Author
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NIELSEN, FORREST - 5450-20-00 |
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Submitted to: North Dakota Academy of Science Proceedings
Publication Type: Other Publication Acceptance Date: 4/30/1998 Publication Date: N/A Citation: N/A Interpretive Summary: Since 1971 circumstantial evidence for the nutritional essentiality of vanadium has appeared. However, this evidence has been questioned. Thus, stronger evidence for essentiality has been sought; this includes finding a specific biochemical role for vanadium in higher animals. An experiment was conducted to obtain further evidence that vanadium is nutritionally important and that it has a biochemical role that affects thyroid metabolism; thyroid hormones are important in the burning of carbohydrates such as glucose in the body to produce heat and energy. Vanadium deprivation affected changes in thyroid weight and the plasma concentrations of the thyroid hormones thyroxine and triiodothyronine caused by feeding deficient and luxuriant amounts of iodine, an element needed for thyroid hormone formation. Vanadium deprivation also increased the activity of pancreatic amylase which is instrumental in the first step in the digestion of dietary starch to glucose. Vanadium deprivation also affected serum lactate dehydrogenase, the last enzyme in the pathway in which glucose is broken down, in an opposite manner when dietary iodine was deficient than when luxuriant. These findings indicate nutritional amounts of vanadium affect thyroid hormone metabolism and carbohydrate metabolism, and when combined with the knowledge that vanadium has defined biochemical functions in lower forms of life, provide circumstantial evidence that vanadium is an essential element for higher forms of life including humans. Thus, vanadium might be of nutritional importance for health and well-being. Technical Abstract: A 2x2x2 factorially arranged experiment was conducted with the objective of gaining further evidence that vanadium has a biochemical role that affects thyroid, and thus carbohydrate, metabolism in higher animals. The variables were deficient and adequate dietary vanadium, or about 2 ng and 500 ng/g diet; low and luxuriant dietary iodine, or about 50 ng and 25 ug/g diet; and type of rat, either diabetes-prone or diabetes-resistant BB/Wor rat. Each treatment group contained eight rats which were fed ad lib their appropriate casein-ground corn-corn oil based diet for 90 days. When rats were fed the low iodine diet, thyroxine concentrations were much less in vanadium-supplemented than -deprived rats. Increasing dietary iodine markedly increased the thyroxine concentrations in the vanadium- supplemented rats but had very little effect on the concentrations in the vanadium-deprived rats. When dietary iodine was low, plasma triiodothyronine was higher in vanadium-supplemented than -deprived rats. Iodine supplementation decreased the triiodothyronine concentration in vanadium-supplemented rats, but increased it in vanadium-deprived rats; this effect was most marked in the diabetes resistant rats. The activity of pancreatic amylase was lower in vanadium-supplemented than -deprived rats; this difference was much greater in the diabetes-resistant than diabetes-prone rat when dietary iodine was low. An interaction between iodine and vanadium also affected the activity of serum lactate dehydrogenase. These findings support the contention that vanadium has a biochemical role that affects thyroid and carbohydrate metabolism in higher animals. |
