Toxicity Studies on One‐Year Treatment of Non‐Diabetic and Streptozotocin‐Diabetic Rats with Vanadyl Sulphate

Dai, Soter; Thompson, Katherine H.; Vera, Erika; McNeill, John H.

doi:10.1111/j.1600-0773.1994.tb00359.x

Cited by 59 publications

(27 citation statements)

References 21 publications

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“…At time of death, vanadium levels (nmol/ml or nmol/g) in DT animals were: plasma, 7.8Ϯ1.0; liver, 30.6Ϯ3.7; muscle, 4.5Ϯ0.2; pancreas, 8.0Ϯ1.0; bone, 415.0Ϯ40.4; kidney, 129.4Ϯ6.9. These levels are similar to previously reported values in diabetic rats after one year of vanadium treatment (18). Vanadium levels were not statistically different between the DT-HC and DT-LC subgroups at 5 weeks.…”

Section: Variable Response To Vanadium Treatmentsupporting

confidence: 81%

Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes

Cam

Rodrigues²,

1999

European Journal of Endocrinology

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Vanadium is an oral insulin-mimetic agent that diminishes hyperglycemia, improves beta-cell insulin store and secretory function, and can reverse the diabetic state chronically after withdrawal from treatment. As food restriction has been reported to enhance insulin sensitivity and reduce insulin demand, we assessed the contribution of a reduced food intake to the glucose lowering and beta-cell protective effects of vanadium. Streptozotocin (STZ)-diabetic rats were untreated (D) or administered vanadyl sulfate in the drinking water (DT) at one week prior to and for 5 weeks following the administration of STZ. An additional group was pair-fed (DP) with an equal amount of food as that consumed by the DT group. Shortly after the induction of diabetes, hyperglycemic D rats demonstrated a significant rise in plasma insulin to levels that initially exceeded that of the controls. This was followed by a steady reduction over several weeks, suggesting a gradual depletion of functional beta-cells. Both vanadium treatment and pair-feeding abolished the insulin hypersecretory response following STZ administration. Glucose lowering was enhanced in DT animals when administered higher concentrations of vanadium, despite no further reduction in food intake, and all DT animals (10/10) were normoglycemic by 5 weeks. Mean pancreatic insulin content in DT rats was improved fourfold and was associated with a greater number of granulated beta-cells. Conversely, food restriction only modestly improved glycemia and the pancreatic insulin store and, unlike DT, DP rats remained highly glucoseintolerant. At 5 weeks of diabetes, fed circulating glucose and insulin levels were strongly correlated (P=0.0002) in the D and DP groups, supporting the notion that glucose lowering with food restriction is dependent on improved plasma insulin levels. A separate correlation was observed in DT animals within a lower range of plasma insulin, suggesting that vanadium, unlike food restriction, reduced plasma glucose by enhancing insulin sensitivity. Thus, vanadium preserves beta-cells in STZ-diabetes at least partially by abolishing the insulin hypersecretory response and the eventual exhaustion of residual insulin stores following a moderate dose of STZ. This property of vanadium would appear to be useful in the treatment of prediabetic and newly diagnosed insulin-dependent diabetes mellitus.

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Section: Variable Response To Vanadium Treatmentsupporting

confidence: 81%

Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes

Cam

Rodrigues²,

1999

European Journal of Endocrinology

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“…Corroborating our results, Dai et al [44] assessed the toxic effects of 0.5-1.5 mg/mL VOSO 4 in the drinking water of diabetic and healthy rats for a period of one year and observed no persistent changes in plasma AST or ALT.…”

Section: Resultssupporting

confidence: 61%

“…Assays of serum enzyme activities that are used as hepato-biliary function markers (ALT, ALP) were carried out, in view of the finding by Dai et al that vanadyl sulfate accumulates in the liver [44]. The results of these toxicity tests indicated (Fig.…”

