SFEBES2026 Poster Presentations Metabolism, Obesity and Diabetes (68 abstracts)
G protein-coupled oestrogen receptor 1 regulates CPT1a expression in human hepatocytes
Jiawen Dong , Kaitlyn Dennis , Hamish Miller , Riccardo Pofi , Tom Potter , Emily Cresswell , Felix Westcott , Nellie Loh , Frederik Karpe , Leanne Hodson & Jeremy Tomlinson
OCDEM, Oxford, United Kingdom
Background: The prevalence and severity of metabolic dysfunction-associated steatotic liver disease (MASLD) rises after the menopause. Preclinical studies have demonstrated that oestrogen signalling regulates metabolic and inflammatory pathways involved in MASLD development in rodents. The precise impact of distinct oestrogen receptor signalling on metabolic pathways involved in MASLD in human hepatocytes is unclear.
Methods: Gene expression levels of oestrogen receptor α (ERα), β (ERβ) and G protein-coupled oestrogen receptor 1 (GPER1) in human hepatoma cell lines (Huh7 and HepG2) and primary human hepatocytes were evaluated using RNA sequencing and western blot analysis. Huh7 cells were treated for 24 hours with oestradiol (E2) or the specific GPER1 agonist (G1), and expression of genes involved in de novo lipogenesis (FASN and ACCA) and fatty acid oxidation (CPT1A and PPARα) were assessed using Taqman qPCR. Additional gene expression studies were conducted following siRNA knockdown of GPER1 in the presence and absence of G1.
Results: GPER1 mRNA was highly expressed in Huh7, HepG2 cells, and in primary human hepatocytes. In comparison, in all 3 cell culture models, expression of ERα and ERβ was minimal. mRNA data were endorsed through western blot analysis confirming protein-level GPER1 expression. Treatment of Huh7 cells with 2μM G1 increased CPT1A mRNA expression (P = 0.02). Successful knockdown of GPER1 in Huh7 cells (64 ± 1.2% knockdown) reversed the G1-induced upregulation of CPT1A (P < 0.001). There were no changes in mRNA expression of FASN or ACCA.
Conclusion: GPER1 is highly expressed in human hepatocytes and has the potential to regulate lipid metabolism. Further study is needed to validate its role in the development of MASLD in humans and specifically its role in the postmenopausal predisposition to MASLD and the putative impact of hormone replacement therapy.
Volume 117
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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