title: Visfatin: a putative biomarker for metabolic syndrome is not influenced by pioglitazone or simvastatin treatment in nondiabetic patients at cardiovascular risk -- results from the PIOSTAT study.
abstract: OBJECTIVE
  The aim of the study was to analyze the effect of pioglitazone (PIO) and simvastatin (SIMVA) on adiponectin and visfatin concentrations in nondiabetic patients with metabolic syndrome and increased risk for cardiovascular complications in a prospective randomized clinical trial.
  
  
  METHODS
  One-hundred twenty-five nondiabetic patients with increased cardiovascular risk [78 females, 47 males, age (mean+/-STD:58.6+/-7.8years, BMI:30.8+/-4.2(kg/m2] were included after randomization to PIO+lacebo, SIMVA+placebo, or PIO+SIMVA treatment for 3 months. At baseline and endpoint, measurements of HbA1c, glucose, insulin, LDL cholesterol, adiponectin and visfatin were performed. Insulin resistance was assessed by means of the HOMAIR-score.
  
  
  RESULTS
  Improvement in the HOMAIR-score was observed with PIO and the combination, but not with SIMVA alone, which was accompanied by an increase in adiponectin with PIO treatment groups, but a decrease with SIMVA alone (baseline/endpoint: PIO: 14.0+/-8.2 mg/l/ 27.6+/- 14.5 mg/l, p<0.05; PIO+SIMVA: 11.7+/-10.0 mg/l/26.7+/-15.7 mg/l, p<0.05; SIMVA: 15.5+/-12.7 mg/l/ 11.6+/-7.0 mg/l, p<0.05). No change could be observed in the visfatin concentrations (PIO: 47.6+/-14.5 ng/ml/48.0+/-11.6 ng/ml, PIO+SIMVA: 45.1+/-10.9 ng/ml/47.9+/-10.1 ng/ml, SIMVA: 49.2+/- 13.4 ng/ml/52.1+/-16.7 ng/ml, n. s. in all cases).
  
  
  CONCLUSIONS
  Insulin resistance and/or cardiovascular risk indicators were not associated with visfatin levels. Regulation of visfatin secretion occurs through biochemical pathways independent from those influenced by pioglitazone or simvastatin.
authors.affiliation: 1Institute for Clinical Research and Development, Mainz, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Pfützner
authors.forename: M
authors.initials: M
authors.lastname: Hanefeld
authors.forename: G
authors.initials: G
authors.lastname: Lübben
authors.forename: M M
authors.initials: MM
authors.lastname: Weber
authors.forename: E
authors.initials: E
authors.lastname: Karagiannis
authors.forename: C
authors.initials: C
authors.lastname: Köhler
authors.forename: C
authors.initials: C
authors.lastname: Hohberg
authors.forename: T
authors.initials: T
authors.lastname: Forst
mesh_terms: D052242:Adiponectin / Q000097:blood; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology*; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D000960:Hypolipidemic Agents / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000150:complications / Q000188:drug therapy*; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood* / Q000378:metabolism; D000077205:Pioglitazone; D010919:Placebos; D012307:Risk Factors; D019821:Simvastatin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D045162:Thiazolidinediones / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D006442:Glycated Hemoglobin; D000960:Hypolipidemic Agents; D054409:Nicotinamide Phosphoribosyltransferase; D000077205:Pioglitazone; D010919:Placebos; D019821:Simvastatin; D045162:Thiazolidinediones; C499918:ADIPOQ protein, human; C517652:hemoglobin A1c protein, human