Gper and erα mediate estradiol enhancement of mitochondrial function in inflamed adipocytes through a pka dependent mechanism
Open accessAbstract
Obesity is associated with inflammation, dysregulated adipokine secretion, and disrupted adipose tissue mitochondrial function. Estradiol (E2) has been previously reported to increase mitochondrial function and biogenesis in several cell lines, but neither the type of oestrogen receptor (ERα, ERβ and GPER) involved nor the mechanism whereby such effects are exerted have been fully described. Considering the anti-inflammatory activity of E2 as well as its effects in enhancing mitochondrial biogenesis, the aim of this study was to investigate the contribution of ERα, ERβ, and GPER signaling to the E2-mediated enhancement of adipocyte mitochondrial function in a pro-inflammatory situation. 3T3-L1 cells were treated for 24 h with ER agonists (PPT, DPN, and G1) and antagonists (MPP, PHTPP, and G15) in the presence or absence of interleukin 6 (IL6), as a pro-inflammatory stimulus. Inflammation, mitochondrial function and biogenesis markers were analyzed. To confirm the involvement of the PKA pathway, cells were treated with a GPER agonist, a PKA inhibitor, and IL6. Mitochondrial function markers were analyzed. Our results showed that activation of ERα and GPER, but not ERβ, was able to counteract the proinflammatory effects of IL6 treatment, as well as mitochondrial biogenesis and function indicators. Inhibition of PKA prevented the E2- and G1-associated increase in mitochondrial function markers. In conclusion E2 prevents IL6 induced inflammation in adipocytes and promotes mitochondrial function through the combined activation of both GPER and ERα. These findings expand our understanding of ER interactions under inflammatory conditions in female rodent white adipose tissue.
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ERα and GPER mediate 17β-estradiol enhancement of mitochondrial respiratory capacity and ATP production via a PKA-dependent mechanism.
“On the other hand, it has been reported that ERα and GPER mediate 17β-estradiol enhancement of mitochondrial respiratory capacity and ATP production via a PKA-dependent mechanism (124).”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [124]
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- Authors
- Bauzá-Thorbrügge, M., Rodríguez-Cuenca, S., Vidal-Puig, A., Galmés-Pascual, B. M., Sbert-Roig, M., Gianotti, M., Lladó, I., & Proenza, A. M.
- Affiliations
- Health Research Institute of the Balearic Islands (ES)
- Instituto de Salud Carlos III (ES)
- Corresponding author
- Gianotti, Magdalena
- Venue
- The Journal of Steroid Biochemistry and Molecular Biology
- Publisher
- Elsevier BV
- Published
- 2019-01
- Volume
- 185
- Pages
- 256-267
- ISSN
- 0960-0760 (ISSN-L)
- OpenAlex
- W2892407828
- Cited by
- 30
- References
- 84
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 3 · 2023: 5 · 2022: 1 · 2021: 7 · 2020: 3 · 2019: 2
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- Locations
- The Journal of Steroid Biochemistry and Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Apollo
- Funders
- FP7-MITIN (223450)
- Medical Research Council Programme (MC_UU_12012/2)
- Agencia Estatal de Investigación (AEI) of the Spanish Government and Fondo Europeo de Desarrollo Regional (FEDER) (SAF2016-80384R)
- Comunitat Autònoma de les Illes Balears, Direcció General d’lnnovació i Recerca, and Fons Europeu de Desenvolupament Regional de la Unió Europea (FEDER) (AAEE43/2014, AAEE52/2015)
- FPU grant from the Ministerio de Educación, Cultura y Deporte (AP2012-1004)
- University of Balearic Islands (07-2014-0303240)
- Balearic Islands Government (FPI11-41523224J)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- G protein-coupled estrogen receptor, estrogen receptor alpha, estrogen receptor beta, estradiol, mitochondrial biogenesis, interleukin-6, adipose tissue inflammation, obesity, protein kinase A, 3T3-L1 adipocytes, white adipose tissue
- MeSH terms
- Animals, Cell Line, Estradiol, Female, Inflammation, Male, Mice, Inbred C57BL, Mitochondria, Obesity, Interleukin-6, 3T3 Cells, Rats, Wistar, Adipocytes, Cyclic AMP-Dependent Protein Kinases, Receptors, G-Protein-Coupled, Estrogen Receptor alpha, Estrogen Receptor beta, Mice, Rats
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