title: Kaiyuqingre formula improves insulin secretion via regulating uncoupling protein-2 and KATP channel.
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 (K(ATP) 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).
  
  
  CONCLUSIONS
  KYQRF can protect islet function by decreasing UCP-2 and sulfonylurea receptor 1.
authors: Department of Endocrinology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053, China.
authors: Xiao-lin
authors: XL
authors: Tong
authors: Jun
authors: J
authors: Song
authors: Lin-hua
authors: LH
authors: Zhao
authors: Hang-yu
authors: HY
authors: Ji
mesh_terms: D018528:ATP-Binding Cassette Transporters / Q000235:genetics; D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D007473:Ion Channels / Q000235:genetics; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D011955:Receptors, Drug / Q000235:genetics; D000077154:Rosiglitazone; D064233:Sulfonylurea Receptors; D045162:Thiazolidinediones / Q000494:pharmacology; D000071246:Uncoupling Protein 2; D000099161:Kcnj11 Channel
chemical_list: D018528:ATP-Binding Cassette Transporters; D004365:Drugs, Chinese Herbal; D005947:Glucose; D007328:Insulin; D007473:Ion Channels; D024101:Mitochondrial Proteins; D024661:Potassium Channels, Inwardly Rectifying; D011955:Receptors, Drug; D000077154:Rosiglitazone; D064233:Sulfonylurea Receptors; D045162:Thiazolidinediones; D000071246:Uncoupling Protein 2; D000099161:Kcnj11 Channel; C000604391:Ucp2 protein, rat