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PubMed2002

Vanadium increases GLUT4 in diabetic rat skeletal muscle.

The effect of vanadium in lowering blood glucose in diabetic animals is well established; however, the exact mechanism of action of vanadium still eludes us. There are several reports from in vitro studies indicating that vanadium increases enzyme activity in insulin signalling pathways; however, these findings have not been duplicated in vivo. Glucose transporters (GLUT) have a major role to play in any glucoregulatory effects. Insulin dependent GLUT4 is a major glucose transporter present in skeletal muscle, adipocytes and heart. In the present study we found that the plasma glucose in streptozotocin (STZ) diabetic animals was restored to normal following treatment with a single dose of BMOV, an organic vanadium compound, given by oral gavage (0.6 mmol/kg), similar to the response with chronic BMOV treatment. The response to BMOV by oral gavage was rapid and the animals were normoglycemic within 24 h of treatment and still demonstrated a significant effect even after 72 h. Using a specific antibody against GLUT4 we found an overall reduction in the GLUT4 in the total membrane fraction in skeletal muscle of diabetic animals. However, with a single dose of BMOV the GLUT4 level was restored to normal. This is the first report that establishes a direct effect of vanadium on the regulation of GLUT4 expression in diabetic animals in vivo, and may at least partially explain the glucoregulatory effects of vanadium.

Animals↗
PubMed1998

Metal-dependent expression of ferritin and lactoferrin by respiratory epithelial cells.

Increased availability of catalytically active metal has been associated with an oxidative injury. The sequestration of transition metals within intracellular ferritin confers an antioxidant function to this protein. Such storage by ferritin requires that the metal be transported across a cell membrane. We tested the hypothesis that, in response to in vitro exposures to catalytically active metal, respiratory epithelial cells increase the production of lactoferrin and ferritin to bind, transport, and store this metal with their coordination sites fully complexed. Residual oil fly ash is an emission source air pollution particle with biological effects that, both in vitro and in vivo, correspond with its metal content. Cell cultures were exposed to 0-200 micrograms/ml of oil fly ash for 2 and 24 h. Concentrations of ferritin and lactoferrin mRNA were estimated by reverse transcription-polymerase chain reaction, and concentrations of ferritin and lactoferrin proteins were measured in parallel. mRNA for ferritin did not change with exposure to oil fly ash. However, ferritin protein concentrations increased. Although mRNA for transferrin receptor decreased, mRNA for lactoferrin increased after incubation with the particle. Similar to changes in mRNA, transferrin concentration decreased, whereas that of lactoferrin increased. Deferoxamine, a metal chelator, inhibited these responses, and exposure of the cells to vanadium compounds alone reproduced elevations in lactoferrin mRNA. We conclude that increases in ferritin and lactoferrin expression can be metal dependent. This response can function to diminish the oxidative stress a metal chelate presents to a living system.

Air Pollutants↗
PubMed2001

Effect of vanadium on insulin and leptin in Zucker diabetic fatty rats.

Vanadium exhibits a variety of insulin-mimetic actions in vitro and in vivo. The mechanism(s) of the effect of vanadium on leptin in Zucker diabetic fatty (ZDF) rats, a model of Type 2 diabetes, is unclear. Since insulin is a stimulator of leptin production and secretion and vanadium is an insulin-mimetic or insulin-enhancing agent, we studied how vanadium affected plasma leptin levels in vivo and the relationship between plasma insulin, leptin and body fat in ZDF rats. Zucker lean and ZDF rats at 9-week old were chronically treated with bis(ethylmaltolato)oxovanadium(IV) (BEOV), an organic vanadium compound, by oral gavage daily for 3 weeks. At termination, the total body fat was weighed and blood was collected for insulin, leptin and glucose assay. BEOV treatment (0.1 mmol/kg/day) significantly decreased plasma glucose levels in ZDF rats and did not change food intake and body fat content either in lean or ZDF rats. Following 3-week treatment, plasma insulin and leptin levels in BEOV treated ZDF rats were significantly higher, 1.5 and 0.5 fold than untreated rats, respectively. The correlation coefficients in ZDF rats showed that plasma leptin levels were correlated to plasma insulin levels, but not to body fat. These data indicate that plasma leptin levels parallel plasma insulin levels, and the effects of vanadium on leptin appear to be mediated by insulin in ZDF rats.

