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

The vanadate and vanadyl forms of vanadium have been shown by many investigators to have insulinlike effects on glucose metabolism. Many investigators have shown that vanadium, or its salts, counteracts the hyperglycemia associated with streptozocin-induced diabetes (STZ-D) in the rat, although insulin secretion remains depressed. Studies of the action of vanadate on insulin secretion and glucose metabolism have not addressed the question of possible long-term effects of this compound on glucose metabolism extending beyond the period of oral administration. This study was undertaken to assess the effects of treatment (3 wk) and withdrawal of vanadyl sulfate (13 wk) on glucose metabolism, insulin secretion, and islet insulin content of STZ-D rats. Our results indicate that STZ-D rats that have had blood glucose levels normalized by 3 wk of vanadyl treatment remain normoglycemic after 13 wk of withdrawal from treatment. Normal glucose tolerance was observed in vanadyl-treated diabetic animals despite depressed fasting and glucose-stimulated plasma insulin levels. Insulin secretion from the isolated perfused pancreas was greater after vanadyl treatment than in untreated diabetic rats, although it was only 12% of values from controls. Three weeks of vanadyl treatment of STZ-D rats, followed by 13 wk of withdrawal, yielded islets close in size and insulin content of control islets, even though in vivo and in vitro insulin secretion was impaired. This study has shown that short-term vanadyl treatment of STZ-D rats yields normalization of glucose tolerance and protection of islets from destruction by STZ.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1989 Nov
PMID:Long-term effects of vanadyl treatment on streptozocin-induced diabetes in rats. 269 73

Although many studies in animal models and in cell cultures have shown that vanadate has insulin-like effects, it has not been studied in human diabetes mellitus. In this study the levels of vanadium in human placentae from 23 pregnancies complicated by gestational diabetes mellitus were compared with 18 uncomplicated non-diabetic pregnancies closely matched for maternal age, gravidity, and gestational age. Using the unpaired Student's t-test, the mid-disc placental levels in gestational diabetes (7.62 +/- 1.29 micrograms/g dry weight) were significantly lower (p less than 0.05) than controls (8.73 +/- 1.85 micrograms/g dry weight). These findings appear to be independent of placental size and birthweight. When these data were analyzed according to treatment, the vanadium levels in insulin-treated cases (8.07 +/- 1.32 micrograms/g dry weight) were not significantly different from the matched controls (8.84 +/- 1.69 micrograms/dry weight); the levels in noninsulin treated cases (7.08 +/- 1.25 micrograms/g dry weight), however, were significantly (p less than 0.005) lower than controls (8.99 +/- 1.96 micrograms/g dry weight). It is interesting to speculate that there may be increased binding of vanadium to maternal tissues in human diabetes mellitus when insulin is deficient.
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PMID:Placental vanadium in gestational diabetes mellitus. 278 May 18

Diabetic changes in small intestinal growth and transport were studied in the rat during the administration of the pentavalent vanadium oxyanion, vanadate. This treatment reversed the effect of diabetes on growth of the intestinal mucosa. It eliminated hyperglycemia and restored the normal rate of absorption of AIB and 3-o-methyl glucose by the intestine. The changes are probably caused by an insulin-like action of vanadate on the intestine.
Diabetes Res 1989 Mar
PMID:Reversal by vanadate of the effect of diabetes on intestinal growth and transport. 280 88

Vanadium compounds are known to affect multiple membrane and cytosolic phosphoenzymes from various tissues; the most characterized effect is the inhibition of Na+-K+-ATPase. Since we previously reported that immunoreactive insulin (IRI) secretagogues tend to inhibit rat islet cation-dependent ATPases, we examined the effects of sodium vanadate on rat IRI secretion from incubated and perifused rat islets. In the presence of 2.4 mM Ca2+, vanadate (10(-3) M) induced biphasic IRI secretion with a background glucose of 100 mg/dl. In the absence of extracellular Ca2+, IRI released from incubated islets by vanadate at 100 and 300 mg/dl glucose was doubled and tripled, respectively. Furthermore, this stimulatory effect was completely abolished by known inhibitors of IRI release such as somatostatin, epinephrine, and diphenylhydantoin. Although we found the expected dose-dependent inhibition by vanadate of islet membrane Na+-K+-ATPase activity, the mechanism of action of vanadate on IRI secretion remains unknown. Vanadate probably interacts in a complex fashion with different islet phosphoenzymes and may prove to be a useful probe to further unravel the mechanisms leading to insulin secretion.
Diabetes 1987 Dec
PMID:Insulinotropic effects of vanadate. 282 62

