Vanadium Abstracts 2

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Oral vanadyl sulfate improves insulin sensitivity in NIDDM but not in obese nondiabetic subjects.
            (Halberstam et al., 1996) Download
We compared the effects of oral vanadyl sulfate (100 mg/day) in moderately obese NIDDM and nondiabetic subjects. Three-hour euglycemic-hyperinsulinemic (insulin infusion 30 mU / m / min) clamps were performed after 2 weeks of placebo and 3 weeks of vanadyl sulfate treatment in six nondiabetic control subjects (age 37 +/- 3 years; BMI 29.5 +/- 2.4 kg/m2 ) and seven NIDDM subjects (age 53 +/- 2 years; BMI 28.7 +/-1.8 kg/m2). Glucose turnover ([3-3 H]glucose), glycolysis from plasma glucose, glycogen synthesis, and whole-body carbohydrate and lipid oxidation were evaluated. Decreases in fasting plasma glucose (by approximately 1.7 mmol/l) and HbAlc (both P < 0.05) were observed in NIDDM subjects during treatment; plasma glucose was unchanged in control subjects. In the latter, the glucose infusion rate (GIR) required to maintain euglycemia (40.1 +/- 5.7 and 38.1 +/- 4.8 micromol / kg fat-free mass FFM / min) and glucose disposal (Rd) (41.7 +/- 5.7 and 38.9 +/-4.7 micromol / kg FFM / min were similar during placebo and vanadyl sulfate administration, respectively. Hepatic glucose output (HGO) was completely suppressed in both studies. In contrast, in NIDDM subjects, vanadyl sulfate increased GIR approximately 82% (17.3 +/- 4.7 to 30.9 +/- 2.7 micromol / kg FFM / min, P < 0.05); this improvement in insulin sensitivity was due to both augmented stimulation of Rd (26.0 +/-4.0 vs. 33.6 +/- 2.22 micromol / kg FFM / min, P < 0.05) and enhanced suppression of HGO (7.7 +/- 3.1 vs. 1.3 +/- 0.9 micromol / kg FFM / min, P < 0.05). Increased insulin-stimulated glycogen synthesis accounted for >80% of the increased Rd with vanadyl sulfate (P < 0.005), but plasma glucose flux via glycolysis was unchanged. In NIDDM subjects, vanadyl sulfate was also associated with greater suppression of plasma free fatty acids (FFAs) (P < 0.01) and lipid oxidation (P < 0.05) during clamps. The reduction in HGO and increase in Rd were both highly correlated with the decline in plasma FFA concentrations during the clamp period (P < 0.001). In conclusion, small oral doses of vanadyl sulfate do not alter insulin sensitivity in nondiabetic subjects, but it does improve both hepatic and skeletal muscle insulin sensitivity in NIDDM subjects in part by enhancing insulin's inhibitory effect on lipolysis. These data suggest that vanadyl sulfate may improve a defect in insulin signaling specific to NIDDM.


 

The biological actions of vanadium. I. Effects upon serum cholesterol levels in man.
            (Lewis, 1959) Download
Lewis selected 32 men who were exposed to vanadium fumes or dust, and a similar group of control subjects from the same localities (Colorado and Ohio). To lessen the effects of age upon cholesterol values, the men chosen were over the age of 40. All were free of apparent disease, and their jobs provided similar physical activity. Because vanadium is excreted rapidly from the kidneys, the author employed determinations of 24-hour urinary excretion of this element to estimate degree of exposure. He eliminated eight men whose jobs did not expose them to excessive amounts of vanadium. In the final analysis, the exposed men excreted four times the quantity of vanadium as did their fellow controls. Next he compared the concentration of cholesterol in their serum, and found a mean difference of 23 mg. per cent (228 compared with 205) which proved to be significant statistically. Other tests such as the electrocardiogram and the hematocrit disclosed no difference between the two groups.