Section: Resultsmentioning

confidence: 99%

Synthesis, characterization and biological analysis of the complex [VO(Hdhp)2] (H2dhp = 2,3-dihydroxypyridine)

Pepato

Alberconi

Rocha

et al. 2007

Transition Met Chem

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A new vanadium (IV) complex with the monoanion of 2,3-dihydroxypyridine (H 2 dhp), or 3-hydroxy-2-(1H)-pyridone, was synthesized, characterized by physicochemical techniques and tested biologically. The EPR data for the [VO(Hdhp) 2 ] complex in DMF are: g x = 1.9768, g y = 1.9768 and g z = 1.9390; A values (10 -4 cm -1 ): A x , 59.4; A y// , 59.4; A z , 171.0. The mV=O band in the IR spectrum of the complex is at 986 cm -1 . The complex is paramagnetic, with l eff = 1.65 BM (d 1 , spin-only) at 25°C. The irreversible oxidation process [V(V)/V(IV)] of the [VO(Hdhp) 2 ] complex, as revealed in a cyclic voltammogram, occurs at 876 mV. The calculated molecular structure of [VO(Hdhp) 2 ] shows the vanadium(IV) center in a distorted square pyramidal environment, with the oxo ligand in the apical position and the oxygen donor atoms of the Hdhp ligands in the basal positions. The ability of [VO(Hdhp) 2 ] to mimic insulin, and its toxicity to hepato-biliary functions, were investigated in streptozotocin-induced diabetic rats and it was concluded that the length of treatment and the amount of [VO(Hdhp) 2 ] administered were effective in reducing experimental diabetes.

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“…They effectively control the diabetic state and prevent the development of complications in both insulin-dependent and noninsulin-dependent diabetes mellitus in experimental animals [6]. Clinical studies in type 1 diabetes patients showed that the daily insulin requirement decreased significantly [7].…”

Section: Introductionmentioning

confidence: 99%

The influence of sodium metavanadate on the process of diabetogenesis in BB rats

Cheţa¹,

Orasanu²,

Nicolaie

et al. 2003

J Cellular Molecular Medi

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Vanadium has been shown to be beneficial in the oral treatment of animal models of type 1 and type 2 diabetes. The aim of the study was to evaluate the short‐term effects of sodium metavanadate in prediabetic BB‐DP rats. To do this, 96 rats were divided into 4 equal groups. Groups VI, V2, V3 were treated with sodium metavanadate (0.1, 0.2 and 0.3 mg/ml respectively) and sodium chloride (0.5 mg/ml) in drinking water for 7 days. Group C received only sodium chloride (0.5 mg/ml). Blood glucose (BG), glycosuria, ketonuria, body weight and insulinemia were determined. The age of onset of diabetes was significantly higher for groups V2, V3 compared to group C, (p < 0.05) and depends on the metavanadate concentration (V3 vs. V1, p=0.006). The incidence of diabetes was lower in the rats treated with metavanadate than in the control group, but this difference was not statistically significant. In diabetic rats, the BG at the onset was higher in group C than in groups V, p < 0.05. Insulinemia, at the onset of the treatment as well as immediately after its cessation showed a drop in the treatment groups, proportionally to the dosage of vanadium, but later increased slowly and continuously until the end of the experiment. In conclusion, metavanadate delays the development of diabetes in BB‐DP rats, but does not prevent its onset. A milder form of diabetes occurs in diabetic rats treated with metavanadate. The effects depend on the metavanadate concentration and 0.2 mg/ml is preferable.

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Toxicity Studies on One‐Year Treatment of Non‐Diabetic and Streptozotocin‐Diabetic Rats with Vanadyl Sulphate

Cited by 59 publications

References 21 publications

Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes

Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes

Synthesis, characterization and biological analysis of the complex [VO(Hdhp)2] (H2dhp = 2,3-dihydroxypyridine)

The influence of sodium metavanadate on the process of diabetogenesis in BB rats

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