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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vanadyl sulfate trihydrate was given by gavage to streptozotocin-induced diabetic rats for 21 days at doses of 0, 25, 50, or 75 mg/kg/day. In marked contrast to the reduction in plasma glucose observed in diabetic animals given vanadyl sulfate via drinking water, diabetic rats given vanadyl by gavage were not characterized by normoglycemia. Similarly, in contrast to the normalizing effect of vanadyl in drinking water, vanadyl by gavage had only a minimal influence on diabetes associated hyperphagia and polydipsia. Despite the lack of marked effect of vanadyl by gavage on the above parameters, tissue vanadium accumulation in the gavaged rats was similar to that reported for rats given vanadium by drinking water. The present results (taken together with previous data) show that the administration of vanadium by gavage is not a viable alternative to the use of insulin in diabetes treatment.
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PMID:Administration of vanadyl sulfate by gavage does not normalize blood glucose levels in streptozotocin-induced diabetic rats. 150 5

Although it has been reported that vanadate is effective in diminishing the expression of diabetes in the rat, the severe toxic side effects noted in the vanadate-treated animals suggest that chronic oral administration of vanadate argues against its use in human diabetes. The present study was conducted to evaluate the effects of the chelator Tiron on the mobilization of vanadium after administration of sodium metavanadate in the drinking water (0.20 mg/ml) of streptozotocin-induced diabetic rats for 35 days. Intraperitoneal treatment with Tiron (300 or 600 mg/kg) was initiated after three weeks of vanadate administration and continued for two weeks. The ameliorative effects of vanadium with respect to diabetes were not diminished by the administration of Tiron, but the accumulation of vanadium in kidney and bone was significantly decreased in the Tiron-treated groups and diabetes associated increases in serum GOT, GPT and cholesterol were diminished with Tiron treatment. It is concluded that the coadministration of metavanadate and Tiron may be of potential value for treatment of diabetes mellitus.
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PMID:Tiron administration minimizes the toxicity of vanadate but not its insulin mimetic properties in diabetic rats. 153 46

Vanadium is a trace metal that has raised increasing interest in diabetology since the discovery of its insulin-like properties in vitro and in vivo. This brief article is a review of the most recent data concerning the cellular mechanisms by which vanadium salts stimulate glucose metabolism. The beneficial effects of vanadium on glucose homeostasis of animal models of insulinopenic or insulin-resistant diabetes are discussed. The perspectives that the use of vanadium opens for the treatment of diabetes are also considered, in the light of the potential toxicity of the element.
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PMID:The insulin-like properties of vanadium: a curiosity or a perspective for the treatment of diabetes? 175 43

Treatment of streptozocin (STZ)-induced diabetic rats with sodium selenate (10-15 mumol.kg-1.day-1) for 7 wk resulted in a decrease in plasma glucose, food intake, and water intake to control or near control levels. Plasma insulin was reduced in control rats given sodium selenate to the level found in the diabetic and treated diabetic group. Treatment did not affect control rats with regard to the other measurements cited. Sodium selenate enhanced weight gain in responding diabetic rats to that seen in controls; sodium selenate's actions thus resembled those of insulin. Thus selenate, like vanadium, appears to have insulinlike effects when administered in vivo.
Diabetes 1991 Dec
PMID:Insulinlike effects of sodium selenate in streptozocin-induced diabetic rats. 175 7

In the present investigation, the effects of oral administration of sodium metavanadate, sodium orthovanadate and vanadyl sulphate to alleviate some signs of diabetes in streptozotocin-treated rats have been evaluated. Streptozotocin-induced diabetic rats drank aqueous solutions (NaCl, 80 mM) containing sodium metavanadate (0.15 mg/ml), sodium orthovanadate (0.23 mg/ml), or vanadyl sulphate pentahydrate (0.31 mg/ml) for 28 days. The vanadium-treated animals were compared to controls, either diabetic or nondiabetic, receiving drinking water containing NaCl (80 mM) only. Daily food and fluid intake were significantly decreased in the vanadium-treated animals relative to diabetic controls. Also, vanadium treatment reduced the level of hyperglycemia in diabetic rats, with sodium metavanadate being the most effective of the vanadium compounds tested. However, daily vanadium intake was significantly lower in the animals receiving sodium metavanadate. Signs of toxicity were observed in all vanadium-treated animals as evidenced by some deaths, decreased weight gain, and increased serum concentrations of urea and creatinine. Moreover, vanadium was detected in all tissues analyzed. Although some signs of diabetes were improved by vanadium treatment, because of the severe toxic side effects noted in all of the vanadium-treated animals, it seems evident that oral vanadium administration is not a suitable therapy of diabetes mellitus in streptozotocin-diabetic rats.
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PMID:Oral vanadium administration to streptozotocin-diabetic rats has marked negative side-effects which are independent of the form of vanadium used. 182 77

