- Relationship between Plasma Leptin Levels and Carotid Intima-Medial Thickness in Korean Adults.
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Hyejin Lee, Eunsoon Hong, Youngsun Hong, Yeon Ah Sung
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J Korean Endocr Soc. 2002;17(1):87-94. Published online February 1, 2002
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 Abstract
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- BACKGROUND
Many studies have recently shown that leptin can promote angiogenesis via endothelial leptin receptors and induce oxidative stress in endothelial cells; These findings suggest the relationship between cardiovascular risk and blood leptin concentration. In the present study, we investigated the relationship between leptin concentration and carotid intima-medial thickness (CIMT) as an indicator of early atherosclerosis in adults. METHEODS: The study subjects comprised 138 (45 men and 93 women; mean age 42.4+/-7.5 years; mean BMI 24.0+/-2.7 kg/m2) without history of diabetes, hypertension or cardiovascular disease. We measured CIMT by high resolution ultrasonography and plasma leptin levels by radioimmunoassay. RESULTS: 1) No significant differences in age, BMI or CIMT between male and female subjects were noted, but the leptin levels in female were significantly higher than those in males. (8.42+/-5.90 ng/mL vs. 3.08+/-1.00 ng/mL, p<0.001) 2) CIMT showed a significant positive correlation with age (r=0.31, p< 0.001), BMI (r=0.25, p<0.01) and level (r=0.42, p<0.05) in simple regression analysis. 3) When male and female subjects were each divided into 3 groups by leptin concentration, no significant difference in CIMT among female subjects was found. In male subjects, CIMT was significantly higher in the highest tertile of leptin level than in the other 2 groups (0.65+/-0.03 mm vs. 0.56+/-0.07 mm and 0.53+/-0.07 mm, p<0.01) after adjustment for BMI and age. However, this difference was not significant after adjustment for smoking. 4) CIMT (0.61+/-0.05 mm vs. 0.53+/-0.07 mm, p<0.01) and leptin concentrations (3.57+/-2.13 ng/mL vs. 2.20+/-1.39 ng/mL, p<0.05) were significantly higher in male smokers than in male non-smokers. CONCLUSION: Our results demonstrated significant correlation of CIMT to plasma leptin level before adjustment for smoking. A possible explanation is the permissive action of smoking on the atherogenic effect of leptin. However, further studies to elucidate the relationships and interactions among smoking, leptin level and the development of atherosclerosis will be needed.
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