Administration, Oral↗
PubMed2000

Vanadate-induced nitric oxide production: role in osteoblast growth and differentiation.

Nitric oxide (NO) has been shown to act as a mediator of cytokines in bone tissue. We have previously demonstrated that vanadium compounds are insulin- and growth factor-mimetic compounds in osteoblasts in culture, although high doses are toxic to these cells. In this study, we measured NO production in two osteoblast-like cells (UMR106 and MC3T3E1) incubated with different concentrations (2.5-100 microM) of vanadate. Vanadate induced NO release in a biphasic manner, with levels being significantly increased at concentrations over 50 microM. The NO donor, sodium nitroprusside, mimicked the vanadate effect: it inhibited cell growth and alkaline phosphatase activity in a dose-dependent manner. Vanadate enhanced the NO synthases, the endothelial and inducible (eNOS and iNOS) isoforms, in a dose-dependent manner. Experiments performed with the ionophore A23187 and EGTA suggested that vanadate-induced NO production involves Ca(2+)-dependent and -independent mechanisms. Altogether, our results suggest that NO may play a critical role in the bioactivity of vanadium in osteoblast-like cells.

Alkaline Phosphatase↗
PubMed2001

Vanadate-induced cell growth regulation and the role of reactive oxygen species.

While vanadium compounds are known as potent toxicants as well as carcinogens, the mechanisms of their toxic and carcinogenic actions remain to be investigated. It is believed that an improper cell growth regulation leads to cancer development. The present study examines the effects of vanadate on cell cycle control and involvement of reactive oxygen species (ROS) in these vanadate-mediated responses in a human lung epithelial cell line, A549. Under vanadate stimulation, A549 cells generated hydroxyl radical (*OH), as determined by electron spin resonance (ESR), and hydrogen peroxide (H2O2) and superoxide anion (O2*-), as detected by flow cytometry using specific dyes. The mechanism of ROS generation involved the reduction of molecular oxygen to O2*- by both a flavoenzyme-containing NADPH complex and the mitochondria electron transport chain. The O2*- in turn generated H2O2, which reacted with vanadium(IV) to generate *OH radical through a Fenton-type reaction (V(IV) + H2O2 --> V(V) +*OH + OH-). The ROS generated by vanadate induced G2/M phase arrest in a time- and dose-dependent manner as determined by measuring DNA content. Vanadate also increased p21 and Chk1 levels and reduced Cdc25C expression, leading to phosphorylation of Cdc2 and a slight increase in cyclin B1 expression as analyzed by Western blot. Catalase, a specific antioxidant for H2O2, decreased vanadate-induced expression of p21 and Chk1, reduced phosphorylation of Cdc2Tyr15, and decreased cyclin B1 levels. Superoxide dismutase, a scavenger of O2*-, or sodium formate, an inhibitor of *OH, had no significant effects. The results obtained from the present study demonstrate that among ROS, H2O2 is the species responsible for vanadate-induced G2/M phase arrest. Several regulatory pathways are involved: (1) activation of p21, (2) an increase of Chk1 expression and inhibition of Cdc25C, which results in phosphorylation of Cdc2 and possible inactivation of cyclin B1/Cdc2 complex.

Anions↗
PubMed2006

Vanadium and insulin increase adiponectin production in 3T3-L1 adipocytes.