Vanadate and vanadyl, two forms of vanadium, have been reported to exert insulin-like effects in vivo and in vitro. In the present study we compared the effectiveness of oral sodium metavanadate (NaVO3), sodium orthovanadate (Na3VO4) and vanadyl sulphate pentahydrate (VOSO4.5H2O) treatment in alleviating some signs of diabetes in streptozotocin-induced diabetic rats. Vanadium compounds were administered in aqueous solutions of NaCl (80 mM) at concentrations of 0.20 mg/ml (NaVO3), 0.50 mg/ml (Na3VO4), and 1.1 mg/ml (VOSO4.5H2O) for two weeks. Control rats, either diabetic or non-diabetic, drank solutions of NaCl (80 mM). Although some signs of diabetes (hyperglycaemia, hyperphagia, polydipsia) were significantly ameliorated by the vanadium treatment, negative side effects were also observed in all of the vanadium-treated diabetic rats. Those effects included some deaths, decreased weight gain, and tissue vanadium accumulation, which are consistent with the reported toxicity of vanadium in non-diabetic rats. Vanadyl sulphate was the most effective compound of those tested in normalizing blood glucose levels. However, the results here reported suggest that chronic administration of vanadyl or vanadate in the drinking water is not a viable alternative treatment to insulin in human diabetes.
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PMID:Improvement of glucose homeostasis by oral vanadyl or vanadate treatment in diabetic rats is accompanied by negative side effects. 186 88

Vanadate, the major oxidized form of the essential trace element vanadium, has rapid effects on glucose transport in vitro and more delayed effects on glucose transport in vivo. We addressed the question that one potential mechanism for the delayed effects of vanadate on glucose homeostasis could be altered expression of one or more of the genes encoding glucose transporters. To do this we studied vanadate regulation of Glut-1 and Glut-4 in NIH3T3 mouse fibroblasts. Vanadate (5-40 microM) induced cells to proliferate to higher cell densities, and in addition, 40 microM vanadate caused the cells to exhibit a transformed morphology. Glut-1 mRNA was maximally induced 4- to 5-fold over the control value after 6-h exposure to 30 microM vanadate. Unlike the response to serum and growth factors, the vanadate-induced increase in Glut-1 mRNA remained elevated over the control value in the presence of vanadate for 5 days. The vanadate effect was serum dependent and was fully reversible when vanadate was removed from the medium. In the absence of vanadate, the half-life of Glut-1 mRNA was 0.5-1 h, whereas after treatment for 5 h with 30 microM vanadate the half-life was increased to 1.5-2 h. Thus, mRNA stabilization accounts for at least a part of the increase in glucose transporter mRNA levels after vanadate treatment. Glut-4 mRNA was not detected in these cells in either the absence or presence of vanadate. While the importance of this increased Glut-1 gene expression for the vanadate effect on normalization of blood glucose in vivo remains to be determined, an association between vanadate-induced cell proliferation and transformed phenotype, and vanadate-induced Glut-1 mRNA in vitro has been made. Possible potential therapeutic use of vanadate for treatment of diabetes must, therefore, be viewed with caution.
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PMID:Vanadate regulates glucose transporter (Glut-1) expression in NIH3T3 mouse fibroblasts. 210 May 13

