The diversity of sex steroid action: regulation of metabolism by estrogen signaling
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The metabolic syndrome is a complex condition characterized by obesity, insulin resistance, decreased high-density lipoproteins, and hypertension associated with high risk of developing type 2 diabetes and cardiovascular disease. A major increase in the incidence of developing metabolic syndrome and related diseases is observed worldwide in association with a change toward a less active lifestyle and increased food consumption. Estrogen and the estrogen receptors (ERs) are well-known regulators of several aspects of metabolism, including glucose and lipid metabolism, and impaired estrogen signaling is associated with the development of metabolic diseases. This review will describe the key effects of estrogen signaling in metabolic and glucose sensing tissues, including the liver, pancreatic β cells, adipose tissue, and skeletal muscle. The impact on metabolic processes of impaired estrogen signaling and knock out of each ER subtype will also be discussed.
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Classical genomic ER action typically occurs within hours, leading to activation or repression of target genes; ligand-activated ER binds as a dimer directly to an estrogen response element in target gene promoters.
“The classical genomic action mechanism of ER action typically occurs within hours, leading to activation or repression of target genes.”
From Estrogen deficiency and the origin of obesity during menopause (2014) · cites this paper as [51]
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- Authors
- Faulds, M. H., Zhao, C., Dahlman-Wright, K., & Gustafsson, J.-Å.
- Affiliations
- Karolinska Institutet (SE)
- ORCID
- Zhao, Chunyan
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2011-04-21
- Volume
- 212
- Issue
- 1
- Pages
- 3-12
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2140387377
- Cited by
- 230
- References
- 105
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 15 · 2023: 14 · 2022: 10 · 2021: 12 · 2020: 18 · 2019: 6 · 2018: 13 · 2017: 17 · 2016: 15 · 2015: 23 · 2014: 24 · 2013: 26 · 2012: 16
- FWCI
- 2.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- estrogen signaling, estrogen receptor, metabolic syndrome, glucose metabolism, lipid metabolism, insulin resistance, obesity, type 2 diabetes, cardiovascular disease, hepatic glucose metabolism, pancreatic beta cells, adipose tissue, skeletal muscle
- MeSH terms
- Animals, Cholesterol, Estrogens, Glucose, Homeostasis, Humans, Inflammation, Insulin Resistance, Lipolysis, Metabolic Syndrome, Lipogenesis
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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.
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