ArticleJournal of diabetes investigation2020
Different pathogenesis of glucose intolerance in two subtypes of primary aldosteronism: Aldosterone-producing adenoma and idiopathic hyperaldosteronism.
Article in Journal of diabetes investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Meta-analysis of blood parameters related to lipid and glucose metabolism between two subtypes of primary aldosteronism.Journal of clinical hypertension (Greenwich, Conn.) · 2023Pooled it
- Gut microbiome dysbiosis is associated with aldosterone overproduction in idiopathic hyperaldosteronism.iScience · 2026Article
- Prospective study of primary aldosteronism in acute ischemic stroke: association with small vessel disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Clinical Significance of Skeletal Fat-to-Muscle Ratio in Idiopathic Hyperaldosteronism.Clinical endocrinology · 2025Article
- Glucocorticoids: The culprit behind metabolic disorders in primary Aldosteronism? A narrative review.Journal of clinical & translational endocrinology · 2025Review
- Prevalence, risk factors and evolution of diabetes mellitus after treatment in primary aldosteronism. Results from the SPAIN-ALDO registry.Journal of endocrinological investigation · 2023Article
- Recovery from diabetes mellitus in primary aldosteronism patients after adrenalectomy.BMC endocrine disorders · 2022Article
- Update on Hypertension Research in 2021.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Aldosterone/direct renin concentration ratio as a screening test for primary aldosteronism: a systematic review and meta-analysis.Annals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AIMS/
introductionAn 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. MATERIALS AND
methodsOral 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.
resultsA 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).
conclusionsInsulin 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.
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