Effects of vanadium treatment on the alterations of cardiac glycogen phosphorylase and phosphorylase kinase in streptozotocin-induced chronic diabetic rats.
            (Liu and McNeill, 1994) Download
Supersensitivity to isoproterenol (ISO) induced activation of cardiac phosphorylase in diabetic rat heart has been previously demonstrated and was also reproduced in this study. To explore further the nature of this supersensitivity, we examined the activity of phosphorylase kinase and the level of cyclic AMP (cAMP) in this tissue. We observed a significantly enhanced activation of phosphorylase kinase but no increase in cAMP levels in response to ISO stimulation in diabetic rat heart, suggesting that the supersensitivity of phosphorylase activation in diabetic heart may result from an enhanced activation of phosphorylase kinase that does not involve the cAMP pathway. On the other hand, perfusion of diabetic rat heart with verapamil (5 x 10(-8) M) prior to ISO stimulation abolished the enhanced cardiac phosphorylase activation, suggesting a role for calcium in the supersensitivity of phosphorylase activation. Furthermore, treatment of the diabetic rats with an insulin-like compound, vanadyl sulphate, completely abolished the enhanced cardiac phosphorylase activation and restored the increase in ISO-induced cAMP elevation in diabetic heart. The present study has provided further information on the changes of phosphorylase activation in the diabetic rat heart and demonstrated beneficial effects of vanadyl sulphate on the pathway leading to phosphorylase activation in diabetic rat heart.


 

Vanadyl sulfate treatment stimulates proliferation and regeneration of beta cells in pancreatic islets.
            (Missaoui et al., 2014) Download
We examined the effects of vanadium sulfate (VOSO4) treatment at 5 and 10 mg/kg for 30 days on endocrine pancreas activity and histology in nondiabetic and STZ-induced diabetic rats. In diabetic group, blood glucose levels significantly increased while insulinemia level markedly decreased. At the end of treatment, VOSO4 at a dose of 10 mg/Kg normalized blood glucose level in diabetic group, restored insulinemia, and significantly improved insulin sensitivity. VOSO4 also increased in a dose-dependent manner the number of insulin immunopositive beta cells in pancreatic islets of nondiabetic rats. Furthermore, in the STZ-diabetic group, the decrease in the number of insulin immunopositive beta cells was corrected to reach the control level mainly with the higher dose of vanadium. Therefore, VOSO4 treatment normalized plasma glucose and insulin levels and improved insulin sensitivity in STZ-experimental diabetes and induced beta cells proliferation and/or regeneration in normal or diabetic rats.

Vanadium: a possible aetiological factor in manic depressive illness.
            (Naylor and Smith, 1981)  Download
The effect of Vitamin C in manic-depressive psychosis was assessed by a double-blind, placebo controlled, crossover trial. Both manic and depressed patients were significantly better following a single 3 g dose of Vitamin C than following a placebo. Preliminary results of a double-blind, crossover comparison of normal vanadium intake with reduced intake in manic and depressed subjects are reported. Both manic and depressed patients were significantly better on reduced intake. These results are in keeping with the suggestion that vanadium may be an aetiological factor in manic depressive illness.

Reduction of vanadate, a possible explanation of the effect of phenothiazines in manic-depressive psychosis.
            (Naylor and Smith, 1982)  Download
It has been suggested that vanadate may be involved in the aetiology of manic-depressive illness. Lithium diminishes the inhibition of Na+-K+ ATPase by vanadate, and drugs which reduce vanadate to vanadyl (e.g., ascorbic acid and methylene-blue) may be of therapeutic value. The following results show that phenothiazines but not thioxanthines nor tricyclic antidepressants catalyse the reduction of vanadate by NADH, hence offering a possible explanation for their therapeutic action in manic-depressive psychosis.


 

Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review.
            (Nielsen and Sandstead, 1974)  Download
Data supporting the view that vanadium essential element for animals was first reported by Hopkins and Mohr.

Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation.
            (Nielsen, 1991)  Download
Definition of specific biochemical functions in higher animals (including humans) for the ultratrace elements boron, silicon, vanadium, nickel, and arsenic still has not been achieved although all of these elements have been described as being essential nutrients. Recently, many new findings from studies using molecular biology techniques, sophisticated equipment, unusual organisms, and newly defined enzymes have revealed possible sites of essential action for these five elements. Based on these findings and the response of animals and/or humans to low intakes of these elements, the following speculations have been presented: 1) Boron has a role that affects cell membrane characteristics and transmembrane signaling. 2) Silicon is necessary for the association between cells and one or more macromolecules such as osteonectin, which affects cartilage composition and ultimately cartilage calcification. 3) Vanadium reacts with hydrogen peroxide to form a pervanadate that is required to catalyze the oxidation of halide ions and/or stimulate the phosphorylation of receptor proteins. 4) Nickel is needed for the CO2-fixation to propionyl-CoA to form D-methylmalonyl-CoA. 5) Arsenic has an important role in the conversion of methionine to its metabolites taurine, labile methyl, and the polyamines. If any of these speculations are found to be true, the element involved will be firmly established as having a nutritional requirement because the body obviously cannot synthesize it. Based on animal findings, the dietary requirement is likely to be small; that is, expressed in micrograms per day.

