Background Type 2 diabetes mellitus （T2DM） results from the complex association of insulin resistance and pancreatic β-cell failure. Recent studies have shown that patients diagnosed with T2DM present with a signif...Background Type 2 diabetes mellitus （T2DM） results from the complex association of insulin resistance and pancreatic β-cell failure. Recent studies have shown that patients diagnosed with T2DM present with a significant decrease in β-cell function, which can be further compromised during the progression of the disease. Several mechanisms have been shown to play a role in this process such as glucotoxicity and lipotoxicity, which contribute to accelerating insulin secretion. In this regard, Chinese medicine has a certain advantage. This experiment was performed to observe the effect of a Chinese medicine named Kaiyuqingre formula （KYQRF） on β-cell function and its mechanisms of action therein. Methods High glucose was used to set up a model of β-cell function failure. At the same time, medicated serum of KYQRF with different doses were administered to the cells. Rosiglitazone was taken as a control to observe the changes in insulin secretion, ATP-sensitive K＋ channels （KATP channel） and uncoupling protein-2 （UCP-2） in each group. Results KYQRF had some effects on the insulin secretion. In a low glucose environment, no effective change in insulin secretion was observed （P 〉0.05）. However, insulin levels increased significantly when INS-1 cells were exposed to a high glucose environment （P 〈0.05）. KYQRF could also enhance cell viability （P 〈0.05） in an effect similar to rosiglitazone. Although KYQRF had no effect on inwardly rectifying potassium channels （Kir6.2） （P 〉0.05）, it could decrease the overexpression of both UCP-2 and sulfonylurea receptor 1 （P〈0.05）. Conclusion KYQRF can protect islet function by decreasing UCP-2 and sulfonylurea receptor 1.展开更多
基金This work was supported in part by grants from the National Natural Science Foundation of China （No. 81001513） and China Postdoctoral Science Foundation （973 Program, No. 2010CB530601）.
文摘Background Type 2 diabetes mellitus （T2DM） results from the complex association of insulin resistance and pancreatic β-cell failure. Recent studies have shown that patients diagnosed with T2DM present with a significant decrease in β-cell function, which can be further compromised during the progression of the disease. Several mechanisms have been shown to play a role in this process such as glucotoxicity and lipotoxicity, which contribute to accelerating insulin secretion. In this regard, Chinese medicine has a certain advantage. This experiment was performed to observe the effect of a Chinese medicine named Kaiyuqingre formula （KYQRF） on β-cell function and its mechanisms of action therein. Methods High glucose was used to set up a model of β-cell function failure. At the same time, medicated serum of KYQRF with different doses were administered to the cells. Rosiglitazone was taken as a control to observe the changes in insulin secretion, ATP-sensitive K＋ channels （KATP channel） and uncoupling protein-2 （UCP-2） in each group. Results KYQRF had some effects on the insulin secretion. In a low glucose environment, no effective change in insulin secretion was observed （P 〉0.05）. However, insulin levels increased significantly when INS-1 cells were exposed to a high glucose environment （P 〈0.05）. KYQRF could also enhance cell viability （P 〈0.05） in an effect similar to rosiglitazone. Although KYQRF had no effect on inwardly rectifying potassium channels （Kir6.2） （P 〉0.05）, it could decrease the overexpression of both UCP-2 and sulfonylurea receptor 1 （P〈0.05）. Conclusion KYQRF can protect islet function by decreasing UCP-2 and sulfonylurea receptor 1.
