title: Aldosterone excess may inhibit insulin secretion: A comparative study on glucose metabolism pre- and post-adrenalectomy in patients with primary aldosteronism.
abstract: Conflicting data have been published on the effects of aldosterone excess on glucose metabolism. Specifically, there are limited data on whether adrenalectomy in patients with aldosterone-producing adenomas (APA) can improve glucose metabolism. In this study we evaluated changes in glucose metabolism, before and after surgery for APA. The subjects were 61 patients treated with unilateral adrenalectomy, localized by adrenal venous sampling. A 75g-oral glucose tolerance test (OGTT) was performed before and 1 year after adrenalectomy. Patients with diabetes mellitus or a serum cortisol level >3 μg/dL after a 1 mg dexamethasone suppression test, were excluded. Using the 75g-OGTT data, insulin secretion and insulin resistance (or sensitivity) indices were calculated. The results showed that immunoreactive insulin levels during the OGTT increased significantly after adrenalectomy, whereas plasma glucose levels, before and after surgery, were comparable. The insulinogenic index significantly increased after surgery (0.5 [0.4-0.8] to 0.8 [0.4-1.1], p < 0.001). The disposition index remained largely unchanged (806.2 [489.4-1,138.9] to 686.6 [479.4-922.1], p = 0.25). The homeostatic model assessment of insulin resistance increased significantly (1.0 [0.6-1.5] to 1.5 [1.0-2.2], p < 0.001) and the ISImatsudadecreased significantly (6.9 [4.5-10.4] to 5.2 [3.4-7.9], p < 0.001). Changes in these indices were not correlated with changes in potassium and aldosterone levels before and after surgery. In conclusion, insulin secretion increased after adrenalectomy for APA, indicating that aldosterone excess inhibits insulin secretion. However, because of a parallel increase in insulin resistance, plasma glucose levels remained unchanged.
authors.affiliation: Endocrinology and Diabetes Center, Yokohama Rosai Hospital, Yokohama 222-0036, Japan.
authors.forename: Yuya
authors.initials: Y
authors.lastname: Tsurutani
authors.forename: Chiho
authors.initials: C
authors.lastname: Sugisawa
authors.forename: Akiko
authors.initials: A
authors.lastname: Ishida
authors.forename: Kosuke
authors.initials: K
authors.lastname: Inoue
authors.forename: Jun
authors.initials: J
authors.lastname: Saito
authors.forename: Masao
authors.initials: M
authors.lastname: Omura
authors.forename: Shoichiro
authors.initials: S
authors.lastname: Nagasaka
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Nishikawa
mesh_terms: D000306:Adrenal Cortex Neoplasms / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D000315:Adrenalectomy; D018246:Adrenocortical Adenoma / Q000378:metabolism / Q000503:physiopathology / Q000601:surgery; D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000378:metabolism*; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D007333:Insulin Resistance; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000378:metabolism*; D007564:Japan; D008297:Male; D008875:Middle Aged; D011184:Postoperative Period; D011188:Potassium / Q000097:blood; D057234:Preoperative Period; D012189:Retrospective Studies
chemical_list: D001786:Blood Glucose; D007328:Insulin; D000450:Aldosterone; D011188:Potassium