Viikari Liisa A, Huupponen Risto K, Viikari Jorma S A, Marniemi Jukka, Eklund Carita, Hurme Mikko, Lehtimäki Terho, Kivimäki Mika, Raitakari Olli T
Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, 20521 Turku, Finland.
J Clin Endocrinol Metab. 2007 Dec;92(12):4753-8. doi: 10.1210/jc.2007-0103. Epub 2007 Sep 18.
Leptin and C-reactive protein (CRP) concentrations are increased in inflammation, and both have been linked to increased risk for cardiovascular diseases.
The objective of the study was to explore in a population-based sample whether the relation between leptin and CRP is independent of obesity level and whether genetic causes of CRP elevation contribute to leptin levels.
This was a population-based study including 1862 young adults (971 women; 891 men) aged 24-39 yr.
The study was conducted at five centers in Finland.
Associations between leptin and CRP adjusted for obesity indices, risk factors, genetic variables, and lifestyle variables were measured.
Women had 3.0-fold higher median concentrations of leptin (12.5 vs. 4.1 ng/ml) and 1.3-fold higher median concentrations of CRP (0.75 vs. 0.56 mg/liter) than men (P < 0.0001 in both comparisons). In univariate analyses, CRP and leptin were significantly intercorrelated (r = 0.47, P < 0.0001 for women; r = 0.46, P < 0.0001 for men). In multiple regression analysis including age, body mass index, waist circumference, insulin, lipids, systolic and diastolic blood pressures, smoking status, and use of oral contraceptives in women, leptin was the main determinant of CRP in men (P < 0.0001) and the second most important determinant in women (P < 0.0001). A Mendelian randomization test based on genetic variants in the CRP gene (five single nucleotide polymorphisms) provided no support for CRP as a causal agent for leptin.
Leptin, obesity, and oral contraceptive use in women were the main factors related to CRP. The relation between leptin and CRP was independent of obesity and cardiovascular risk factors.
炎症时瘦素和C反应蛋白(CRP)浓度升高,且二者均与心血管疾病风险增加有关。
本研究旨在基于人群样本探讨瘦素与CRP之间的关系是否独立于肥胖水平,以及CRP升高的遗传原因是否影响瘦素水平。
这是一项基于人群的研究,纳入了1862名年龄在24 - 39岁的年轻人(971名女性;891名男性)。
该研究在芬兰的五个中心进行。
测量调整肥胖指数、危险因素、遗传变量和生活方式变量后瘦素与CRP之间的关联。
女性瘦素的中位数浓度(12.5对4.1 ng/ml)比男性高3.0倍,CRP的中位数浓度(0.75对0.56 mg/升)比男性高1.3倍(两项比较P均<0.0001)。在单变量分析中,CRP与瘦素显著相关(女性r = 0.47,P < 0.0001;男性r = 0.46,P < 0.0001)。在多因素回归分析中,纳入年龄、体重指数、腰围、胰岛素、血脂、收缩压和舒张压、吸烟状况以及女性口服避孕药使用情况后,瘦素是男性CRP的主要决定因素(P < 0.0001),是女性第二重要的决定因素(P < 0.0001)。基于CRP基因中的遗传变异(五个单核苷酸多态性)进行的孟德尔随机化检验不支持CRP是瘦素的因果因素。
瘦素、肥胖以及女性口服避孕药的使用是与CRP相关的主要因素。瘦素与CRP之间的关系独立于肥胖和心血管危险因素。