Department of Endocrinology, Diabetes and Metabolism, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
J Diabetes Investig. 2020 Nov;11(6):1511-1519. doi: 10.1111/jdi.13312. Epub 2020 Jun 26.
AIMS/INTRODUCTION: An increased risk of diabetes mellitus has been reported in primary aldosteronism, but the pathogenesis of glucose intolerance between the primary aldosteronism subtypes remains unclear. This study aimed to evaluate glucose metabolism in oral glucose tolerance test between aldosterone-producing adenoma and idiopathic hyperaldosteronism, and characterize patients with improved glucose intolerance after primary aldosteronism treatment.
Oral glucose tolerance test was carried out in 116 patients who were diagnosed with primary aldosteronism and received adrenal venous sampling for subtyping. Oral glucose tolerance test was re-evaluated after starting the treatment of primary aldosteronism for those who had glucose intolerance before the treatment.
A total of 46.4% and 52.3% of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism, respectively, were diagnosed with impaired glucose tolerance or diabetes. The insulinogenic index was significantly lower in aldosterone-producing adenoma than in idiopathic hyperaldosteronism (P = 0.045), whereas the Matsuda insulin sensitivity index was significantly higher in aldosterone-producing adenoma than in idiopathic hyperaldosteronism (P = 0.022). After the treatment of primary aldosteronism, glucose intolerance was improved in 66.6% and 45.8% of aldosterone-producing adenoma and idiopathic hyperaldosteronism, respectively. The presence of obesity and central obesity were significantly lower in patients who improved glucose intolerance after the treatment of primary aldosteronism as compared with those not improved (P = 0.013 and P = 0.033, respectively).
Insulin secretion impairment and insulin resistance play pathogenic roles for glucose intolerance in aldosterone-producing adenoma and idiopathic hyperaldosteronism, respectively. In addition, primary aldosteronism treatments can ameliorate glucose intolerance more effectively in patients without obesity and/or central obesity.
目的/引言：原发性醛固酮增多症患者发生糖尿病的风险增加，但醛固酮增多症亚型之间葡萄糖耐量异常的发病机制尚不清楚。本研究旨在评估醛固酮瘤和特发性醛固酮增多症患者口服葡萄糖耐量试验中的葡萄糖代谢情况，并描述原发性醛固酮增多症治疗后葡萄糖耐量改善的患者特征。
对 116 例经诊断为原发性醛固酮增多症并接受肾上腺静脉取样分型的患者进行口服葡萄糖耐量试验。对治疗前有葡萄糖耐量异常的患者开始原发性醛固酮增多症治疗后，重新评估口服葡萄糖耐量试验。
醛固酮瘤和特发性醛固酮增多症患者分别有 46.4%和 52.3%被诊断为糖耐量受损或糖尿病。醛固酮瘤患者的胰岛素生成指数明显低于特发性醛固酮增多症（P=0.045），而醛固酮瘤患者的Matsuda 胰岛素敏感性指数明显高于特发性醛固酮增多症（P=0.022）。原发性醛固酮增多症治疗后，醛固酮瘤和特发性醛固酮增多症患者的葡萄糖耐量分别改善了 66.6%和 45.8%。与未改善的患者相比，原发性醛固酮增多症治疗后葡萄糖耐量改善的患者中肥胖和中心性肥胖的发生率明显更低（P=0.013 和 P=0.033）。
胰岛素分泌受损和胰岛素抵抗分别在醛固酮瘤和特发性醛固酮增多症患者的葡萄糖耐量异常中起致病作用。此外，原发性醛固酮增多症治疗在无肥胖和/或中心性肥胖的患者中更能有效改善葡萄糖耐量。
