Cited by 114Hormonal Regulation and HypertensionPancreatic function and diabetesPotassium and Related Disorders

Effects of aldosterone on insulin sensitivity and secretion

Open access
Luther, James M.·2014·Steroids

Abstract

Dr. Conn originally reported an increased risk of diabetes in patients with hyperaldosteronism in the 1950’s, although the mechanism remains unclear. Aldosterone-induced hypokalemia was initially described to impair glucose tolerance by impairing insulin secretion. Correction of hypokalemia by potassium supplementation only partially restored insulin secretion and glucose tolerance, however. Aldosterone also impairs glucose-stimulated insulin secretion in isolated pancreatic islets via reactive oxygen species in a mineralocorticoid receptor-independent manner. Aldosterone-induced mineralocorticoid receptor activation also impairs insulin sensitivity in adipocytes and skeletal muscle. Aldosterone may produce insulin resistance secondarily by altering potassium, increasing inflammatory cytokines, and reducing beneficial adipokines such as adiponectin. Renin-angiotensin system antagonists reduce circulating aldosterone concentrations and also the risk of type 2 diabetes in clinical trials. These data suggest that primary and secondary hyperaldosteronism may contribute to worsening glucose tolerance by impairing insulin sensitivity or insulin secretion in humans. Future studies should define the effects of MR antagonists and aldosterone on insulin secretion and sensitivity in humans.

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Crossref · 10.1016/j.steroids.2014.08.016

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  • Reduced insulin sensitivity has been reported in patients with primary aldosteronism when they are compared with normotensive cohorts.

    “However, when compared with normotensive cohorts, reduced insulin sensitivity has been reported in PA patients [19,9,20,13,8,21,22].”

    From Insulin sensitivity and pancreatic β-cell function in patients with primary aldosteronism (2021) · cites this paper as [9]

    Section 3.1 reports reduced insulin sensitivity in patients with primary aldosteronism in some studies, but not all. Its comparison is with hypertensive controls, not normotensive cohorts; the separate finding in normotensive subjects concerns an association between aldosterone levels and insulin sensitivity. No page number is available in our copy. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Primary aldosteronism is associated with an increased risk of dysglycemia.

    “Primary aldosteronism (PA) is associated with increased risk for dysglycemia.”
  • The effects of hyperaldosteronism on insulin sensitivity and β-cell function are unclear.

    “However, the effects of hyperaldosteronism on insulin sensitivity and β-cell function are unclear.”

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Authors
Luther, J. M.
Affiliations
Vanderbilt University (US)
Corresponding author
Luther, James M.
Venue
Steroids
Publisher
Elsevier BV
Published
2014-12
Volume
91
Pages
54-60
ISSN
0039-128X (ISSN-L)
OpenAlex
W2000737837
Cited by
114
References
120
Citations by year
2026: 6 · 2025: 11 · 2024: 10 · 2023: 16 · 2022: 11 · 2021: 10 · 2020: 13 · 2019: 10 · 2018: 10 · 2017: 2 · 2016: 10 · 2015: 4 · 2014: 1
FWCI
0.90
Type
journal article
Language
en
Open access
Locations
  • Steroids (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
NIH (DK081662, DK096994)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
Keywords
aldosterone, hyperaldosteronism, insulin sensitivity, insulin secretion, glucose tolerance, insulin resistance, hypokalemia, potassium supplementation, glucose-stimulated insulin secretion, pancreatic islets, reactive oxygen species, mineralocorticoid receptor, adipocytes, skeletal muscle, adiponectin, inflammatory cytokines, renin-angiotensin system inhibitors, type 2 diabetes
MeSH terms
Insulin Secretion, Aldosterone, Clinical Trials as Topic, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Resistance, Models, Biological

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