The trace element vanadium has an unclear biological function. Vanadate, an oxidized form of vanadium, appears to have an insulin-like action. The effect of vanadate on blood glucose and cardiac performance was assessed in female Wistar rats 6 weeks after they were made diabetic with streptozotocin. When vanadate was administered for a 4-week period to the diabetic rats, their blood glucose was not significantly different from that of nondiabetic controls despite a low serum insulin. In contrast, blood glucose was increased about threefold in the diabetic rats that were not treated with vanadate; these rats also had low insulin levels. Cardiac performance was depressed in the untreated diabetic animals, but the cardiac performance of the vanadate-treated diabetic animals was not significantly different from that of nondiabetic controls. Thus vanadate controlled the high blood glucose and prevented the decline in cardiac performance due to diabetes.
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PMID:Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats. 315 5

Myocardial contractile function is often depressed in patients with diabetes mellitus. Vanadate is an essential trace element that has purportedly an insulin-like action and has been suggested as a therapeutic agent for the treatment of diabetes mellitus. The purpose of the present study was to compare the prophylactic efficacy of oral vanadate therapy (0.8 mg of sodium orthovanadate per milliliter drinking water) to that of insulin treatment (5 units/day s.c.) in terms of its ability to reduce or prevent the progressive cardiodepression that occurs in untreated diabetes mellitus. Diabetes was induced in male rats by i.v. streptozotocin injection (50 mg/kg). Diabetes rats were assigned randomly to one of three regimens for 8 weeks: untreated, insulin-treated or vanadate-treated. Noninjected rats served as controls. In vivo myocardial contractile function was measured under basal conditions and after i.v. norepinephrine infusions in ketamine-xylazine-anesthetized rats using a miniature catheter-tip pressure transducer inserted in the right carotid artery and advanced into the left ventricle. Vanadate and insulin treatment resulted in comparable increases in body weight and reductions in plasma glucose, which were improved relative to untreated diabetics. These findings suggest that vanadium may possess an insulin-like action. Basal in vivo myocardial contractile performance was depressed significantly in untreated diabetic rats as compared to control and insulin-treated diabetic rats. The contractile performance of vanadate-treated diabetic rats was in between untreated diabetic and control groups. In vivo myocardial reactivity to norepinephrine based on assessments of left intraventricular developed pressure, positive and negative dP/dt and delta dP/dt was depressed significantly in untreated diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of vanadate on in vivo myocardial reactivity to norepinephrine in diabetic rats. 354

There is accumulating evidence that the metabolism of several trace elements is altered in insulin-dependent diabetes mellitus and that these nutrients might have specific roles in the pathogenesis and progress of this disease. Magnesium deficiency is the most evident disturbance of metal metabolism in diabetes mellitus. Hypomagnesemia might increase the risk of ischemic heart disease and severe retinopathy. Increased urinary loss of zinc is a commonly encountered feature of diabetes. High-dose oral zinc might enhance wound healing, although data regarding diabetes are lacking. Chromium increases tissue sensitivity to insulin and tends to raise high-density lipoprotein (HDL) cholesterol and the HDL:low-density lipoprotein ratio. Selenium is involved in processes which protect the cell against oxidative damage by peroxides produced from lipid metabolism. There is one report of elevated serum selenium in diabetic children although the clinical significance of this finding is still unclear. An insulin-like effect has recently been attributed to vanadium in experimental animals, a finding of potential interest to man. Current knowledge does not implicate iron, iodine, manganese, cobalt, nickel, silicone, fluoride, molybdenum or tin in the pathophysiology of diabetes. Appropriate trace element supplementation might prove beneficial in ameliorating some physiological deficiencies associated with diabetes and prevent or retard secondary complications. However, properly designed and well-documented trials, especially on magnesium supplementation, need to be performed before rationales for such supplementation are developed. The potential roles of vanadium, chromium and selenium in diabetes constitute challenging areas for further experimental and clinical research.
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PMID:The role of trace elements in juvenile diabetes mellitus. 640 Apr 52

