Aldosterone and Risk for Insulin Resistance.
Aldosterone and Risk for Insulin Resistance.
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醛固酮和胰岛素抵抗的风险。
DOI：
10.1161/hypertensionaha.111.182782
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Sowers,JamesR
中科院分区：
文献类型：
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作者：
Whaley-Connell,Adam;Sowers,JamesR
作为胰岛素抵抗和代谢综合征其他组分之间的统一机制，探索肾素-血管紧张素-醛固酮系统的不适当激活越来越受到关注。1，2最近的数据表明，血浆醛固酮水平升高与胰岛素抵抗相关，与血管紧张素II的其他成分无关。在探索原发性醛固酮增多症（其中存在低水平的肾素活性和血管紧张素II）与胰岛素抵抗之间的关联的研究中观察到了这种关系。1在本期中，Kumagai等3在一项为期10年的前瞻性队列研究中探讨了基线时醛固酮在正常范围内的增加作为胰岛素抵抗发生的预测因素。通过胰岛素抵抗的稳态模型评估来确定胰岛素抵抗。作者使用了一个由1088名非糖尿病患者组成的日本队列，以探讨基线醛固酮水平与胰岛素抵抗发生之间的关联强度。然后，他们进一步排除了在基线时具有明显胰岛素抵抗的个体，并前瞻性地跟踪了其余564人10年。在基线单变量回归分析中，醛固酮水平与年龄、胰岛素抵抗指标（空腹血糖和胰岛素）、肥胖（体重指数[BMI]/腰围）和血脂异常相关，但与高血压或钾水平无关。使用逐步回归方法，年龄、血脂异常和稳态模型评估-胰岛素抵抗仍然与醛固酮水平显著相关（参考文献3的表2）。本报告的独特之处在于对血浆醛固酮水平与胰岛素抵抗发生之间的关系进行了前瞻性分析。在前瞻性队列中，151名个体发生了胰岛素抵抗。与未发生胰岛素抵抗的患者相比，发生胰岛素抵抗的患者年龄更大，醛固酮、BMI/腰围和甘油三酯水平更高。作者使用接受者操作特征和c-统计方法创建了增加醛固酮水平的三分位数，并确定了每个醛固酮三分位数内发生胰岛素抵抗的相对风险（表5）。作者报告了第二和第三个三分位数中未调整分析的风险增加，在第二个三分位数中调整年龄，性别和BMI（模型2）后，在第三个三分位数中调整测量的临床变量（通过模型6）后，仍然存在。因此，这些观察结果表明，在正常范围内增加醛固酮水平预测胰岛素抵抗的发展。这一领域的先前工作已经评估了主要由原发性醛固酮增多症、高血压和代谢综合征的其他组分的个体组成的队列中醛固酮和胰岛素抵抗之间的关联。1，4，5稳态模型评估-胰岛素抵抗已被用于评估原发性醛固酮增多症患者的胰岛素抵抗，并探索这种相关关系，5，6和一些研究探索了醛固酮生成肿瘤切除术后胰岛素抵抗的改善。6，7当前研究的结果与前瞻性分析FRADIOR数据的结果相反，FRADIOR数据中正常范围内的醛固酮增加与基线时的胰岛素抵抗相似;然而，这种关系在纵向随访队列中丢失。这2项研究中不同的纵向结果可能归因于人群特征（美国与日本）的差异或...
There is increasing interest in exploring inappropriate activation of the renin-angiotensin-aldosterone system as a unifying mechanism between insulin resistance and other components of the metabolic syndrome. 1, 2 Recent data suggest that elevations in plasma aldosterone levels are associated with the insulin resistance independent of other components of angiotensin II. This relationship has been observed in studies exploring the association between primary aldosteronism, in which there are low levels of renin activity and angiotensin II, and insulin resistance. 1 In this issue, Kumagai et al3 explored increases in aldosterone in the normal range at baseline as a predictor of development of insulin resistance in a prospective cohort of 10 years. Insulin resistance was ascertained by a homeostatic model assessment of insulin resistance. The authors used a Japanese cohort of 1088 individuals without diabetes mellitus to explore the strength of the association between baseline aldosterone levels and development of insulin resistance. They then further excluded individuals with demonstrable insulin resistance at baseline and tracked the remaining 564 persons prospectively for 10 years. On univariate regression analysis at baseline, aldosterone levels correlated with age, measures of insulin resistance (fasting glucose and insulin), obesity (body mass index [BMI]/waist circumference), and dyslipidemia but not with the presence of hypertension or potassium level. Using a stepwise regression approach, age, dyslipidemia, and homeostatic model assessment-insulin resistance remained significantly correlated with aldosterone levels (Table 2 of Reference3). Unique to this report is the prospective analysis of the relationship between plasma aldosterone levels and the development of insulin resistance. In the prospective cohort, 151 individuals developed insulin resistance. Those who developed insulin resistance were older and had higher levels of aldosterone, BMI/waist circumference, and triglycerides compared with those who did not develop insulin resistance. The authors created tertiles for increasing levels of aldosterone using a receiver operating characteristic with c-statistic approach and determined relative risk for the development of insulin resistance within each aldosterone tertile (Table 5). The authors report an increased risk on unadjusted analysis in the second and third tertiles that remained after adjustment for age, sex, and BMI (model 2) in the second tertile and after adjustment for measured clinical variables (through model 6) in the third tertile. Thus, these observations suggest that increasing levels of aldosterone in the normal range predict the development of insulin resistance. Previous work in this area has evaluated the association between aldosterone and insulin resistance in cohorts mostly composed of individuals with primary aldosteronism, hypertension, and other components of the metabolic syndrome. 1, 4, 5 Homeostatic model assessment-insulin resistance has been used to assess insulin resistance in those with primary aldosteronism and to explore this correlative relationship, 5, 6 and a few studies have explored improvements in insulin resistance postresection of aldosterone-producing tumors. 6, 7 Results of the current investigation contrast with findings from a prospective analysis of Framingham data wherein increases in aldosterone in the normal range were similarly associated with insulin resistance at baseline; however, this relationship was lost in the longitudinal follow-up cohort. Disparate longitudinal results in these 2 studies may be attributed to differences in population characteristics (US versus Japanese) or …