Both adiponectin, an adipokine secreted by adipocytes, and vanadium compounds, have been extensively shown to enhance insulin sensitivity in vivo and in vitro. In this study we examined whether insulin and vanadyl sulfate (VS) affected adiponectin release and cell content from 3T3-L1 adipocytes, and whether they acted through a similar signaling pathway. Adiponectin cell content, but not release, consistently increased in cells treated with insulin (100 nM) and VS (10 and 50 microM) after 24 h. On the other hand, VS-induced adiponectin release only occurred after 4 days of incubation. The protein kinase B (PKB) inhibitor, NL-71-101, decreased both insulin and VS-induced adiponectin cell content, while neither wortmannin nor LY 294002, inhibitors of phosphatidylinositol 3-kinase (PI3-K), attenuated insulin or VS-induced adiponectin cell content. Furthermore, VS-induced adiponectin accumulation occurred in the presence of AGL2263, an insulin receptor (IR) inhibitor. These studies provide the first evidence that vanadium could exert its insulin sensitizing effects through the stimulation of adiponectin through a PKB-dependent transduction pathway.

3T3-L1 Cells↗
PubMed2005

Restoration of ultrastructural and biochemical changes in alloxan-induced diabetic rat sciatic nerve on treatment with Na3VO4 and Trigonella--a promising antidiabetic agent.

Vanadium has been reported to have broad pharmacological activity both in vitro and in vivo. Vanadium compound, sodium orthovanadate, Na3VO4, is well known for its hypoglycaemic effects. However, Na3VO4 exerts these effects at relatively high doses (0.6 mg/ml) and exhibit several toxic effects. In the present study lower doses of Na3VO4 (0.2 mg/ml) are combined with Trigonella foenum graecum seed powder (TSP), another hypoglycaemic agent, to reduce its toxicity without compromising its antidiabetic potential. The efficacy of the lower doses of Na3VO4 has been investigated in restoring the altered glucose metabolism and histological structure in the sciatic nerves in 21 and 60 days alloxan diabetic rats. A portion of the glucose was found to be channelled from the normal glycolytic route to polyol pathway, evident by the reduced hexokinase activity and increased polyol pathway enzymes aldose reductase and sorbitol dehydrogenase activity causing accumulation of sorbitol and fructose in diabetic conditions. Ultrastructural observation of the sciatic nerve showed extensive demylination and axonal loss after eight weeks of diabetes induction. Blood glucose levels increased in diabetic rats were normalized with the lower dose of vanadium and Trigonella treatment. The treatment of the diabetic rats with vanadium and Trigonella prevented the activation of the polyol pathway and sugar accumulations. The sciatic nerves were also protected against the structural abnormalities found in diabetes with Trigonella foenum graecum as well as Na3VO4. Results suggest that lower doses of Na3VO4 may be used in combination with TSP as an efficient antidiabetic agent to effectively control the long-term complications of diabetes in tissues like peripheral nerve.

Aldehyde Reductase↗
PubMed1994

Vanadium induced hemolysis of vitamin E deficient erythrocytes in Hepes buffer.

Several vanadium compounds were tested for their ability to induce in vitro hemolysis of vitamin E-deficient hamster erythrocytes. Free vanadyl caused hemolysis in Hepes buffer but not in Tris or phosphate buffer, while hemolysis was inhibited by catalase, chelators such as deferoxamine mesylate and EDTA, and hydroxyl radical scavengers such as ethanol and D-mannitol. Although metavanadate itself could not induce hemolysis, metavanadate with NAD(P)H caused hemolysis in Hepes buffer only, and superoxide dismutase prevented it. Hydrogen peroxide, hydroxyl radical and Hepes radical were involved in vanadyl-induced hemolysis, superoxide anion was further involved in metavanadate plus NAD(P)H-induced hemolysis. Vitamin E prevented hemolysis under both conditions.

Analysis of Variance↗
PubMed2001

Effect of vanadium on insulin sensitivity and appetite.

