title: [Mechanism of BVT.2733 and pioglitazone in the improvement of insulin resistance].
abstract: OBJECTIVE
  To investigate the mechanism of BVT.2733 on insulin resistance, by using diet-induced obese (DIO) mice model.
  
  
  METHODS
  After having been balanced for 3 days, the C57BL/6J mice were randomly divided into a normal diet group and a high-fat diet (HFD) group. After 20 weeks, the obese mice were further randomly divided into an obese control group, a BVT.2733 group and a pioglitazone (PGZ) group and they were orally administered with placebo, BVT.2733 and PGZ separately for two weeks. Adiponectin and leptin mRNA expression levels from adipose tissue were analyzed with real-time quantitative PCR. The levels of plasma glucose, serum insulin and adiponectin were measured with biochemical technology, radioimmunoassay and ELISA. Adipocyte sizes were observed with immunohistochemistry.
  
  
  RESULTS
  The body weight, plasma glucose and serum insulin levels raised (P < 0.05) in the HFD group and the adipocyte sizes were bigger. Serum insulin levels significantly reduced (P < 0.05) and adipocyte sizes reduced, while plasma adiponectin level raised (P < 0.01) in the two treatment groups as compared with those in obese controls. Both the mRNA expressions of adiponectin and leptin upregulated (P < 0.05) in the PGZ group, but their expressions in the BVT.2733 group did not alter significantly. The body weight of the mice reduced significantly in the BVT.2733 group.
  
  
  CONCLUSIONS
  BVT.2733 can reduce body weight significantly and improve insulin resistance, but cannot influence the expression of adipocytokines.
authors.affiliation: Department of Geriatrics, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China. gxding@njmu.edu.cn
authors.forename: Yu
authors.initials: Y
authors.lastname: Xie
authors.forename: Ting
authors.initials: T
authors.lastname: Zhu
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhong
authors.forename: Juan
authors.initials: J
authors.lastname: Liu
authors.forename: Jing
authors.initials: J
authors.lastname: Yu
authors.forename: Juan-ming
authors.initials: JM
authors.lastname: Zha
authors.forename: Wen-juan
authors.initials: WJ
authors.lastname: DI
authors.forename: Guo-xian
authors.initials: GX
authors.lastname: Ding
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D000077205:Pioglitazone; D010879:Piperazines / Q000494:pharmacology*; D013449:Sulfonamides / Q000494:pharmacology*; D013844:Thiazoles / Q000494:pharmacology*; D045162:Thiazolidinediones / Q000494:pharmacology*; D000096926:Benzenesulfonamides
chemical_list: D007004:Hypoglycemic Agents; D000077205:Pioglitazone; D010879:Piperazines; D013449:Sulfonamides; D013844:Thiazoles; D045162:Thiazolidinediones; C474501:3-chloro-2-methyl-N-(4-(2-(4-methyl-1-piperazinyl)-2-oxoethyl)-1,3-thiazol-2-yl)benzenesulfonamide; D000096926:Benzenesulfonamides