Does the relief of glucose toxicity act as a mediator in proliferative actions of vanadium on pancreatic islet beta cells in streptozocin diabetic rats
            (Pirmoradi et al., 2014)  Download
BACKGROUND:  Data shows vanadium protects pancreatic beta cells (BC) from diabetic animals. Whether this effect is direct or through the relief of glucose toxicity is not clear. This study evaluated the potential effect of oral vanadyl sulfate (vanadium) on glycemic status and pancreatic BC of normal and diabetic rats. METHODS:  Rats were divided into five groups of normal and diabetic. Diabetes was induced with streptozocin (40 mg/kg, i.v.). Normal rats used water (CN) or vanadium (1 mg/ml VOSO4, VTN). Diabetic rats used water (CD), water plus daily neutral protamine Hagedorn insulin injection (80 U/kg, ITD) or vanadium (VTD). Blood samples were taken for blood glucose (BG, mg/dL) and insulin (ng/dL) measurements. After two months, the pancreata of sacrificed rats were prepared for islet staining. RESULTS:  Pre-treated normal BG was 88 ± 2, and diabetic BG was 395 ± 9. The final BG in CD, VTD, and ITD was 509 ± 22, 138 ± 14, and 141 ± 14, respectively. Insulin in VTN (0.75 ± 0.01) and VTD (0.78 ± 0.01) was similar, higher than CD (0.51 ± 0.07) but lower than CN (2.51 ± 0.02). VTN islets compared to CN had larger size and denser central core insulin immunoreactivity with plentiful BC. CD and ITD islets were atrophied and had scattered insulin immunoreactivity spots and low BC mass. VTD islets were almost similar to CN. CONCLUSION:  Besides insulin-like activity, vanadium protected pancreatic islet BC, and the relief of glucose toxicity happening with vanadium had a little role in this action.

Quantitative Assessment of Proliferative Effects of Oral Vanadium on Pancreatic Islet Volumes and Beta Cell Numbers of Diabetic Rats.
            (Pirmoradi et al., 2016)  Download
BACKGROUND:  Oral vanadyl sulfate (vanadium) induces normoglycemia, proliferates beta cells and prevents pancreatic islet atrophy in streptozotocin-induced diabetic rats. Soteriological method is used to quantitate the proliferative effects of vanadium on beta-cell numbers and islet volumes of normal and diabetic rats. METHODS:  Adult male Sprague-Dawley rats were made diabetic with intravenous streptozotocin injection (40 mg/kg). Normal and diabetic rats were divided into four groups. While control normal and diabetic (CD) groups used water, vanadium-treated normal (VTN) and diabetic (VTD) groups used solutions containing vanadyl sulfate (0.5-1 mg/mL, VOSO4+5H2O). Tail blood samples were used to measure blood glucose (BG) and plasma insulin. Two months after treatment, rats were sacrificed, pancreata prepared, and stereology method was used to quantitatively evaluate total beta cell numbers (TBCN) and total islet volumes (TISVOL). RESULTS:  Normoglycemia persisted in VTN with significantly decreased plasma insulin (0.19±0.08 vs. 0.97±0.27 ng/dL, P<0.002). The respective high BG (532±49 vs. 144±46 mg/dL, P<0.0001) and reduced plasma insulin (0.26±0.15 vs. 0.54±0.19 ng/dL, P<0.002) seen in CD were reversed in VTD during vanadium treatment or withdrawal. While the induction of diabetes, compared to their control, significantly decreased TISVOL (1.9±0.2 vs. 3.03±0.6 mm3, P<0.003) and TBCN (0.99±0.1 vs. 3.2±0.2 x 106, P<0.003), vanadium treatment significantly increased TISVOL (2.9±0.8 and 4.07±1.0 mm3, P<0.003) and TBCN (1.5±0.3 and 3.8±0.6 x 106, P<0.03). CONCLUSION:  Two-month oral vanadium therapy in STZ-diabetic rats ameliorated hyperglycemia by partially restoring plasma insulin. This action was through proliferative actions of vanadium in preventing islet atrophy by increasing beta-cell numbers.