Diabetes mellitus results from an absolute or relative deficiency in insulin secretion and a resistance of target tissues to the action of insulin, in proportions that vary with the type of the disease. The shortage of insulin can be corrected by administration of exogenous insulin or stimulation of pancreatic beta-cells with sulphonylureas. However, insulin resistance remains a major therapeutic problem. Here, Sonia Brichard and Jean-Claude Henquin review the recent discoveries that indicate a possible role for vanadium in management of the disease. In vitro, vanadium salts mimic most effects of insulin on the main target tissues of the hormone, and in vivo they induce a sustained fall in blood glucose levels in insulin-deficient diabetic rats, and improve glucose homeostasis in obese, insulin-resistant diabetic rodents. Recent short-term clinical trials with vanadium salts also seem promising in type II (non-insulin-dependent) diabetic patients in whom liver and peripheral insulin resistance was attenuated, indicating the therapeutic potential of vanadium salts, pending demonstration of their long-term innocuity.
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PMID:The role of vanadium in the management of diabetes. 748 87

When rats with streptozotocin (STZ)-induced diabetes were given a daily intraperitoneal (i.p.) injection of VOSO4 (+4 oxidation state of vanadium), their serum glucose dropped from hyperglycemic level to normal level within 2d and serum free fatty acid (FFA) level also dropped to normal level. Vanadium was incorporated in most organs as well as in the adipose tissues, as detected by neutron activation analysis (NAA). The mechanism for the insulin-like action vanadium in terms of FFA release from isolated rat adipocytes was investigated: (1) Vanadyl (IV) and vanadic (III) ions normalize the FFA release in the adipocytes treated with epinephrine; (2) vanadate (V) ion treated with ascorbic acid, cysteine or glucose is effective in normalizing the FFA release but vanadate ion alone has no effect on FFA release; (3) vanadyl ion is incorporated into the adipocytes, while vanadate ion is not, as indicated by ESR spectroscopy; and (4) vanadyl ion can act on the glucose transporter, as indicated by experiments using cytochalasin B which is an inhibitor of this transporter. From these results, the normalization of both serum glucose and FFA levels by vanadyl ion was concluded to be due to the incorporation of vanadyl ion into the adipocytes, in which the metal ion acts on the glucose transporter and induces both the promotion of glucose uptake and the decrease of FFA release form peripheral adipocytes. The vanadyl state was suggested to be a possible pharmacologically active form of vanadium allowing the insulin-like action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism on insulin-like action of vanadyl sulfate: studies on interaction between rat adipocytes and vanadium compounds. 749 89

The mitogen-activated protein (MAP) kinases and ribosomal S6 protein kinases in the skeletal muscle of insulin-resistant long-term (2 and 6 months' duration) diabetic rats were investigated to understand further the changes in insulin intracellular signaling pathways that accompany diabetes. The effects of insulin-mimetic vanadium compounds on the activity of these kinases were also examined. In the insulin-resistant 2-month diabetic rats, the basal activities of MAP kinases were relatively unchanged, while the basal activities of S6 kinases were significantly increased. Intravenous injection of insulin moderately activated both the 42-kDa MAP kinase (p42mapk) and a 44-kDa MAP kinase (p44erk1) in the 2-month control rats but not in the 2-month diabetic rats. Insulin treatment markedly stimulated the activity of a novel 31-kDa S6 kinase and the previously described 90-kDa ribosomal S6 kinase encoded by one of the rsk genes (p90rsk) in the 2-month control rats, while the effect was substantially reduced in the diabetic rats. In the 6-month diabetic rats, the basal phosphotransferase activities of both MAP kinases were depressed threefold or greater. This correlated with reductions in the amount of immunoreactive p42mapk and p44erk1 proteins in extracts from the diabetic rats. The basal activity of the 31-kDa S6 kinase activity was also reduced fourfold in the 6-month diabetic rats. Treatment of the 2-month diabetic rats with vanadyl sulfate resulted in euglycemia, prevented the increase in the basal activity of S6 kinase, and improved the activation of S6 kinase by insulin.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1995 Oct
PMID:Skeletal muscle mitogen-activated protein kinases and ribosomal S6 kinases. Suppression in chronic diabetic rats and reversal by vanadium. 755 49


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