Aldosterone stimulated differentiation of mouse 3T3-L1 cells into adipocytes
Abstract
We find that 1-10 nM aldosterone can induce differentiation of 3T3-L1 cells into adipose cells as evaluated by microscopic accumulation of fat droplets and quantitative measurement of triglycerides and of glycerol-3-phosphate dehydrogenase, an enzyme specific for adipocyte differentiation. Moreover, the aldosterone antagonist ZK91587 inhibits aldosterone-but not glucocorticoid-mediated differentiation of 3T3-L1 cells. Steroid binding assays with 3T3-L1 cells indicate the presence of specific binding sites for aldosterone. We conclude that there is an aldosterone receptor-mediated pathway for terminal differentiation of 3T3-L1 cells into adipose cells. Receptors for aldosterone have also been found in a variety of cells that do not function to regulate sodium and potassium transport. The aldosterone receptor may have a role in regulation expression of genes involved in differentiation of these cells.
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Mineralocorticoid receptors on adipocytes promote inflammatory adipokine expression, leading to lower insulin receptor expression and impaired insulin-induced glucose uptake.
“MRs on adipocytes promoted the expression of inflammatory adipokines (-), giving rise to lower insulin receptor expression and impaired insulin-induced glucose uptake ().”
From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [174]
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Armani, A., Marzolla, V., Feraco, A., Gorini, S., Mammi, C., Infante, M., & Caprio, M. (2019) · IntechOpen eBooks · doi:10.5772/intechopen.87231
Metabolic effects of aldosterone
Валерьевна, И. К., Mazurina, N. V., Platonova, N. M., & Troshina, E. A. (2024) · Obesity and metabolism · doi:10.14341/omet13040
Gideon, A., von Känel, R., Degroote, C., Thomas, L., Zuccarella‐Hackl, C., Wiest, R., & Wirtz, P. H. (2026) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1655896
Mineralocorticoid receptor genetics: A scoping review
Jaurretche, S. P. A., Balañá, C., & Bascolo, R. (2026) · World Journal of Medical Genetics · doi:10.5496/wjmg.115237
- Authors
- Rondinone, C. M., Rodbard, D., & Baker, M. E.
- Affiliations
- National Institutes of Health (US)
- ORCID
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 1993-06
- Volume
- 132
- Issue
- 6
- Pages
- 2421-2426
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2073760548
- Cited by
- 101
- References
- 3
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 4 · 2023: 1 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 2 · 2016: 5 · 2015: 5 · 2014: 9 · 2013: 5 · 2012: 6
- FWCI
- 0.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- aldosterone, adipogenesis, 3T3-L1 cells, mineralocorticoid receptor, glucocorticoid receptor, steroid binding sites, triglycerides, glycerol-3-phosphate dehydrogenase, gene expression regulation
- MeSH terms
- Adipose Tissue, Aldosterone, Androstanols, Animals, Binding, Competitive, Cell Differentiation, Glycerolphosphate Dehydrogenase, Hydrocortisone, Receptors, Glucocorticoid, Spironolactone, Triglycerides, 3T3 Cells, Mice
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