Quantitative Assessment of Proliferative Effects of Oral Vanadium on Pancreatic Islet Volumes and Beta Cell Numbers of Diabetic Rats

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 solutions containing vanadyl sulfate (0.5-1 mg/mL, VOSO4 + 5H2O). 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). Normoglycemia persisted in VTN with significantly decreased plasma insulin (0.19 +/- 0.08 vs. 0.97 +/- 0.27 ng/dL, P<0.002). The respective high BG (532 +/- 49 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 mm3, P<0.003) and TBCN (0.99 +/- 0.1 vs. 3.2 +/- 0.2 x 106, P<0.003), vanadium treatment significantly increased TISVOL (2.9 +/- 0.8 and 4.07 +/- 1.0 mm3, P<0.003) and TBCN (1.5 +/- 0.3 and 3.8 +/- 0.6 x 106, P<0.03). Two-month oral vanadium therapy in STZ-diabetic rats ameliorated hyperglycemia by partially restoring plasma insulin. This was through proliferative actions of vanadium in preventing islet atrophy by increasing beta-cell numbers.