 

Vanadium and diabetes.
            (Poucheret et al., 1998)  Download
We demonstrated in 1985 that vanadium administered in the drinking water to streptozotocin (STZ) diabetic rats restored elevated blood glucose to normal. Subsequent studies have shown that vanadyl sulfate can lower elevated blood glucose, cholesterol and triglycerides in a variety of diabetic models including the STZ diabetic rat, the Zucker fatty rat and the Zucker diabetic fatty rat. Long-term studies of up to one year did not show toxicity in control or STZ rats administered vanadyl sulfate in doses that lowered elevated blood glucose. In the BB diabetic rat, a model of insulin-dependent diabetes, vanadyl sulfate lowered the insulin requirement by up to 75%. Vanadyl sulfate is effective orally when administered by either single dose or chronic doses. It is also effective by the intraperitoneal route. We have also been able to demonstrate marked long-term effects of vanadyl sulfate in diabetic animals following treatment and withdrawal of vanadyl sulfate. Because vanadyl sulfate is not well absorbed we have synthesized and tested a number of organic vanadium compounds. One of these, bismaltolato-oxovanadium IV (BMOV), has shown promise as a therapeutic agent. BMOV is 2-3x more potent than vanadyl sulfate and has shown less toxicity. Recent studies from our laboratory have shown that the effects of vanadium are not due to a decrease in food intake and that while vanadium is deposited in bone it does not appear to affect bone strength or architecture. The mechanism of action of vanadium is currently under investigation. Several studies indicate that vanadium is a phosphatase inhibitor and that vanadium can activate serine/threonine kinases distal to the insulin receptor presumably by preventing dephosphorylation due to inhibition of phosphatases Short-term clinical trials using inorganic vanadium compounds in diabetic patients have been promising.

Influence of vanadium on acclimatization of humans to high altitude.
            (Rawal et al., 1997)  Download
The study was conducted on human volunteers as controls as well as after administration of vanadyl sulphate on induction to high altitude (HA) at 3500 m. The plasma vanadium contents were significantly reduced in the control group on abrupt induction to HA on days 3 and 10, indicating redistribution to other organs/tissues under the stressful situation. In the vanadium salt-treated group, plasma vanadium contents were similar to those obtained at sea-level. Administration of vanadyl sulphate did not act as a diuretic. Moreover the vanadium supplemented group drank more water and also excrete less urine than the control group.


 

Why Antidiabetic Vanadium Complexes are Not in the Pipeline of "Big Pharma" Drug Research? A Critical Review.
            (Scior et al., 2016)  Download
Public academic research sites, private institutions as well as small companies have made substantial contributions to the ongoing development of antidiabetic vanadium compounds. But why is this endeavor not echoed by the globally operating pharmaceutical companies, also known as "Big Pharma"? Intriguingly, today's clinical practice is in great need to improve or replace insulin treatment against Diabetes Mellitus (DM). Insulin is the mainstay therapeutically and economically. So, why do those companies develop potential antidiabetic drug candidates without vanadium (vanadium- free)? We gathered information about physicochemical and pharmacological properties of known vanadium-containing antidiabetic compounds from the specialized literature, and converted the data into explanations (arguments, the "pros and cons") about the underpinnings of antidiabetic vanadium. Some discoveries were embedded in chronological order while seminal reviews of the last decade about the Medicinal chemistry of vanadium and its history were also listed for further understanding. In particular, the concepts of so-called "noncomplexed or free" vanadium species (i.e. inorganic oxido-coordinated species) and "biogenic speciation" of antidiabetic vanadium complexes were found critical and subsequently documented in more details to answer the question.

Effect of vanadium on serum cholesterol.
            (Somerville and Davies, 1962)  Download
Twelve patients were treated with diammonium vanado-tartrate* for 6 months. Statistical analysis of the results showed that there was no significant effect on serum cholesterol during administration of vanadium (Table I). There were no changes in the lipoprotein pattern, blood urea, or hemoglobin, and no patient developed albuminuria.

Long- term efficacy and safety of vanadium in the treatment of type 1 diabetes.
            (Soveid et al., 2013)  Download
BACKGROUND:  Vanadium compounds are able to reduce blood glucose in experimentally- induced diabetic rats and type 2 diabetic patients, but data about their long- term safety and efficacy in diabetic patients are scarce. METHODS:  Fourteen type 1 diabetic patients received oral vanadyl sulfate (50 - 100 mg TID) for a period of 30 months. Fasting blood sugar (FBS), lipid levels, hematologic, and biochemical parameters were measured before and periodically during the treatment. RESULTS:  The daily doses of insulin decreased from 37.2 ± 5.5 to 25.8 ± 17.3 units/day and at the same time the mean FBS decreased from 238 ± 71 to 152 ± 42 mg/dL. Meanwhile, there was a decrease in plasma total cholesterol without any change in triglyceride level. No significant clinical or paraclinical side effects, with the exception for mild diarrhea at the beginning of treatment, were observed during 30 months therapy. CONCLUSION:  Vanadium is effective and safe for long- term use in type 1 diabetic patients.

