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Cardiac Performance During Diabetes
Published in Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla, Heart Dysfunction in Diabetes, 2019
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla
Another method used to prevent the decline in cardiac performance during diabetes was vanadate treatment. Vanadate is the oxidized form of the trace element vanadium. It has an insulin-like action in the cell.92 Vanadate, when included in the drinking water of diabetic rats, restored plasma glucose levels to control without influencing plasma insulin concentration.93 The left ventricular developed pressure and + and -dP/dt were significantly depressed in the diabetic animals. After vanadate treatment, these functional parameters were normalized in the diabetic rats. Unfortunately, side effects may limit its clinical usefulness, at least in the near future. Since cardiac dysfunction recovered without any improvement in plasma insulin concentrations but with a dramatic improvement in blood sugar levels, this would support a role for hyperglycemia and not hypoinsulinemia in the cardiac disease. However, the validity of this contention is complicated and seriously threatened by the knowledge that the molecular mode of action of vanadate is very much like that of insulin.92
Vanadium
Published in Linda M. Castell, Samantha J. Stear (Nottingham), Louise M. Burke, Nutritional Supplements in Sport, Exercise and Health, 2015
At supraphysiological levels, in vitro and animal studies indicate that vanadate and other vanadium compounds exert measurable biological effects (Rehder, 2012). Effects on glucose transport activity and pancreatic β-cell function, via phosphatases and kinases, are currently the subject of research into antidiabetic therapeutics (Smith et al., 2008). The role of vanadium as a transcription modulator of genes in oxidative stress and oncogenesis has also been described (Willsky et al., 2006; Manna et al., 2011) in studies investigating anti-cancer agents.
Boron, Manganese, Molybdenum, Nickel, Silicon and Vanadium
Published in Judy A. Driskell, Ira Wolinsky, Sports Nutrition, 2005
When vanadate appears in the blood, it is quickly converted into the vanadyl cation.225 However, as a result of oxygen tension, vanadate still exists in blood. Vanadyl, the most prevalent form of vanadium in blood, is bound and transported by transferrin and albumin.225 Vanadate is transported by transferrin only.226 Vanadyl also complexes with ferritin in plasma and body fluids.227,228 It remains to be determined whether vanadyl-transferrin can transfer vanadium into cells through the transferrin receptor or whether ferritin is a storage vehicle for vanadium. Vanadium is rapidly removed from plasma and is generally retained in tissues under normal conditions at concentrations less than 10 ng/g fresh weight.220 Bone apparently is a major sink for excessive retained vanadium.
The impact of concomitant administration of vanadium and insulin on endothelial dysfunction markers (PAI-1 and ET-1) in type 1 diabetic rats
Published in Archives of Physiology and Biochemistry, 2021
M. D. Morsy, I. Bin-Jaliah, S. O. Bashir, A. Shatoor, M. A. Haidara
In group DIV, we observed that there were maximum significant improvements in lipid profile, markers of oxidative stress, inflammatory and endothelial dysfunction markers. Several studies reported other mechanisms of action of vanadate. Vanadium in its peroxo oxidation form rapidly oxidised thiol groups in cysteine residues of proteins giving a potential mechanism for regulating enzyme activity (Huyer et al.1997). The inhibition of phosphorylases by vanadate is due to its similarity to phosphate in the transition state of phosphate ester hydrolysis. Also, due to the similarity between the vanadyl cation and Mg2+, the enzymes depending on Mg2+ as a cofactor are likely regulated competitively by vanadyl (Stankiewicz et al.1987). Also, vanadium exerted its therapeutic effects through several other mechanisms, including increased protein kinase B (Akt) and endothelial NO synthase activity, modulation of endothelin and angiotensin expression, inhibition of dystrophin breakdown, calpastatin, and inhibition of stress of the endoplasmic reticulum (Cong et al.2016). Vanadium compounds stimulated the expression of Akt in a receptor tyrosine kinase-dependent manner by inhibiting both protein tyrosine phosphatases and production of ROS (Shioda et al.2007). By activating Akt, vanadium suppresses pancreatic β cell apoptosis through enhanced phosphorylation of several substrates (Datta et al.1997). Also, vanadium induced insulin sensitivity is caused by the inhibition of phosphotyrosine phosphatases thereby stimulating insulin receptor tyrosine kinase (IRTK) activity. Another study suggested that vanadium stimulates glucose uptake independently of IRTK activation (García-Vicente et al.2007).
Evaluation of sodium orthovanadate as a radioprotective agent under total-body irradiation and partial-body irradiation conditions in mice
Published in International Journal of Radiation Biology, 2021
Yuichi Nishiyama, Akinori Morita, Bing Wang, Takuma Sakai, Dwi Ramadhani, Hidetoshi Satoh, Kaoru Tanaka, Megumi Sasatani, Shintaro Ochi, Masahide Tominaga, Hitoshi Ikushima, Junji Ueno, Mitsuru Nenoi, Shin Aoki
Vanadate was purchased from Sigma-Aldrich (St. Louis, MO, USA) and dissolved in a normal saline (NS) solution. After 7 days of acclimatization, the mice were given a single intraperitoneal injection of vanadate (20 mg/kg body weight, 2 mg/mL in NS solution) or vehicle (NS solution) 30 min before irradiation. TBI and PBI were then performed using an X-ray generator (MBR-1520R-3, Hitachi, Ltd., Tokyo, Japan) under a tube voltage of 150 kV, a tube current of 20 mA, and a dose rate of approximately 1.0 Gy/min. Dosimetry was carried out with a 0.3 cc N31003 ionization chamber (PTW Freiburg, Freiburg, Germany).
Dual character of GABA action on Cl–-transport by the reconstituted Cl–/
Published in Journal of Receptors and Signal Transduction, 2018
Vanadate in low concentrations (1–10 μM) is a known potent inhibitor of certain plasma membrane P-type ATPases as well as the Cl–-ATPase [13]. Preincubation of the proteoliposomes with vanadate (10 μM) did not change the GABA-induced Cl– inflow into the liposomes, but completely inhibited the ATP-dependent Cl– input (Figure 1(c)). These data are similar to those of previously reported electrophysiological studies of Cl–-transport by recombinant GABAAR [14]. The GABA-induced Cl–-current was not much changed by the application of vanadate (100 μM).