Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Fish Oil Supplementation Mitigates High-Fat Diet-Induced Obesity: Exploring Epigenetic Modulation and Genes Associated with Adipose Tissue Dysfunction in Mice

Version 1 : Received: 21 May 2024 / Approved: 22 May 2024 / Online: 22 May 2024 (07:52:25 CEST)

How to cite: Simão, J. D. J.; Bispo, A. F. D. S.; Plata, V. T. G.; Armelin-Correa, L. M.; Cardoso Alonso Vale, M. I. Fish Oil Supplementation Mitigates High-Fat Diet-Induced Obesity: Exploring Epigenetic Modulation and Genes Associated with Adipose Tissue Dysfunction in Mice. Preprints 2024, 2024051423. https://doi.org/10.20944/preprints202405.1423.v1 Simão, J. D. J.; Bispo, A. F. D. S.; Plata, V. T. G.; Armelin-Correa, L. M.; Cardoso Alonso Vale, M. I. Fish Oil Supplementation Mitigates High-Fat Diet-Induced Obesity: Exploring Epigenetic Modulation and Genes Associated with Adipose Tissue Dysfunction in Mice. Preprints 2024, 2024051423. https://doi.org/10.20944/preprints202405.1423.v1

Abstract

This study investigated the effects of fish oil (FO) treatment, particularly enriched with eicosapentaenoic acid (EPA), on obesity induced by a high-fat diet (HFD) in mice. The investigation focused on elucidating the impact of FO on epigenetic modifications in white adipose tissue (WAT) and the involvement of adipose-derived stem cells (ASCs). C57BL/6j mice were submitted to a control diet or a HFD for 16 weeks, treated (or not) with FO for the last 8 weeks. WAT was removed for RNA and protein extraction, while ASCs were isolated, cultured, and treated with Leptin. All samples were analyzed using functional genomics tools, including PCR-array, RT-PCR and Western Blot assays. Mice receiving HFD displayed increased body mass, fat accumulation, and altered gene expression associated with WAT inflammation and dysfunction. FO supplementation attenuated these effects, a potential protective role against HFD-induced obesity. Analysis of H3K27 revealed HFD-induced changes in histone, which were partially reversed by FO treatment. The study further explored leptin signaling in ASCs, suggesting a potential mechanism for ASC dysfunction in the leptin-rich environment of obese WAT. Overall, FO supplementation demonstrated efficacy in mitigating HFD-induced obesity, influencing epigenetic and molecular pathways, and shedding light on the role of ASCs and leptin signaling in WAT dysfunction associated with obesity.

Keywords

obesity; inflammation; H3K27; n-3 PUFA; WAT; leptin

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

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