Recent studies have indicated that the blood glucose level of rats with streptozotocin (STZ)-induced diabetes (type 1) is normalized without an increase in the plasma insulin level by administration of sodium orthovanadate in the drinking water. The mechanism of this insulin-like effect of vanadate is unknown. In this study, we investigated whether vanadyl ion, which is less toxic than vanadate to rats, also has an insulin-like effect in rats with STZ-induced diabetes. When rats with STZ-induced diabetes were given a daily i.p. injection of vanadyl sulphate (9.3 and 4.6 mg vanadium/kg body weight), their blood glucose level decreased from about 22.2 to about 7.2 mmol glucose/l within 2 days and remained low for at least 12 weeks. This treatment did not affect their low plasma insulin level. Quantitative electron spin resonance (ESR) spectrometry showed that most of the vanadium (about 90%) in their tissues was present as a vanadyl form (VO2+). ESR analysis also showed that the vanadyl ion in tissues was bound endogenously with four oxygen ligands from either water or oxyamino acid residues in proteins. Vanadyl sulphate accelerated glucose incorporation into adipocytes of rats, suggesting that the action of vanadyl ion is peripheral. Interestingly, vanadyl sulphate at a high concentration (about 10 mmol/l) was more effective than insulin in enhancing glucose uptake. This study demonstrated that: (1) vanadyl sulphate (+4 oxidation state), like vanadate ion, normalizes the blood glucose levels of rats with STZ-induced diabetes; (2) the action of vanadyl ion is peripheral; and (3) the active form of vanadium for an insulin-like effect may be a vanadyl form, not vanadate.
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PMID:Insulin-like effect of vanadyl ion on streptozotocin-induced diabetic rats. 217 May 56

The trace element vanadium exerts insulinlike effects in vitro and decreases hyperglycemia in insulin-deficient animals. This study examined whether vanadate can improve glucose homeostasis in genetically obese hyperglycemic insulin-resistant ob/ob mice, which present metabolic abnormalities similar to those of human non-insulin-dependent diabetes. Sodium orthovanadate (0.3 mg/ml) was administered for 7 wk in H2O. Vanadate treatment induced a fall in fed and fasted plasma glucose and insulin levels and improved tolerance to oral glucose; the stimulated glucose area was decreased by 65%, and an early peak of insulin secretion was restored. During an intravenous glucose tolerance test, the glucose disappearance rate was twofold higher in vanadate-treated mice, and the reappearance of a significant insulin response was also observed. Moreover, vanadate produced a twofold increase in hepatic glycogen content and prevented the exhaustion of pancreatic insulin stores. The hypoglycemic response to exogenous insulin was similar in control and treated mice. In vitro experiments showed that basal glucose oxidation by hemidiaphragms was 32% higher in vanadate-treated mice than in controls, although stimulation by insulin was similar in both groups. In conclusion, oral vanadate caused a marked and sustained improvement of glucose homeostasis in diabetic insulin-resistant mice by exerting an insulinlike effect on peripheral tissues and apparently preventing the exhaustion of pancreatic insulin stores.
Diabetes 1990 Nov
PMID:Marked improvement of glucose homeostasis in diabetic ob/ob mice given oral vanadate. 222 6

This study explored some toxicological aspects of vanadyl sulphate (VOSO4) treatment of rats made diabetic with a single intravenous injection of streptozotocin (60 mg/kg). Administered in drinking water (0.25, 0.5, 0.75 or 1 mg of VOSO4, 5H2O ml) VOSO4 treatment partially or totally corrected some of the alterations associated with the diabetic state (hyperglycaemia, polydipsia, polyphagia, high cholesterol and triglycerides levels) and did not produce any changes in various plasma or blood cell parameters which were not previously altered by diabetes. Measurement of vanadium levels indicated that tissues accumulated vanadium in the following order of concentrations: bone greater than kidney greater than spleen greater than liver greater than lung greater than or equal to muscle greater than blood. Histopathological studies did not reveal any difference in liver, stomach, ileum, spleen, heart and lung from control, non-treated diabetic or VOSO4-treated diabetic animals. Kidney of all non-treated diabetic animals showed an epithelial cellular swelling of distal tubules while only 2 of 6 VOSO4-treated diabetic animals showed this alteration. Cellular degeneration of pancreas B-cells was less marked in VOSO4-treated that in non-treated diabetic animals. The study indicates that VOSO4 may be a potential antidiabetic agent.
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PMID:Toxicological aspects of vanadyl sulphate on diabetic rats: effects on vanadium levels and pancreatic B-cell morphology. 225 74


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