title: The relationship between plasma adiponectin concentration and insulin resistance is altered in smokers.
abstract: BACKGROUND
  Low plasma adiponectin concentrations in smokers may contribute to the adverse consequences that occur in these individuals.
  
  
  OBJECTIVE
  The objective of the study was to define the relationship among smoking, plasma adiponectin concentrations, insulin resistance, and inflammation.
  
  
  METHODS
  This was a cross-sectional, observational study with a 2 x 2 factorial design and a prospective longitudinal arm.
  
  
  METHODS
  The study was conducted at a general clinical research center.
  
  
  METHODS
  Apparently healthy smokers (n = 30) and nonsmokers (n = 30), subdivided into insulin resistant (IR) (n = 15) and insulin sensitive (IS) (n = 15) subgroups participated in the study.
  
  
  METHODS
  Intervention included pioglitazone administration for 3 months to 12 IR smokers and eight IS smokers.
  
  
  METHODS
  Measures included fasting plasma adiponectin and C-reactive protein (CRP) concentrations and changes in adiponectin after pioglitazone treatment in IR and IS smokers.
  
  
  RESULTS
  Being either a smoker or having insulin resistance was independently associated with lower adiponectin concentrations (P = 0.046 and 0.001, respectively). The difference in mean adiponectin concentration between smokers and nonsmokers did not depend on the insulin resistance status of the subjects. No difference was detected in average CRP concentrations between smokers and nonsmokers (P = 0.18) and between IR and IS subjects (P = 0.13). CRP concentrations were unrelated to adiponectin in smokers (r = -0.05, P = 0.78) and nonsmokers (r = 0.03, P = 0.86). Finally, pioglitazone treatment increased adiponectin concentrations in both IR (P < 0.001) and IS smokers (P = 0.001).
  
  
  CONCLUSIONS
  Plasma adiponectin concentrations are lower in smokers and IR subjects and are unrelated to CRP concentrations. These findings suggest that low levels of adiponectin in smokers may be independent of both insulin resistance and a generalized inflammatory response.
authors.affiliation: Department of Medicien, Stanford University School of Medicine, CA 94305, USA.
authors.forename: Fahim
authors.initials: F
authors.lastname: Abbasi
authors.forename: Helke M F
authors.initials: HM
authors.lastname: Farin
authors.forename: Cindy
authors.initials: C
authors.lastname: Lamendola
authors.forename: Tracey
authors.initials: T
authors.lastname: McLaughlin
authors.forename: Eric A
authors.initials: EA
authors.lastname: Schwartz
authors.forename: Gerald M
authors.initials: GM
authors.lastname: Reaven
authors.forename: Peter D
authors.initials: PD
authors.lastname: Reaven
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D003430:Cross-Sectional Studies; D004341:Drug Evaluation; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D000077205:Pioglitazone; D012907:Smoking / Q000009:adverse effects*; D045162:Thiazolidinediones / Q000494:pharmacology*
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D045162:Thiazolidinediones; D002097:C-Reactive Protein; D000077205:Pioglitazone