Adiponectin levels and the risk of hypertension: a systematic review and meta-analysis.
Adiponectin levels and the risk of hypertension: a systematic review and meta-analysis.
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DOI：
10.1161/hypertensionaha.113.01453
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发表时间：
2013-07
期刊：
影响因子：
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通讯作者：
Lipsitz LA
中科院分区：
文献类型：
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作者：
Kim DH;Kim C;Ding EL;Townsend MK;Lipsitz LA
动物研究和人类小型对照研究表明，脂联素可能通过脑介导和内皮介导的机制调节血压。我们进行了一项系统回顾和荟萃分析，以评估自由生活成年人血浆脂联素水平和高血压的流行病学证据。截至2013年2月，对Medline和EMBASE进行系统检索，确定了43项非前瞻性研究和5项前瞻性研究，包括17,598名成人（8,220名高血压患者，平均年龄19-69岁，平均体重指数22-38 kg/m2）。两名研究者独立提取了脂联素水平与高血压状态和剂量-反应关系的数据。我们采用随机效应模型计算高血压和正常成人之间脂联素水平的加权平均差异，并采用两阶段广义线性平方法计算每增加1 μg/ml脂联素导致高血压的比值比。高血压成人的脂联素水平比正常成人低1.64 μg/ml（95%可信区间：−2.07,−1.21）。脂联素水平每增加1 μg/ml，高血压风险降低6%（95%可信区间：0.92,0.97）。这些发现在研究设计和特征中是一致的，包括年龄、性别和体重指数（p>0.05）。然而，我们的荟萃分析受到无法解释的大型研究间异质性、少量前瞻性研究和选择性报告剂量-反应数据的限制。总之，流行病学证据表明，血浆脂联素水平是肥胖相关性高血压发展的生物标志物和可能的中介。关于脂联素作为一种潜在的治疗靶点及其与其他脂肪因子在血压调节中的关系的问题仍然存在。
Animal studies and small-controlled studies in humans suggest that adiponectin may regulate blood pressure via brain-mediated and endothelium-mediated mechanisms. We conducted a systematic review and meta-analysis to evaluate the epidemiologic evidence on plasma adiponectin levels and hypertension in free-living adult population. A systematic search of Medline and EMBASE, up to February 2013, identified 43 non-prospective and 5 prospective studies that included 17,598 adults (8,220 with hypertension; mean age 19–69 years; and mean body mass index 22–38 kg/m2). Two investigators independently extracted data on adiponectin levels by hypertension status and dose-response relationship. We used a random-effects model to compute the weighted mean difference in adiponectin levels between hypertensive and normotensive adults and a 2-stage generalized linear-square methods to compute the odds ratio of hypertension per 1 μg/ml increase in adiponectin. Hypertensive adults had 1.64 μg/ml (95% confidence interval: −2.07, −1.21) lower adiponectin levels than normotensive adults. Every 1 μg/ml increase in adiponectin levels was associated with 6% reduced risk of hypertension (95% confidence interval: 0.92, 0.97). These findings were consistent across study design and characteristics, including age, gender, and body mass index (p>0.05). However, our meta-analysis was limited by unexplained large between-study heterogeneity, a small number of prospective studies, and selective reporting of dose-response data. In conclusion, epidemiologic evidence suggests that plasma adiponectin level is a biomarker and possible mediator in the development of adiposity-related hypertension. The question remains as to adiponectin as a potential therapeutic target and its relationship with other adipokines in blood pressure regulation.