title: Plasma resistin concentration, hepatic fat content, and hepatic and peripheral insulin resistance in pioglitazone-treated type II diabetic patients.
abstract: OBJECTIVE
  To study the effect of pioglitazone (PIO) on plasma resistin concentration, endogenous glucose production (EGP), and hepatic fat content (HFC) in patients with type II diabetes (T2DM).
  
  
  METHODS
  A total of 13 T2DM patients (age=51+/-2 y, BMI=29.7+/-1.1 kg/m(2), HbA(1c)=8.0+/-0.5%).
  
  
  METHODS
  HFC (magnetic resonance spectroscopy) and basal plasma resistin concentration were quantitated before and after PIO treatment (45 mg/day) for 16 weeks. Subjects received a 3 h euglycemic insulin (100 mU/m(2)/min) clamp with 3-[(3)H] glucose to determine rates of EGP and tissue glucose disappearance (Rd) before and after PIO.
  
  
  RESULTS
  PIO reduced fasting plasma glucose (10.3+/-0.7 to 7.6+/-0.6 mmol/l, P<0.001) and HbA(1c) (8.0+/-0.4 to 6.8+/-0.3%, P<0.001) despite increased body weight (83.2+/-3.4 to 86.3+/-3.4 kg, P<0.001). PIO improved Rd (4.9+/-0.4 to 6.6+/-0.5 mg/kg/min, P<0.005) and reduced EGP (0.22+/-0.04 to 0.06+/-0.02 mg/kg/min, P<0.01) during the insulin clamp. Following PIO, HFC decreased from 21.1+/-3.5 to 11.2+/-2.1% (P<0.005), and plasma resistin decreased from 5.3+/-0.6 to 3.5+/-0.3 ng/ml (P<0.01). Plasma resistin concentration correlated positively with HFC before (r=0.58, P<0.05) and after (r=0.55, P<0.05) PIO treatment. Taken collectively, plasma resistin concentration, before and after PIO treatment, correlated positively with hepatic fat content (r=0.66, P<0.001) and EGP during the insulin clamp (r=0.41, P<0.05). However, the plasma resistin concentration did not correlate with whole body glucose disposal (Rd) during the insulin clamp either before (r=-0.18, P=NS) or after (r=-0.13, P=NS) PIO treatment.
  
  
  CONCLUSIONS
  PIO treatment in T2DM causes a significant decrease in plasma resistin concentration. The decrease in plasma resistin is positively correlated with the decrease in hepatic fat content and improvement in hepatic insulin sensitivity.
authors.affiliation: Diabetes Division, Department of Medicine, University of Texas Health Science Center at San Antonio, Texas, USA. mandeepbajaj@hotmail.com
authors.forename: M
authors.initials: M
authors.lastname: Bajaj
authors.forename: S
authors.initials: S
authors.lastname: Suraamornkul
authors.forename: L J
authors.initials: LJ
authors.lastname: Hardies
authors.forename: T
authors.initials: T
authors.lastname: Pratipanawatr
authors.forename: R A
authors.initials: RA
authors.lastname: DeFronzo
mesh_terms: D001786:Blood Glucose / Q000032:analysis; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism; D006729:Hormones, Ectopic / Q000097:blood*; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007333:Insulin Resistance / Q000502:physiology*; D008055:Lipids / Q000032:analysis*; D008099:Liver / Q000737:chemistry* / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D008875:Middle Aged; D000077205:Pioglitazone; D052243:Resistin; D045162:Thiazolidinediones / Q000627:therapeutic use*; D015430:Weight Gain / Q000502:physiology
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D006729:Hormones, Ectopic; D007004:Hypoglycemic Agents; D008055:Lipids; C499624:RETN protein, human; D052243:Resistin; D045162:Thiazolidinediones; D005947:Glucose; D000077205:Pioglitazone