Kaiyuqingre formula improves insulin secretion via regulating uncoupling protein-2 and KATP channel |
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Authors: | Tong Xiao-lin Song Jun Zhao Lin-hua Ji Hang-yu |
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Institution: | Department of Endocrinology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China. |
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Abstract: | 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 (KATpchannel) 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. |
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Keywords: | diabetes Kaiyuqingre formula uncoupling protein-2 KATP channel β-cell function |
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