Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, MA, USA.
Hypertension. 2013 Jul;62(1):27-32. doi: 10.1161/HYPERTENSIONAHA.113.01453. Epub 2013 May 28.
Animal studies and small controlled studies in humans suggest that adiponectin may regulate blood pressure via brain-mediated and endothelium-mediated mechanisms. We performed a systematic review and meta-analysis to evaluate the epidemiological 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 nonprospective and 5 prospective studies that included 17 598 adults (8220 with hypertension; mean age 19-69 years; and mean body mass index 22-38 kg/m(2)). 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 adults with hypertension and normotensive adults and a 2-stage generalized least-square trend methods to compute the odds ratio of hypertension per 1 µg/mL increase in adiponectin. Adults with hypertension 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, sex, 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, epidemiological 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.
动物研究和人体小型对照研究表明，脂联素可能通过脑介导和内皮细胞介导的机制来调节血压。我们进行了系统评价和荟萃分析，以评估有关游离生活成年人群体血浆脂联素水平与高血压的流行病学证据。通过 MEDLINE 和 EMBASE 进行了系统搜索，截至 2013 年 2 月，共确定了 43 项非前瞻性和 5 项前瞻性研究，其中包括 17598 名成年人（8220 名患有高血压；平均年龄 19-69 岁；平均体重指数 22-38kg/m2）。两名研究人员独立根据高血压状态和剂量-反应关系提取脂联素水平的数据。我们使用随机效应模型计算高血压和正常血压成年人之间的脂联素水平的加权平均差异，使用 2 阶段广义最小二乘趋势方法计算每增加 1µg/mL 脂联素的高血压的比值比。与正常血压成年人相比，高血压成年人的脂联素水平低 1.64µg/mL（95%置信区间，-2.07，-1.21）。脂联素水平每增加 1µg/mL，高血压的风险降低 6%（95%置信区间，0.92，0.97）。这些发现与研究设计和特征（包括年龄、性别和体重指数）一致（P>0.05）。然而，我们的荟萃分析受到未解释的大研究间异质性、前瞻性研究数量少和剂量-反应数据选择性报告的限制。总之，流行病学证据表明，血浆脂联素水平是肥胖相关高血压发生的生物标志物和可能的中介物。脂联素作为潜在的治疗靶点及其与血压调节中其他脂肪因子的关系仍有待探讨。