Vanadium, a potent nonselective inhibitor of protein tyrosine phosphatases, has been shown to mimic many of the metabolic actions of insulin both in vivo and in vitro. The mechanism(s) of the effect of vanadium on the decrease in appetite and body weight in Zucker fa/fa rats, an insulin-resistant model, is still unclear. Because insulin may inhibit hypothalamic neuropeptide Y (NPY), which is known to be related to appetite, and increase leptin secretion in adipose tissue, we studied the possibility that the changes in appetite produced by vanadium may be linked to altered NPY levels in the hypothalamus. We also examined effects of vanadium on leptin. Zucker lean and fatty rats were chronically treated with bis(maltolato)oxovanadium(IV) (BMOV), an organic vanadium compound, in the drinking water. Plasma and adipose tissue leptin levels were measured by radioimmunoassay and immunoblotting, respectively. Hypothalamic NPY mRNA and peptide levels were measured using in situ hybridization and immunocytochemistry, respectively. BMOV treatment significantly reduced food intake, body fat, body weight, plasma insulin levels, and glucose levels in fatty Zucker rats. Fifteen minutes after insulin injection (5 U/kg, intravenous [IV]), circulating leptin levels (+100%) and adipose leptin levels (+60%) were elevated in BMOV-treated fatty rats, although these effects were not observed in untreated fatty rats. NPY mRNA levels in the arcuate nucleus (ARC) (-29%), NPY peptide levels in ARC (-31%), as well as in the paraventricular nucleus (PVN) (-37%) were decreased with BMOV treatment in these fatty rats. These data indicate that BMOV may increase insulin sensitivity in adipose tissue and decrease appetite and body fat by decreasing NPY levels in the hypothalamus. BMOV-induced reduction in appetite and weight gain along with normalized insulin levels in models of obesity, suggest its possible use as a therapeutic agent in obesity.

Adipose Tissue↗
PubMed2006

Synthesis, characterization, antitumoral and osteogenic activities of quercetin vanadyl(IV) complexes.

The development of new vanadium derivatives with organic ligands, which improve the beneficial actions (insulin-mimetic, antitumoral) and decrease the toxic effects, is of great interest. A good candidate for the generation of a new vanadium compound is the flavonoid quercetin because of its own anticarcinogenic effect. The complex [VO(Quer)(2)EtOH]( n ) (QuerVO) has been synthesized and characterized by means of different spectroscopic techniques (UV-vis, Fourier transform IR, electron paramagnetic resonance) and its magnetic and stability properties. The inhibitory effect on bovine alkaline phosphatase (ALP) activity has been tested for the free ligand, the complex as well as for the vanadyl(IV) (comparative purposes). The biological activity of the complex on the proliferation of two osteoblast-like cells in culture, a normal one (MC3T3E1) and a tumoral one (UMR106), has been compared with that of the vanadyl(IV) cation and quercetin. The differentiation osteoblast markers ALP specific activity and collagen synthesis have been also tested. In addition, the effect of QuerVO on the activation of the extracellular regulated kinase (ERK) pathway is reported. The bone antitumoral effect of quercetin alone was established with the cell proliferation assays (it inhibits the proliferation of the tumoral cells and does not exert any effect on the normal osteoblasts). Moreover, the complex exerts osteogenic effects since it stimulates the type I collagen production and is a weak inhibitory agent upon ALP activity. Finally, QuerVO stimulated the ERK phosphorylation in a dose-response manner and this activation seems to be involved as one of the possible mechanisms for the biological effects of the complex.

3T3-L1 Cells↗
PubMed2004

An experimental and theoretical study of the Cp2VO2CO: use of 13CO3(2-) for structure investigation of d1-metallocene complexes.

EPR study has shown that the anticancer agent vanadocene dichloride (Cp2VCl2) interacts with carbonate contained in physiological solutions. Chelate complex Cp2VO2CO (|A(iso)(51V)| = 175.1 MHz, g(iso) = 1.9861) is the only paramagnetic species formed in the range about the physiological pH (5.5-11.0). The super-hyperfine coupling (|a(iso)(13C)| = 24.1 MHz) was evidenced at measurements using 13C labelled carbonate. The structure of carbonate complex was validated by comparison of observed and theoretical calculated HFC tensors (at the density functional level of theory).

