Pancreatic protective effects of sodium tungstate in streptozotocin-induced diabetic rats

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• 作者：Parichehreh Yaghmaei ; Kazem Parivar ; Farid Niksereshet ; Shahab Amini ; Amirhadi Masoudi ; Elham Amini
• 关键词：Diabetes mellitus ; Sodium tungstate ; Beta-cell ; Rat
• 刊名：Diabetes Metabolic Syndrome: Clinical Research Reviews
• 出版年：2008
• 出版时间：December 2008
• 年：2008
• 卷：2
• 期：4
• 页码：259-265
• 全文大小：1047 K

文摘

Summary

Aims

A number of chemical compounds such as sodium tungstate and vanadyl sulfate have been assessed for their anti-diabetic effects in several animal models of diabetes. This study investigates the proper time for initiation of sodium tungstate treatment in diabetic Wistar rats and its histopathological effects on pancreas.

Materials and methods

Animals were divided into five groups (n = 10). Control (C), sodium tungstate-treated control (TC), streptozotocin-induced diabetic (D), streptozotocin-induced diabetic rats were treated by sodium tungstate form 1 week before streptozotocin (STZ) injection (TD₁), and diabetic rats treated with sodium tungstate 1 week after STZ administration (TD₂). The histopathologic changes in pancreas were investigated by light microscopy. Body weight, blood glucose, insulin levels, food intake and fluid intake were compared between groups. Serum insulin levels were determined by ultra-sensitive rat insulin kit, using double-antibody ELISA.

Results

Group D and TD₂ showed significant weight loss, polydipsia, polyuria and polyphagia compared to groups C and TC (p < 0.01). TD₁ group protects diabetic-induced rats from elevation of glucose compared to groups D and TD₂ (p < 0.01). Group TD₁ showed significant decrease in fasting glucose levels and oral glucose tolerance test in comparison to groups D and TD₂ (p < 0.01). Microscopic evaluation of pancreas showed that in TD₁ group, tungstate protects STZ-induced beta-cells degenerations.

Conclusion

Pre-treatment with sodium tungstate leads to amelioration of diabetic complications and short-term pre-treatment with tungstate can converts the diabetic state by sustaining a few, although it is critical, amount of beta-cells that adequately maintain normoglycemia.