Vanadium Inhibits Type 2 Diabetes Mellitus-Induced Aortic Ultrastructural Alterations Associated with the Inhibition of Dyslipidemia and Biomarkers of Inflammation in Rats (original) (raw)
Related papers
The impact of vanadium on endothelial dysfunction in type 2 diabetic rats: Histological insight
Introduction: The aim of this research is to investigate the effect of vanadium and or insulin on endothelial dysfunction in type 2 diabetic rats (T2DM). Material and methods:60 white albino rats were included in this research and randomly divided into 6 groups(n=10) as follows: Control group (Control): rats injected once intraperitoneally (i.p.) with citrate buffer (0.1 M, pH 4.5), vanadium treated group (Vanadium): rats received vanadyl sulfate of 0.64 mmol/kg weight freshly dissolved in 1 ml of distilled water daily through a nesophageal tube, diabetic type 2group(D type 2) : rats received high fat diet for 15 days followed by streptozotocin (25 mg/kg body weight ), diabetic type 2 and insulin group (D type 2 +I): D type 2 rats received mixtard insulin subcutaneously in a dose of 0.75 IU/100 gm weight in 0.75 ml volume once daily, diabetic type 2 and vanadium group (D type 2+V): type 2 diabetic ratsreceived the same dose of vanadium as in vanadium group after 48 h of induction of...
Health Promotion Perspectives
Background: Oxidative stress has a significant role in the commencement and development of hyperglycemia. Vanadium, as a transitional metal with redox properties, enters the redox process, produces free radicals, and distracts the pro-antioxidant balance. The present animal systematic review aimed to assess the effect of vanadium supplementation on inflammation and oxidative stress biomarkers in diabetes-induced animals. Methods: A systematic search was conducted using the PubMed, Scopus, and web of science databases from 1990 to 2021, according to the inclusion and exclusion criteria. The search strategy was based on the guidelines for systematic review of animal experiments and Preferred Reporting Items for Systematic Reviews (PRISMA). Criteria for eligibility were animal-based studies, evaluating the therapeutic effects of vanadium on inflammatory and oxidative stress biomarkers in diabetes. The Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE) tool was used...
Biological trace element research, 2018
Vanadium compounds have been primarily investigated as potential therapeutic agents for the treatment of various major health issues, including cancer, atherosclerosis, and diabetes. The translation of vanadium-based compounds into clinical trials and ultimately into disease treatments remains hampered by the absence of a basic pharmacological and metabolic comprehension of such compounds. In this review, we examine the development of vanadium-containing compounds in biological systems regarding the role of the physiological environment, dosage, intracellular interactions, metabolic transformations, modulation of signaling pathways, toxicology, and transport and tissue distribution as well as therapeutic implications. From our point of view, the toxicological and pharmacological aspects in animal models and humans are not understood completely, and thus, we introduced them in a physiological environment and dosage context. Different transport proteins in blood plasma and mechanistic...
Ameliorative effect of vanadium on oxidative stress in stomach tissue of diabetic rats
Bosnian journal of basic medical sciences / Udruženje basičnih mediciniskih znanosti = Association of Basic Medical Sciences, 2014
Between their broad spectrum of action, vanadium compounds are shown to have insulin mimetic/enhancing effects. Increasing evidence in experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of diabetes and on the onset of diabetic complications. Thus, preventive therapy can alleviate the possible side effects of the disease. The aim of the present study was to investigate the effect of vanadyl sulfate supplementation on the antioxidant system in the stomach tissue of diabetic rats. Male Swiss albino rats were randomly divided into 4 groups: control; control+vanadyl sulfate; diabetic; diabetic+vanadyl sulfate. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ; 65 mg/kg body weight). Vanadyl sulfate (100 mg/kg body weight) was given daily by gavage for 60 days. At the last day of the experiment, stomach tissues were taken and homogenized to make a 10% (w/v) homogenate. Catalase (CAT), superoxide dismutase (SOD), g...
Iranian Biomedical Journal, 2014
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 VOSO 4 , 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.
Molecular and Cellular Biochemistry, 1998
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-terrn 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 vanaditun compounds. One of these, bismaltolato-oxovanadiurn 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 vanadiun is a phosphatase inhibitor and that vanadium can activate serine/threonine kineses distal to tbe 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.
1999
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.
Effects of oral vanadium on glycaemic and lipid profile in rats
JPMA. The Journal of the Pakistan Medical Association, 2016
Vanadyl sulphate, an inorganic tetravalent salt of transition metal vanadium is conventionally used to treat diabetes and by athletes as body-building supplement. Vanadyl sulphate is a constituent of many supplements and herbal preparations available over the counter in many parts of the world. In this study the efficacy of the salt as hypoglycaemic agent and its effects on lipid profile were determined when administered in therapeutic dose range (in humans) to healthy Sprague Dawley rats for a considerable duration. One hundred and five rats were randomly divided into three groups of 35 rats each. Animals of all three groups were provided normal rodent diet and water ad libitum. Group I animals were administered 0.5 ml plain water through oral gavage while group II and group III rats, 0.25mg/Kg/day and 1.2mg/Kg/day vanadyl sulphate respectively for 24 weeks. At the end of 24 weeks intra-cardiac blood sampling was done and blood glucose, insulin and lipid profile were measured. Ther...
Vanadium increases GLUT4 in diabetic rat skeletal muscle
Molecular and cellular biochemistry, 2002
The effect of vanadium in lowering blood glucose in diabetic animals is well established; however, the exact mechanism of action of vanadium still eludes us. There are several reports from in vitro studies indicating that vanadium increases enzyme activity in insulin signalling pathways; however, these findings have not been duplicated in vivo. Glucose transporters (GLUT) have a major role to play in any glucoregulatory effects. Insulin dependent GLUT4 is a major glucose transporter present in skeletal muscle, adipocytes and heart. In the present study we found that the plasma glucose in streptozotocin (STZ) diabetic animals was restored to normal following treatment with a single dose of BMOV, an organic vanadium compound, given by oral gavage (0.6 mmol/kg), similar to the response with chronic BMOV treatment. The response to BMOV by oral gavage was rapid and the animals were normoglycemic within 24 h of treatment and still demonstrated a significant effect even after 72 h. Using a...