title: Leptin, leptin soluble receptor and coronary atherosclerosis.
abstract: BACKGROUND
  The adipose tissue-related hormone leptin plays an important role in the regulation of body weight. The associations of leptin and leptin soluble receptor (sOb-R) with coronary artery disease (CAD) are not clear.
  
  
  METHODS
  We measured leptin and sOb-R in 543 consecutive patients (379 men, 164 women) referred for coronary angiography for the evaluation of CAD. Coronary artery stenoses with lumen narrowing > or = 50% were considered significant.
  
  
  RESULTS
  Serum leptin correlated significantly with body mass index (r(s) = 0.443), with insulin resistance as assessed by the homeostasis model for the assessment of insulin resistance (r(s) = 0.339), with serum triglycerides (r(s) = 0.181), with systolic as well as diastolic blood pressure (r(s) = 0.170 and r(s) = 0.133, respectively) and, inversely, with sOb-R (r(s) = -0.346; P < 0.01 for all correlations). Coronary angiography revealed significant coronary artery stenoses in 331 (61%) of our patients. Serum leptin was significantly lower in patients with significant coronary artery stenoses than in patients without such lesions (8.5 +/- 7.8 vs. 13.2 +/- 12.2 ng mL(-1); P < 0.001). Multivariate logistic regression analysis proved serum leptin inversely and independently associated with the presence of significant coronary artery stenoses (standardized adjusted odds ratio 0.746, 95% confidence interval 0.566-0.983, P = 0.038). In contrast to serum concentrations of leptin, serum concentrations of sOb-R did not significantly differ between patients with significant stenoses and those without such lesions (22.4 +/- 8.3 vs. 23.1 +/- 12.1 ng mL(-1); P = 0.655).
  
  
  CONCLUSIONS
  Serum leptin but not sOb-R is significantly lower in patients with angiographically determined CAD. Despite its association with cardiovascular risk factors, leptin should not be simply regarded as a promoter of atherosclerosis.
authors.affiliation: Academic Teaching Hospital, Feldkirch, Austria.
authors.forename: G
authors.initials: G
authors.lastname: Hoefle
authors.forename: C H
authors.initials: CH
authors.lastname: Saely
authors.forename: L
authors.initials: L
authors.lastname: Risch
authors.forename: P
authors.initials: P
authors.lastname: Rein
authors.forename: L
authors.initials: L
authors.lastname: Koch
authors.forename: F
authors.initials: F
authors.lastname: Schmid
authors.forename: S
authors.initials: S
authors.lastname: Aczél
authors.forename: T
authors.initials: T
authors.lastname: Marte
authors.forename: P
authors.initials: P
authors.lastname: Langer
authors.forename: H
authors.initials: H
authors.lastname: Drexel
mesh_terms: D000368:Aged; D000792:Angiography; D015992:Body Mass Index; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000097:blood*; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood; D054411:Receptors, Leptin / Q000097:blood*; D012044:Regression Analysis; D012307:Risk Factors
chemical_list: D020738:Leptin; D054411:Receptors, Leptin