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

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. METHODS: 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). 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 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). 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.

Rosiglitazone ameliorates the histological parameters of the dorsal root ganglion and functional assessment after sciatic nerve injury in the rat.

BACKGROUND: This study investigates the effects of rosiglitazone (a peroxisome proliferator-activated receptor-gamma) on the histological parameters of the dorsal root ganglion (DRG) and the recovery potential of the injured sciatic nerve in rats using stereological methods. METHODS: The rats were divided into four groups including control, sham-operated, sciatic nerve crush (SNC), and SNC + rosiglitazone treatment (5 mg/kg body weight/day). The sciatic functional index (SFI) was used to evaluate functional recovery. The main DRG neurons were defined as either A cells (the larger cell with a central nucleolus in the nucleus and granulated cytoplasm) or B cells (the smaller cell with multiple peripherally located nucleoli and homogenous cytoplasm). Satellite cells (supporting) surround the neuron cell body. RESULTS: The volume and surface of A and B cells decreased in the SNC group compared to the sham-operated group. In the SNC + rosiglitazone group, the volume of A and B cells decreased to a lesser extent, and was 30% and 48% higher in comparison with the SCN group. In the SNC + rosiglitazone rats the surface of the A and B cells decreased to a minor extent, and was 45% and 21% higher in comparison with the SNC animals. In rosiglitazone-treated rats the number of the A, B, and satellite cells decreased less, and was 38%, 34%, and 29% higher than in the SNC rats. The SFI score improved in SNC + rosiglitazone rats in comparison with non-treated animals. CONCLUSION: Rosiglitazone has an ameliorative effect on the DRG and enhances the functional recovery after SNC in rats.