Effects of vanadyl derivatives on animal models of diabetes

Cros, Gérard; Mongold, J. J.; Serrano, Jean-Jacques; Ramanadham, Sasanka; McNeill, John H.

doi:10.1007/bf00229771

Cited by 26 publications

(20 citation statements)

References 28 publications

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“…Nephropathy, a major complication of diabetes mellitus, is characterized by mesangial cell activation with development of mesangial matrix expansion, mesangial cell hypertrophy, and proliferation (4,5). Since vanadate administered in vivo is concentrated in the kidney (32,36) (41,42). Although extrapolation from in vitro to in vivo studies should be cautious, our data may have implications relevant to the use of vanadate as a therapeutic modality for diabetes.…”

Section: Discussionmentioning

confidence: 83%

“…In streptozotocin-treated diabetic rats and in mouse models of non-insulindependent diabetes mellitus, treatment with vanadate has a beneficial effect, resulting in reduction of blood glucose levels and correction of several of the metabolic abnormalities (1,2). These studies prompted the evaluation of vanadate as a therapeutic adjunct to insulin for the treatment of diabetes mellitus in humans (31,32). The mechanism by which vanadate is thought to potentiate the effect of insulin is not precisely known.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Activation of mesangial cells by the phosphatase inhibitor vanadate. Potential implications for diabetic nephropathy.

Wenzel¹,

Fouqueray²,

Biswas³

et al. 1995

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Activation of mesangial cells by the phosphatase inhibitor vanadate. Potential implications for diabetic nephropathy.

Wenzel¹,

Fouqueray²,

Biswas³

et al. 1995

J. Clin. Invest.

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“…Although the vanadate (+V) form of vanadium has been shown to affect the activities of various intracellular enzymes in vitro (mostly at pharmacological concentrations), vanadate is reduced intracellularly to the vanadyl ( + IV) state. 38 ' 39 Vanadyl in turn is a very poor inhibitor of cellular enzyme systems. 38 ' 40 Since it was not possible to alter the rate of insulin release with the type of implants used in this study, plasma insulin values in the vanadyl-treated SHR given insulin implants exceeded those seen in the untreated SHR 3 weeks post-implant (causing a decrease in plasma glucose and an increase in plasma catecholamines).…”

Section: Discussionmentioning

confidence: 99%

“…38 ' 39 Vanadyl in turn is a very poor inhibitor of cellular enzyme systems. 38 ' 40 Since it was not possible to alter the rate of insulin release with the type of implants used in this study, plasma insulin values in the vanadyl-treated SHR given insulin implants exceeded those seen in the untreated SHR 3 weeks post-implant (causing a decrease in plasma glucose and an increase in plasma catecholamines). However, it is perhaps important that a reversal of the antihypertensive effects of vanadyl was evident even 1 week after implant, when plasma glucose and insulin levels in the rats with implants were similar to those of the untreated SHR.…”

Section: Discussionmentioning

confidence: 99%

Vanadyl sulfate lowers plasma insulin and blood pressure in spontaneously hypertensive rats.

Bhanot

McNeill

1994

Hypertension

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Spontaneously hypertensive rats (SHR) are hyperinsulinemic compared with their Wistar-Kyoto (WKY) controls. Since previous studies have demonstrated that vanadyl sulfate lowers insulin levels in nondiabetic rats, we used vanadyl to explore the relation between hyperinsulinemia and hypertension. In a prevention study, 5-week-old SHR and WKY rats were started on long-term vanadyl sulfate treatment. Vanadyl in doses of 0.4 to 0.6 mmol/kg per day lowered plasma insulin (252±22.8 versus 336±12.6 pmol/L, treated versus untreated, P<.01) and systolic blood pressure (158±2 versus 189±1 mm Hg, P<.001) in SHR without causing any change in plasma glucose. No changes were seen in the treated WKY rats. At 11 weeks of age, a group of untreated rats from the prevention study was started on vanadyl treatment as before. Again, vanadyl caused significant and sustained decreases in plasma insulin (264±12.6 versus 342±6.6 pmol/L, treated versus untreated, P<.001) and blood pressure (161 ±1 versus E ssential hypertension is associated with multiple metabolic defects in carbohydrate and lipoprotein metabolism 13 that include insulin resistance, hyperinsulinemia, and dyslipidemia.1 ' 45 Insulin resistance in hypertension is often accompanied by hyperinsulinemia, 67 and these metabolic defects persist when blood pressure (BP) is reduced by conventional antihypertensive drugs.58 Hyperinsulinemia in hypertension is probably a reflection of the resistance to the peripheral uptake and utilization of glucose, with high levels of insulin needed to maintain and/or sustain euglycemia in the presence of insulin resistance.9 -10 However, the precise nature of this relation remains unexplained. The primary question that needs resolution is whether or not these defects in carbohydrate metabolism are causally related to hypertension.Insulin resistance and hyperinsulinemia have also been documented in three models of experimental hypertension 1114 including the genetically predisposed spontaneously hypertensive rat (SHR).13 Furthermore, SHR exhibit a decreased insulin clearance, which may also result in increased plasma insulin

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“…Vanadium [reviewed in 48,49] Vanadium salts (vanadate and vanadyle) can mimic insulin activity. In normal rats, administration of vana dium decreases plasma insulin levels without inducing hypoglycemia.…”

Section: Potential Treatments Of Insulin Resistancementioning

confidence: 99%

Pharmacological Approach in the Treatment of Insulin Resistance

Vialettes¹,

Silvestre²

1992

Horm Res

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Insulin resistance syndromes are heterogeneous in either severity or mechanism. Many drugs have been shown to counteract various elements of insulin resistance. Some of them, by normalization of metabolic parameters, decrease insulin resistance induced by chronic hyperglycemia in diabetes. Insulin and, to some extent, sulfonylureas are in this group, but these drugs are not stricto sensu medication of insulin resistance. Some drugs sensitize peripheral tissues to the action of insulin. For instance, biguanides and thiazolidine-dione facilitate translocation to the membrane of glucose transporter in presence of insulin. Other compounds as vanadate or IGF-1 mimic some peripheral action of insulin. Finally, blockade of FFA oxidation by specific inhibitors (methylpalmoxyrate) can limit insulin resistance. In 1992, among these compounds, specific of insulin resistance, biguanides are mostly used. However, the efficacy of these drugs is moderate and limited to type 2 diabetes.

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Effects of vanadyl derivatives on animal models of diabetes

Cited by 26 publications

References 28 publications

Activation of mesangial cells by the phosphatase inhibitor vanadate. Potential implications for diabetic nephropathy.

Activation of mesangial cells by the phosphatase inhibitor vanadate. Potential implications for diabetic nephropathy.

Vanadyl sulfate lowers plasma insulin and blood pressure in spontaneously hypertensive rats.

Pharmacological Approach in the Treatment of Insulin Resistance

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