Carbon Isotopes↗
PubMed1992

The effects of orthovanadate, vanadyl and peroxides of vanadate on glucose metabolism in skeletal muscle preparations in vitro.

The insulin-like effects of various vanadium compounds (orthovanadate, vanadyl and peroxides of vanadate) on rates of glucose oxidation, lactate formation and glycogen synthesis were measured in isolated incubated epitrochlearis (mainly type II fibres) and soleus (mainly type I fibres) muscle preparations. There was a small stimulation of the rate of glucose utilisation in soleus muscle preparations in vitro by orthovanadate (1 mM). Orthovanadate or vanadyl, at 1 mM, had little effect on the rates of lactate formation or glycogen synthesis in isolated incubated epitrochlearis muscle preparations. In contrast, peroxides of vanadate (peroxovanadates, at 1 mM) significantly stimulated glucose utilisation in both soleus and epitrochlearis muscle preparations in vitro. The stimulation of the rate of glycogen synthesis was associated with an increase in the percentage of glycogen synthase in the I (or a) form. Peroxovanadates were administered in the drinking water to rats made insulin deficient by streptozotocin treatment. There was no decrease in the elevated level of blood glucose over an 8 day administration period.

Animals↗
PubMedDate not supplied

Modulation of insulin action by vanadate: evidence of a role for phosphotyrosine phosphatase activity to alter cellular signaling.

UNLABELLED: A number of vanadium compounds (vanadate, vanadyl sulfate, metavanadate) have insulin-mimicking actions both in vitro and in vivo. They have multiple biological effects in cultured cells and interact directly with various enzymes. The inhibitory action on phosphoprotein tyrosine phosphatases (PTPs) and enhancement of cellular tyrosine phosphorylation appear to be the most relevant to explain the ability to mimic insulin. We demonstrated that in rat adipocytes both acute insulin effects, e.g. stimulation of IGF-II and transferrin binding and a chronic effect, insulin receptor downregulation, were stimulated by vanadate. Vanadate also enhanced insulin binding, particularly at very low insulin concentrations, associated with increased receptor affinity. This resulted in increased adipocyte insulin sensitivity. Finally vanadate augmented the extent of activation of the insulin receptor kinase by submaximal insulin concentrations. This was associated with a prolongation of the insulin biological response, lipogenesis, after removal of hormone. IN CONCLUSION: in rat adipocytes vanadate promotes insulin action by three mechanisms, 1) a direct insulin-mimetic action, 2) an enhancement of insulin sensitivity and 3) a prolongation of insulin biological response. These data suggest that PTP inhibitors have potential as useful therapeutic agents in insulin-resistant and relatively insulin-deficient forms of diabetes mellitus.

Adipocytes↗
PubMedDate not supplied

Effects of vanadate on the expression of genes involved in fuel homeostasis in animal models of Type I and Type II diabetes.

Vanadium is a trace element that has raised increasing interest in diabetology since the discovery of its insulin-like properties in vitro and in vivo. This brief article reviews the most recent data concerning the beneficial effects of vanadium compounds on fuel homeostasis in animal models of insulinopenic (Type I) or insulin-resistant (Type II) diabetes. These studies open obvious therapeutic possibilities in diabetes, and more particularly, in states of insulin resistance.

Animals↗
PubMedDate not supplied

Regulation and control of glucose overutilization in erythrocytes by vanadate.

The insulin mimetic effect of vanadate in in vitro incubation of erythrocytes with high glucose concentrations showed an increase in sorbitol accumulation and glucose utilization using U-14C-glucose. Aldose reductase inhibitors and vanadate addition reversed the sorbitol accumulation, whereas insulin could not reverse it. Increased glucose utilization was also normalized with vanadium compounds. Increased activity of aldose reductase and sorbitol levels in diabetic animals were also normalized with vanadate treatment.

