ArticleActa pharmacologica Sinica2011
17β-Estradiol inhibition of PPARγ-induced adipogenesis and adipocyte-specific gene expression.
Article in Acta pharmacologica Sinica, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- Estrogen Deficiency and the Origin of Obesity during Menopause.BioMed research international · 2014Pooled it
- Influence of Biological Sex on Metabolic and Adipokine Responses after Metabolic-Bariatric Surgery: A Narrative Review.Current obesity reports · 2026Review
- Paraben exposures and satiety hormones in preschool children: an ENVIRONAGE study.Environmental research · 2025Article
- Depression mediates the association between lipid accumulation products and overactive bladder.Scientific reports · 2025Article
- Comparative analysis of β-Estradiol and testosterone on lipid droplet accumulation, and regulatory protein expression in palmitate/oleate-induced fatty HepG2 cells.BMC gastroenterology · 2025Article
- Metabolic Changes in Patients with Premature Ovarian Insufficiency: Adipose Tissue Focus-A Narrative Review.Metabolites · 2025Review
- Oestrogen suppresses the adipogenesis of fibro/adipogenic progenitors through reactivating the METTL3-ESR1-mediated loop in post-menopausal females.Clinical and translational medicine · 2025Article
- Association between lifetime endogenous estrogen exposure and body composition metrics in postmenopausal women: findings from the Tehran Lipid and Glucose Study.BMC women's health · 2024Article
- Cxcr4 regulates a pool of adipocyte progenitors and contributes to adiposity in a sex-dependent manner.Nature communications · 2024Article
- Effect ofInternational journal of molecular sciences · 2024Article
- A Multifunctional Therapeutic Strategy Using P7C3 as A Countermeasure Against Bone Loss and Fragility in An Ovariectomized Rat Model of Postmenopausal Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Effect of β-Estradiol on Adipogenesis in a 3T3-L1 Cell Model of Prelamin A Accumulation.International journal of molecular sciences · 2024Article
- A PRDM16-driven signal regulates body composition in testosterone-treated hypogonadal men.Frontiers in endocrinology · 2024Article
- The evolutionary impact and influence of oestrogens on adipose tissue structure and function.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Estrogens in Adipose Tissue Physiology and Obesity-Related Dysfunction.Biomedicines · 2023Review
- Impact of Prenatal Exposure to Maternal Diabetes and High-Fat Diet on Postnatal Myocardial Ketone Body Metabolism in Rats.International journal of molecular sciences · 2023Article
- 17α-estradiol, a lifespan-extending compound, attenuates liver fibrosis by modulating collagen turnover rates in male mice.American journal of physiology. Endocrinology and metabolism · 2023Article
- The Role of Persistent Organic Pollutants in Obesity: A Review of Laboratory and Epidemiological Studies.Toxics · 2022Review
- The Regulation of Adipose Tissue Health by Estrogens.Frontiers in endocrinology · 2022Review
- Metabolic and Epigenetic Regulation by Estrogen in Adipocytes.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
aimTo investigate the molecular interaction of peroxisome proliferator-activated receptor γ (PPARγ) with 17β-estradiol (E) in the regulation of adipogenesis.
methodsFemale ovariectomized (OVX) mice and differentiated 3T3-L1 adipocytes were treated with combinations of the PPARγ agonist troglitazone or E, and the variables and determinants of adipogenesis were measured using in vivo and in vitro approaches.
resultsTroglitazone (250 mg·kg(-1)·d(-1) for 13 weeks) decreased the size of adipocytes without the change in white adipose tissue (WAT) mass and increased the expression of adipocyte-specific genes, such as PPARγ, adipocyte fatty acid binding protein, and lipoprotein lipase, compared with OVX control mice. E (0.05 mg/pellet, sc implanted) significantly reduced WAT mass, adipocyte size, and adipose marker gene expression. When mice were concomitantly treated with troglitazone and E, E blunted the effects of troglitazone on WAT mass, adipocyte size, and adipose PPARγ target gene expression. Consistent with the in vivo data, E (10 μmol/L) treatment inhibited lipid accumulation and the expression of adipocyte-specific genes caused by troglitazone (10 μmol/L) in 3T3-L1 cells. E (10 μmol/L) also decreased troglitazone-induced PPARγ reporter activity through both estrogen receptor (ER) α and ERβ. Mechanistic studies indicated that E (0.1 μmol/L) decreased the DNA binding of PPARγ induced by troglitazone (1 μmol/L) and inhibited the recruitment of the PPARγ coactivator CREB-binding protein.
conclusionThese results suggest that in vivo and in vitro treatment of E interferes with the actions of PPARγ on adipogenesis by down-regulating adipogenesis-related genes, which are mediated through the inhibition of PPARγ coactivator recruitment. In addition, it is likely that the activities of PPARγ activators may be enhanced in estrogen-deficient states.
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