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Leptin, leptin soluble receptor and coronary atherosclerosis
Author(s) -
Hoefle G.,
Saely C. H.,
Risch L.,
Rein P.,
Koch L.,
Schmid F.,
Aczél S.,
Marte T.,
Langer P.,
Drexel H.
Publication year - 2007
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2007.01842.x
Subject(s) - leptin , medicine , coronary artery disease , body mass index , insulin resistance , endocrinology , cardiology , odds ratio , adipose tissue , artery , confidence interval , coronary atherosclerosis , leptin receptor , blood pressure , insulin , obesity
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. Design 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 ≥ 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.