Impact of Adiposity on Incident Hypertension Is Modified by Insulin Resistance in Adults: Longitudinal Observation From the Bogalusa Heart Study.
Impact of Adiposity on Incident Hypertension Is Modified by Insulin Resistance in Adults: Longitudinal Observation From the Bogalusa Heart Study.
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成人胰岛素抵抗改变了肥胖对高血压事件的影响：Bogalusa 心脏研究的纵向观察。
DOI：
10.1161/hypertensionaha.115.06509
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发表时间：
2016-01
期刊：
影响因子：
--
通讯作者：
Chen W
中科院分区：
文献类型：
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作者：
Zhang T;Zhang H;Li S;Li Y;Liu Y;Fernandez C;Harville E;Bazzano L;He J;Chen W
肥胖和胰岛素抵抗与高血压密切相关。本研究的目的是调查肥胖和高血压之间的联系是否受到胰岛素抵抗的影响。该队列包括1,624名中年血压正常的黑人和白色成年人，基线年龄为18至43岁，平均随访16年。基线时超重/肥胖定义为BMI≥25，使用胰岛素抵抗稳态模型评估（HOMA）测量胰岛素抵抗。比较胰岛素敏感性肥胖和胰岛素抵抗性肥胖组的高血压发病率。胰岛素抵抗性肥胖组的高血压患病率高于胰岛素敏感性肥胖组（32.1% vs22.1%，P<0.001）。在多变量logistic分析中，校正基线年龄、种族、性别、随访年数和吸烟，基线胰岛素抵抗性肥胖与高血压事件相关（比值比，OR=1.9，p=0.008）。黑人和白人之间的OR无差异（p=0.238）。值得注意的是，随着基线HOMA四分位数的增加，BMI与高血压相关的OR显著增加（四分位数I、II、III和IV的OR分别为1.3、1.1、1.5和2.5，趋势p=0.006）。随访血压（BP）随基线BMI增加的斜率，以回归系数（β）测量，胰岛素抵抗个体显著大于胰岛素敏感个体（收缩压β=0.60 vs β=0.33，差异p=0.039;舒张压β=0.41 vs β=0.20，差异p=0.019）。这些研究结果表明，胰岛素抵抗对年轻人的肥胖-高血压关联具有协同作用，表明肥胖在高血压发展中的作用被胰岛素抵抗所改变。
Adiposity and insulin-resistance are closely associated with hypertension. This study aims to investigate whether the association between adiposity and hypertension is modified by insulin resistance. The cohort consisted of 1,624 middle-aged normotensive black and white adults aged 18 to 43 years at baseline who followed for 16 years on average. Overweight/obesity at baseline was defined as BMI≥25, and insulin resistance was measured using homeostasis model assessment of insulin resistance (HOMA). Prevalence of incident hypertension was compared between the insulin-sensitive adiposity and insulin-resistant adiposity groups. The prevalence of incident hypertension was higher in the insulin-resistant adiposity than in the insulin-sensitive adiposity group (32.1% vs 22.1%, p<0.001). In multivariable logistic analyses, adjusted for baseline age, race, gender, follow-up years, and smoking, baseline insulin-resistant obesity was associated with incident hypertension (odds ratio, OR=1.9, p=0.008). ORs did not differ between blacks and whites (p=0.238). Of note, the ORs of BMI associated with hypertension significantly increased with increasing quartiles of baseline HOMA (OR=1.3, 1.1, 1.5, and 2.5 in quartiles I, II, III, and IV, respectively, p=0.006 for trend). Slopes of increasing follow-up blood pressure (BP) with baseline BMI, measured as regression coefficients (β), were significantly greater in insulin-resistant than in insulin-sensitive individuals (β=0.60 vs β=0.33 for systolic BP, p=0.039 for difference; β=0.41 vs β=0.20 for diastolic BP, p=0.019 for difference). These findings suggest that insulin-resistance has a synergistic effect on the obesity-hypertension association in young adults, indicating that the role of adiposity in the development of hypertension is modified by insulin resistance.