Aldosterone Stimulates Gene Expression of Hepatic Gluconeogenic Enzymes through the Glucocorticoid Receptor in a Manner Independent of the Protein Kinase B Cascade
Open accessAbstract
Primary aldosteronism is associated with glucose intolerance and diabetes, which is due in part to impaired insulin release caused by reduction of potassium, although other possibilities remain to be elucidated. To evaluate the in vivo effects of aldosterone on glucose metabolism, a single dose of aldosterone was administered to mice, which resulted in elevation of the blood glucose level. In primary cultured mouse hepatocytes, the gene expression of gluconeogenic enzymes such as glucose-6-phosphatase (G6Pase), fructose-1,6-bisphosphatase and phosphoenolpyruvate carboxykinase increased in response to aldosterone in a dose-dependent manner even at a concentration similar to a physiological condition (10(-9) M). The inhibitory effect of insulin on G6Pase gene expression was partially suppressed by aldosterone. Furthermore, aldosterone enhanced G6Pase promoter activity in human hepatoma cell line HepG2, which was prevented by co-treatment with a glucocorticoid antagonist RU-486, but not a mineralocorticoid antagonist spironolactone. In contrast, aldosterone had no effects on major insulin signaling pathways including insulin receptor substrate-1, protein kinase B, and forkhead transcription factor. These results suggest that aldosterone may affect the inhibitory effect of insulin on hepatic gluconeogenesis through the glucocorticoid receptor, which may be one of the causes of impaired glucose metabolism in primary aldosteronism.
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Aldosterone stimulates hepatic glucose production by increasing gluconeogenesis.
“Aldosterone stimulates hepatic glucose production by increased gluconeogenesis [47,48].”
From Insulin sensitivity and pancreatic β-cell function in patients with primary aldosteronism (2021) · cites this paper as [47]
The Abstract reports that aldosterone increased blood glucose in mice and increased expression of gluconeogenic-enzyme genes in cultured mouse hepatocytes. The Discussion concludes that aldosterone can influence hepatic gluconeogenesis, but the paper does not establish that it increased hepatic glucose production or that increased gluconeogenesis caused the observed rise in blood glucose. (LLM, conf=0.87)
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- Authors
- YAMASHITA, R., KIKUCHI, T., MORI, Y., AOKI, K., KABURAGI, Y., YASUDA, K., & SEKIHARA, H.
- Affiliations
- Yokohama City University (JP)
- Department of Metabolic Disorder, Research Institute, International Medical Center of Japan
- Venue
- Endocrine Journal
- Publisher
- Japan Endocrine Society
- Published
- 2004
- Volume
- 51
- Issue
- 2
- Pages
- 243-251
- ISSN
- 0918-8959 (ISSN-L)
- 1348-4540
- OpenAlex
- W2004674731
- Semantic Scholar
- 0a2f4e686a61388bd52f054561a5839a6763f34f
- Cited by
- 55
- References
- 34
- Citations by year
- 2026: 2 · 2024: 4 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 4 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 2 · 2014: 3 · 2013: 2 · 2012: 1
- FWCI
- 2.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Journal (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- aldosterone, glucocorticoid receptor, hepatic gluconeogenesis, glucose-6-phosphatase, fructose-1,6-bisphosphatase, phosphoenolpyruvate carboxykinase, insulin signaling, Akt, forkhead transcription factor, primary aldosteronism, impaired glucose tolerance, hepatocytes, gene expression regulation
- MeSH terms
- Aldosterone, Mineralocorticoid Receptor Antagonists, Animals, Blood Glucose, Carboxy-Lyases, Cells, Cultured, Female, Gene Expression Regulation, Gluconeogenesis, Glucose-6-Phosphatase, Fructose-Bisphosphatase, Humans, Insulin, Liver, Mice, Inbred ICR, Promoter Regions, Genetic, Proto-Oncogene Proteins, Receptors, Glucocorticoid, Spironolactone, Signal Transduction, Mifepristone, Gene Expression, Protein Serine-Threonine Kinases, Hepatocytes, Proto-Oncogene Proteins c-akt, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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