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Vanadium in Biosphere and Its Role in Biological Processes. | LitMetric

AI Article Synopsis

  • Ultra-trace elements, like vanadium (V), play critical roles in biological processes such as glucose and lipid metabolism and may help alleviate stress in diabetes when used in low doses.
  • Vanadium competes with iron for transport in the body and inhibits certain enzymes that can help promote glucose uptake in cells, particularly with insulin present.
  • While most research has been conducted on lab animals, there is emerging evidence supporting vanadium's potential benefits and risks as a therapeutic agent for various diseases in humans and larger animals.

Article Abstract

Ultra-trace elements or occasionally beneficial elements (OBE) are the new categories of minerals including vanadium (V). The importance of V is attributed due to its multifaceted biological roles, i.e., glucose and lipid metabolism as an insulin-mimetic, antilipemic and a potent stress alleviating agent in diabetes when vanadium is administered at lower doses. It competes with iron for transferrin (binding site for transportation) and with lactoferrin as it is secreted in milk also. The intracellular enzyme protein tyrosine phosphatase, causing the dephosphorylation at beta subunit of the insulin receptor, is inhibited by vanadium, thus facilitating the uptake of glucose inside the cell but only in the presence of insulin. Vanadium could be useful as a potential immune-stimulating agent and also as an antiinflammatory therapeutic metallodrug targeting various diseases. Physiological state and dose of vanadium compounds hold importance in causing toxicity also. Research has been carried out mostly on laboratory animals but evidence for vanadium importance as a therapeutic agent are available in humans and large animals also. This review examines the potential biochemical and molecular role, possible kinetics and distribution, essentiality, immunity, and toxicity-related study of vanadium in a biological system.

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Source
http://dx.doi.org/10.1007/s12011-018-1289-yDOI Listing

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