title: Resistin production from adipose tissue is decreased in db/db obese mice, and is reversed by rosiglitazone.
abstract: OBJECTIVE
  This study was designed to (1) investigate the expression profiles of resistin in db/db mice and its dynamic association with metabolic parameters; and (2) evaluate the effects of Rosiglitazone on production of resistin.
  
  
  METHODS
  Db/db mice and their lean litter mates were used for this study. Epididymal fat tissue was excised from mice of different age (from 5 to 12 weeks) for ex vivo incubation. Resistin,along with adiponectin,in serum and conditioned culture medium of epididymal fat pads were measured with immunoassays. The gene expression of resistin was determined by real-time PCR. Rosiglitazone or the vehicle (PBS) was administered into db/db mice by daily intra-gastric gavage. Differentiated 3T3-L1 adipocytes were used for in vitro evaluation.
  
  
  RESULTS
  The secretion of resistin from the fat pads in db/db mice was significantly lower than that in lean mice (P<0.01). The mRNA expression of the resistin gene in fat tissue of db/db mice at the age of 5 weeks was decreased by 60.5% compared to lean controls (p<0.05). Serum levels of resistin were comparable between the obese and lean groups, perhaps due to the increased total fat mass in db/db mice. Correlation analysis showed that serum resistin levels were positively correlated to resistin secretion from fat pads(r = 0.844,P = 0.000), while negatively associated with the body weight (r = -0.515, P = 0.000) and fasting glucose level (r = -0.357, P = 0.002). Notably, treatment with rosiglitazone increased the serum resistin levels by 66.4%(P<0.05)in db/db mice. In 3T3-L1 adipocytes, Rosiglitazone (10 uM) markedly enhanced the secretion of resistin by 120% (P<0.01) and its gene expression by 78.1% (P<0.05).
  
  
  CONCLUSIONS
  Both resistin gene expression and its secretion from the epididymal adipose tissue were decreased in db/db obese mice, while the insulin-sensitizing drug rosiglitazone increased resistin production. Our results do not support the role of resistin as an etiological link between obesity and diabetes.
authors.affiliation: Department of Medicine, The University of Hong Kong, Hong Kong, China.
authors.forename: Hongying
authors.initials: H
authors.lastname: Ye
authors.forename: Herbert J
authors.initials: HJ
authors.lastname: Zhang
authors.forename: Aimin
authors.initials: A
authors.lastname: Xu
authors.forename: Ruby L C
authors.initials: RL
authors.lastname: Hoo
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D005786:Gene Expression Regulation / Q000187:drug effects*; D007118:Immunoassay; D051379:Mice; D008820:Mice, Obese; D060888:Real-Time Polymerase Chain Reaction; D052243:Resistin / Q000097:blood / Q000378:metabolism*; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology*
chemical_list: D052242:Adiponectin; D052243:Resistin; D045162:Thiazolidinediones; D000077154:Rosiglitazone