Vanadium in Biosphere and Its Role in Biological Processes.
            (Tripathi et al., 2018)  Download
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.

Effect of vanadium(IV) compounds in the treatment of diabetes: in vivo and in vitro studies with vanadyl sulfate and bis(maltolato)oxovandium(IV).
            (Willsky et al., 2001)  Download
Vanadyl sulfate (VOSO(4)) was given orally to 16 subjects with type 2 diabetes mellitus for 6 weeks at a dose of 25, 50, or 100 mg vanadium (V) daily [Goldfine et al., Metabolism 49 (2000) 1-12]. Elemental V was determined by graphite furnace atomic absorption spectrometry (GFAAS). There was no correlation of V in serum with clinical response, determined by reduction of mean fasting blood glucose or increased insulin sensitivity during euglycemic clamp. To investigate the effect of administering a coordinated V, plasma glucose levels were determined in streptozotocin (STZ)-induced diabetic rats treated with the salt (VOSO(4)) or the coordinated V compound bis(maltolato)oxovandium(IV) (abbreviated as VO(malto)(2)) administered by intraperitoneal (i.p.) injection. There was no relationship of blood V concentration with plasma glucose levels in the animals treated with VOSO(4), similar to our human diabetic patients. However, with VO(malto)(2) treatment, animals with low plasma glucose tended to have high blood V. To determine if V binding to serum proteins could diminish biologically active serum V, binding of both VOSO(4) and VO(malto)(2) to human serum albumin (HSA), human apoTransferrin (apoHTf) and pig immunoglobulin (IgG) was studied with EPR spectroscopy. Both VOSO(4) and VO(malto)(2) bound to HSA and apoHTf forming different V-protein complexes, while neither V compound bound to the IgG. VOSO(4) and VO(malto)(2) showed differences when levels of plasma glucose and blood V in diabetic rodents were compared, and in the formation of V-protein complexes with abundant serum proteins. These data suggest that binding of V compounds to ligands in blood, such as proteins, may affect the available pool of V for biological effects.

Influence of vanadium on serum lipid and lipoprotein profiles: a population-based study among vanadium exposed workers.
            (Zhang et al., 2014)  Download
BACKGROUND:  Some experimental animal studies reported that vanadium had beneficial effects on blood total cholesterol (TC) and triglyceride (TG). However, the relationship between vanadium exposure and lipid, lipoprotein profiles in human subjects remains uncertain. This study aimed to compare the serum lipid and lipoprotein profiles of occupational vanadium exposed and non-exposed workers, and to provide human evidence on serum lipid, lipoprotein profiles and atherogenic indexes changes in relation to vanadium exposure. METHODS:  This cross-sectional study recruited 533 vanadium exposed workers and 241 non-exposed workers from a Steel and Iron Group in Sichuan, China. Demographic characteristics and occupational information were collected through questionnaires. Serum lipid and lipoprotein levels were measured for all participants. The ratios of total cholesterol to high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) to HDL-C and apoB to apoA-I were used as atherogenic indexes. A general linear model was applied to compare outcomes of the two groups while controlling possible confounders and multivariate logistic regression was performed to evaluate the relationship between low HDL-C level, abnormal atherogenic index and vanadium exposure. RESULTS:  Higher levels of HDL-C and apoA-I could be observed in the vanadium exposed group compared with the control group (P < 0.05). Furthermore, atherogenic indexes (TC/HDL-C, LDL-C/HDL-C, and apoB/apoA-I ratios) were found statistically lower in the vanadium exposed workers (P < 0.05). Changes in HDL-C, TC/HDL-C, and LDL-C/HDL-C were more pronounced in male workers than that in female workers. In male workers, after adjusting for potential confounding variables as age, habits of smoking and drinking, occupational vanadium exposure was still associated with lower HDL-C (OR 0.41; 95% CI, 0.27-0.62) and abnormal atherogenic index (OR 0.38; 95% CI, 0.20-0.70). CONCLUSION:  Occupational vanadium exposure appears to be associated with increased HDL-C and apoA-I levels and decreased atherogenic indexes. Among male workers, a significantly negative association existed between low HDL-C level, abnormal atherogenic index and occupational vanadium exposure. This suggests vanadium has beneficial effects on blood levels of HDL-C and apoA-I.

