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Open Access | Online First

Role of selenium and 17β oestradiol in modulating lipid accumulation in in vitro models of obesity and NAFLD

Sarah K Walsh†, Katy Pettigrew†, Isabella Mezzani†, Intisar Alaswad, Giovanna Bermano( )
Centre for Obesity Research and Education (CORE), School of Pharmacy and Life Sciences, Robert Gordon University, Aberdeen AB10 7GJ, United Kingdom

†These authors contributed equally to this work# These authors share co-senior authorship

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Highlights

(1) Abdominal obesity is a risk factor for the development of metabolic syndrome and associated diseases such as non-alcoholic fatty liver disease (NAFLD) in menopausal/postmenopausal women.

(2) Supplementation of Selenium (Se) reduces lipid deposition in adipocytes in vitro by modulating gene expression of markers of redox status, energy metabolism, inflammation, and adipocyte differentiation.

(3) Administration of oestrogen, as 17β oestradiol (E2), regulates lipid synthesis and metabolism in the same in vitro model of obesity.

(4) Both Se and E2 reduce lipid accumulation via regulation of lipid and energy metabolism and inflammatory genes in an in vitro model of NAFLD.

(5) Both hormonal treatment and micronutrient supplementation may be beneficial in obesity and NAFLD management.

Graphical Abstract

This study explored the cellular mechanisms by which the micronutrient selenium (Se) and oestrogen, as 17β oestradiol (E2), modulate lipid accumulation in in vitro models of both obesity and non-alcoholic fatty liver disease (NAFLD). Se supplementation reduced lipid deposition in adipocytes by increasing the expression of genes related to redox status (Gpx1, Selenow, and Ucp2) and reducing the expression of markers of inflammation (Cox-2 and Lep); while administration of E2 regulated lipid synthesis and metabolism (reductions in Fasn, Pparg, and Hsl expression and increased Fabp4 and Glut4 expression). In fatty acid treated hepatocytes, both Se and E2 reduced lipid accumulation via regulation of lipid and energy metabolism (SCD1 and SREBF1) and inflammatory genes (COX2 and LEP). These results suggest that both hormonal treatment and micronutrient supplementation may be beneficial in obesity and NAFLD management. If such in vitro findings were subsequently demonstrated in vivo, they could provide valuable data to support the use of either Se supplementation and/or oestrogen-based therapies to prevent and/or manage obesity and NAFLD in postmenopausal women.

Abstract

Abdominal obesity is prevalent in women and during menopause, making them more susceptible to weight gain, fat redistribution, and subsequent development of metabolic syndrome and associated diseases such as non-alcoholic fatty liver disease (NAFLD). Evidence from menopausal/postmenopausal women has demonstrated an association between declining oestrogen (i.e. 17β oestradiol; E2) levels and the development/progression of both obesity and associated diseases. Furthermore, dietary intake of the micronutrient selenium (Se) is reduced in obese postmenopausal women and a negative correlation between Se level and body mass index (BMI) has been reported. This suggests that novel nutritional and hormonal solutions are needed to moderate fat deposition in postmenopausal women. This study used mouse 3T3-L1 and human HepG2/C3A cells, as in vitro models of obesity and NAFLD, respectively, to understand basic cellular mechanisms associated with lipogenesis, and to study the role of Se and oestrogen, as E2, in modulating lipid deposition. Supplementation of 3T3-L1 cells during differentiation to adipocytes with 200 nmol/L Se reduced lipid deposition (~20%) by increasing the expression of genes related to redox status (Gpx1, Selenow, and Ucp2) and reducing the expression of markers of energy metabolism, inflammation and adipocyte differentiation (Lep, Cox-2, and Fabp4); whereas administration of 10 nmol/L E2 regulated lipid synthesis and metabolism (reductions in Fasn, Pparg, and Hsl expression and increased Fabp4 and Glut4 expression). In HepG2/C3A cells, both Se and E2 reduced lipid accumulation (15%−20%), via regulation of lipid and energy metabolism and inflammatory genes (SREBF1, SCD1, COX2, and LEP). These results suggest that both hormonal treatment and micronutrient supplementation may be beneficial in obesity and NAFLD management. If our current in vitro findings were subsequently demonstrated in vivo, they could provide valuable data to support the use of either Se supplementation and/or oestrogen-based therapies to prevent and manage obesity and NAFLD in postmenopausal women.

Keywords

inflammationseleniumobesityoxidative stressadipogenesisnon-alcoholic fatty liver disease17β oestradiol

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Food & Medicine Homology
DOI: 10.26599/FMH.2025.9420056
Cite this article:
Walsh SK, Pettigrew K, Mezzani I, et al. Role of selenium and 17β oestradiol in modulating lipid accumulation in in vitro models of obesity and NAFLD. Food & Medicine Homology, 2025, https://doi.org/10.26599/FMH.2025.9420056

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Received: 09 July 2024
Revised: 06 August 2024
Accepted: 07 August 2024
Published: 05 November 2024
© National R & D Center for Edible Fungus Processing Technology 2024. Published by Tsinghua University Press.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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