as NH4VO3 in a low Cr diet containing < 0.07 microgram Cr/g diet. After 21 weeks on this diet, guinea pigs receiving more ascorbate had lower liver weight/body weight ratios and increased bone copper. Testes weight/body weight ratios, hepatic glycogen and bone copper decreased while hepatic lipids, fecal bile acids, plasma cortisol and bone calcium and magnesium were increased by vanadium supplementation. An interaction between vanadium and ascorbate affected cholesterol excretion in feces, hepatic iron, plasma cholesterol concentration and the activity of HMG CoA reductase. This study provides evidence of increased bone mineral concentrations with vanadium supplementation and of an interaction between vanadium and ascorbate which affected cholesterol metabolism.
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