 


References

Halberstam, M, et al. (1996), ‘Oral vanadyl sulfate improves insulin sensitivity in NIDDM but not in obese nondiabetic subjects.’, Diabetes, 45 (5), 659-66. PubMed: 8621019
Lewis, CE (1959), ‘The biological actions of vanadium. I. Effects upon serum cholesterol levels in man.’, AMA Arch Ind Health, 19 (4), 419-25. PubMed: 13626260
Liu, H and JH McNeill (1994), ‘Effects of vanadium treatment on the alterations of cardiac glycogen phosphorylase and phosphorylase kinase in streptozotocin-induced chronic diabetic rats.’, Can J Physiol Pharmacol, 72 (12), 1537-43. PubMed: 7736346
Missaoui, S, et al. (2014), ‘Vanadyl sulfate treatment stimulates proliferation and regeneration of beta cells in pancreatic islets.’, J Diabetes Res, 2014 540242. PubMed: 25215302
Naylor, GG and AH Smith (1982), ‘Reduction of vanadate, a possible explanation of the effect of phenothiazines in manic-depressive psychosis.’, Lancet, 1 (8268), 395-96. PubMed: 6120371
Naylor, GJ and AH Smith (1981), ‘Vanadium: a possible aetiological factor in manic depressive illness.’, Psychol Med, 11 (2), 249-56. PubMed: 6791192
Nielsen, FH and HH Sandstead (1974), ‘Are nickel, vanadium, silicon, fluorine, and tin essential for man? A review.’, Am J Clin Nutr, 27 (5), 515-20. PubMed: 4596029
Nielsen, FH (1991), ‘Nutritional requirements for boron, silicon, vanadium, nickel, and arsenic: current knowledge and speculation.’, FASEB J, 5 (12), 2661-67. PubMed: 1916090
Pirmoradi, L, et al. (2014), ‘Does the relief of glucose toxicity act as a mediator in proliferative actions of vanadium on pancreatic islet beta cells in streptozocin diabetic rats’, Iran Biomed J, 18 (3), 173-80. PubMed: 24842144
Pirmoradi, L, et al. (2016), ‘Quantitative Assessment of Proliferative Effects of Oral Vanadium on Pancreatic Islet Volumes and Beta Cell Numbers of Diabetic Rats.’, Iran Biomed J, 20 (1), 18-25. PubMed: 26459400
Poucheret, P, et al. (1998), ‘Vanadium and diabetes.’, Mol Cell Biochem, 188 (1-2), 73-80. PubMed: 9823013
Rawal, SB, et al. (1997), ‘Influence of vanadium on acclimatization of humans to high altitude.’, Int J Biometeorol, 40 (2), 95-98. PubMed: 9140210
Scior, T, et al. (2016), ‘Why Antidiabetic Vanadium Complexes are Not in the Pipeline of “Big Pharma” Drug Research? A Critical Review.’, Curr Med Chem, 23 (25), 2874-91. PubMed: 26997154
Somerville, J and B Davies (1962), ‘Effect of vanadium on serum cholesterol.’, Am Heart J, 64 54-56. PubMed: 13915099
Soveid, M, GA Dehghani, and GR Omrani (2013), ‘Long- term efficacy and safety of vanadium in the treatment of type 1 diabetes.’, Arch Iran Med, 16 (7), 408-11. PubMed: 23808778
Tripathi, D, V Mani, and RP Pal (2018), ‘Vanadium in Biosphere and Its Role in Biological Processes.’, Biol Trace Elem Res, 186 (1), 52-67. PubMed: 29524196
Willsky, GR, et al. (2001), ‘Effect of vanadium(IV) compounds in the treatment of diabetes: in vivo and in vitro studies with vanadyl sulfate and bis(maltolato)oxovandium(IV).’, J Inorg Biochem, 85 (1), 33-42. PubMed: 11377693
Zhang, Y, et al. (2014), ‘Influence of vanadium on serum lipid and lipoprotein profiles: a population-based study among vanadium exposed workers.’, Lipids Health Dis, 13 39. PubMed: 24558984