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