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Primary Aldosteronism Decreases Insulin Secretion and Increases Insulin Clearance in Humans
Hypertension ( IF 6.9 ) Pub Date : 2020-05-01 , DOI: 10.1161/hypertensionaha.119.13922
Gail K Adler 1 , Gillian R Murray 1 , Adina F Turcu 2 , Hui Nian 3 , Chang Yu 3 , Carmen C Solorzano 4 , Robert Manning 5 , Dungeng Peng 5 , James M Luther 5
Affiliation  

Supplemental Digital Content is available in the text. Primary aldosteronism is a frequent cause of resistant hypertension and is associated with an increased risk of developing diabetes mellitus. Aldosterone impairs insulin secretion in isolated islets, and insulin secretion is increased in aldosterone synthase–deficient mice. We hypothesized that treatment for primary aldosteronism increases insulin secretion and insulin sensitivity in humans. We conducted a prospective cohort study in patients with primary aldosteronism, with assessment of glucose metabolism before and 3 to 12 months after treatment. Participants underwent treatment for primary aldosteronism with adrenalectomy or a mineralocorticoid receptor antagonist at the discretion of their treating physician. We assessed insulin secretion and insulin sensitivity by hyperglycemic and hyperinsulinemic-euglycemic clamps, respectively, on 2 study days after a 5-day standardized diet. After treatment, the C-peptide and insulin response during the hyperglycemic clamp increased compared with pretreatment (ΔC-peptide at 90–120 minutes +530.5±384.1 pmol/L, P=0.004; Δinsulin 90–120 minutes +183.0±122.6, P=0.004). During hyperinsulinemic-euglycemic clamps, insulin sensitivity decreased after treatment (insulin sensitivity index 30.7±6.2 versus 18.5±4.7 nmol·kg−1·min−1·pmol−1·L; P=0.02). Insulin clearance decreased after treatment (872.8±207.6 versus 632.3±178.6 mL/min; P=0.03), and disposition index was unchanged. We conclude that the insulin response to glucose increases and insulin clearance decreases after treatment for primary aldosteronism, and these effects were not due to alterations in creatinine clearance or plasma cortisol. These studies may provide further insight into the mechanism of increased diabetes mellitus risk in primary aldosteronism.

中文翻译:

原发性醛固酮增多症会减少人体的胰岛素分泌并增加胰岛素清除率

文本中提供了补充数字内容。原发性醛固酮增多症是顽固性高血压的常见原因,并与患糖尿病的风险增加有关。醛固酮损害孤立胰岛的胰岛素分泌,醛固酮合酶缺陷小鼠的胰岛素分泌增加。我们假设治疗原发性醛固酮增多症会增加人类的胰岛素分泌和胰岛素敏感性。我们对原发性醛固酮增多症患者进行了一项前瞻性队列研究,评估了治疗前和治疗后 3 至 12 个月的葡萄糖代谢。参与者根据主治医师的判断,接受肾上腺切除术或盐皮质激素受体拮抗剂治疗原发性醛固酮增多症。在 5 天标准化饮食后的 2 个研究日,我们分别通过高血糖钳和高胰岛素-正常血糖钳来评估胰岛素分泌和胰岛素敏感性。治疗后,高血糖钳夹期间的C肽和胰岛素反应较治疗前增加(90-120分钟ΔC肽+530.5±384.1 pmol/L,P=0.004;Δ胰岛素90-120分钟+183.0±122.6,P =0.004)。在高胰岛素-正常血糖钳夹期间,治疗后胰岛素敏感性降低(胰岛素敏感性指数 30.7±6.2 对 18.5±4.7 nmol·kg-1·min-1·pmol-1·L;P=0.02)。治疗后胰岛素清除率下降(872.8±207.6 vs 632.3±178.6 mL/min;P=0.03),处置指数没有变化。我们得出结论,在原发性醛固酮增多症治疗后,胰岛素对葡萄糖的反应增加,胰岛素清除率降低,这些影响不是由于肌酐清除率或血浆皮质醇的改变。这些研究可以进一步深入了解原发性醛固酮增多症中糖尿病风险增加的机制。
更新日期:2020-05-01
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