ABSTRACT
Background: Oral vanadyl sulfate [vanadium] induces normoglycemia, proliferates beta cells and prevents pancreatic islet atrophy in streptozotocin-induced diabetic rats. Soteriological method is used to quantitate the proliferative effects of vanadium on beta-cell numbers and islet volumes of normal and diabetic rats. Adult male Sprague-Dawley rats were made diabetic with intravenous streptozotocin injection [40 mg/kg]. Normal and diabetic rats were divided into four groups. While control normal and diabetic [CD] groups used water, vanadium-treated normal [VTN] and diabetic [VTD] groups used solu ons containing vanadyl sulfate [0.51 mg/mL, VOSO[4]+5H[2]O]. Tail blood samples were used to measure blood glucose [BG] and plasma insulin. Two months after treatment, rats were sacrificed, pancreata prepared, and stereology method was used to quantitatively evaluate total beta cell numbers [TBCN] and total islet volumes [TISVOL]
Results: Normoglycemia persisted in VTN with significantly decreased plasma insulin [0.19 +/- 0.08 vs. 0.97+/-0.27 ng/dL, P<0.002]. The respec ve high BG [532h49 vs. 144+/-46 mg/dL, P<0.0001] and reduced plasma insulin [0.26 +/- 0.15 vs. 0.54+0.19 ng/dL, P<0.002] seen in CD were reversed in VTD during vanadium treatment or withdrawal. While the induction of diabetes, compared to their control, significantly decreased TISVOL [1.9 +/- 0.2 vs. 3.03 +/- 0.6 mm[3], P<0.003] and TBCN [0.99 +/- 0.1 vs. 3.2 +/- 0.2 x 10[6], P<0.003], vanadium treatment significantly increased TISVOL [2.9 +/- 0.8 and 4.07 +/- 1.0 mm[3], P<0.003] and TBCN [1.5 +/- 0.3 and 3.8 +/- 0.6 x 10[5], P<0.03
Conclusion: Two-month oral vanadium therapy in STZ-diabetic rats ameliorated hyperglycemia by partially restoring plasma insulin. This action was through proliferative actions of vanadium in preventing islet atrophy by increasing beta-cell numbers
ABSTRACT
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. 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 VOSO4, 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. 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. 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