Animals↗
PubMed1995

Oxidative stress-regulated gene expression and promotion of morphological transformation induced in C3H/10T1/2 cells by ammonium metavanadate.

Promoters of C3H/10T1/2 cell morphological transformation that elevate intracellular oxidant levels can be distinguished by a spectrum of induced gene expression, which includes the oxidant-responsive murine proliferin gene family. Proliferin transcripts were induced 40- to 100-fold by 20 microM ammonium metavanadate, 20-fold by 5 microM vanadium pentoxide but only three-fold by vanadium oxide sulfate. Consistent with its response to other oxidant chemicals, induction of proliferin by ammonium metavanadate was inhibited almost completely by the antioxidant N-acetylcysteine (8 mM). Ammonium metavanadate (5 microM), added as promoter in two-stage morphological transformation assays, amplified yields of Type II and Type III foci in monolayers of 20-methylcholanthrene-initiated C3H/10T1/2 cells. Ammonium metavanadate also induced formation of Type II foci in single-step transformation assays. The results suggest that pentavalent vanadium compounds could promote morphological transformation in C3H/10T1/2 cells by creating a cellular state of oxidative stress, sufficient to induce elevated expression of the proliferin gene family.

Animals↗
PubMed1994

Vanadate treatment reverses gastrointestinal complications in the streptozotocin-diabetic rats.

1. Insulin-like effects of vanadium compounds have been reported in various experimental conditions. Effects of vanadate on the decreased beta-adrenergic responsiveness of the rat duodenum due to streptozotocin diabetes were investigated to determine its influence on diabetic gastro-intestinal complications as well as its effects on the carbohydrate metabolism. 2. Administration of sodium orthovanadate to streptozoticin-diabetic rats in drinking water (0.7 mg/ml) for 4 weeks resulted in an improvement of carbohydrate metabolism noticed by increased serum levels of insulin and decreased blood levels of glucose as reported in previous studies. 3. Vanadate treatment of streptozotocin-diabetic rats also corrected the diabetic changes in the beta-adrenergic responsiveness of the rat duodenum to salbutamol suggesting a beneficial effect on the diabetic complications of rat gastro-intestinal tract. The same treatment with vanadate did not cause any alteration in the beta-adrenergic responsiveness of isolated duodenum from non-diabetic rats. 4. From the findings obtained, it is concluded that vanadate possesses an insulin-like effect on the beta-adrenergic responsiveness of the rat gastro-intestinal tract. Since vanadate treatment did not alter the beta-adrenergic responses of isolated duodenum from non-diabetic rats it seems likely that the insulin-like effect of vanadate is dependent on increased responsiveness of the gastrointestinal tract to circulating insulin.

Animals↗
PubMed2006

Improvement of diabetes, obesity and hypertension in type 2 diabetic KKAy mice by bis(allixinato)oxovanadium(IV) complex.

Previously, we found that bis(allixinato)oxovanadium(IV) (VO(alx)(2)) exhibits a potent hypoglycemic activity in type 1-like diabetic mice. Since the enhancement of insulin sensitivity is involved in one of the mechanisms by which vanadium exerts its anti-diabetic effects, VO(alx)(2) was further tested in type 2 diabetes with low insulin sensitivity. The effect of oral administration of VO(alx)(2) was examined in obesity-linked type 2 diabetic KKA(y) mice. Treatment of VO(alx)(2) for 4 weeks normalized hyperglycemia, glucose intolerance, hyperinsulinemia, hypercholesterolemia and hypertension in KKA(y) mice; however, it had no effect on hypoadiponectinemia. VO(alx)(2) also improved hyperleptinemia, following attenuation of obesity in KKA(y) mice. This is the first example in which a vanadium compound improved leptin resistance in type 2 diabetes by oral administration. On the basis of these results, VO(alx)(2) is proposed to enhance not only insulin sensitivity but also leptin sensitivity, which in turn improves diabetes, obesity and hypertension in an obesity-linked type 2 diabetic animal.

Animals↗