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

  • 0Post-Graduate Program in Chemical Biology, Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo-UNIFESP, Diadema 09913-030, Brazil.
Pharmaceuticals (basel, Switzerland) +

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July 27, 2024

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July 27, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Fish oil (FO) rich in eicosapentaenoic acid (EPA) supplementation helps reduce high-fat diet (HFD)-induced obesity in mice. FO treatment also reversed epigenetic changes in white adipose tissue (WAT) and improved adipose-derived stem cell (ASC) function.

Area Of Science

  • Nutritional Epigenetics
  • Obesity Research
  • Adipose Tissue Biology

Background

  • High-fat diets (HFD) induce obesity, characterized by white adipose tissue (WAT) inflammation and dysfunction.
  • Epigenetic modifications and adipose-derived stem cell (ASC) behavior are implicated in obesity pathogenesis.
  • Fish oil (FO), particularly eicosapentaenoic acid (EPA), is investigated for its potential anti-obesity effects.

Purpose Of The Study

  • To investigate the effects of FO supplementation on HFD-induced obesity in mice.
  • To elucidate the impact of FO on epigenetic modifications in WAT and ASCs.
  • To explore the role of leptin signaling in ASC dysfunction within the context of obesity.

Main Methods

  • C57BL/6j mice were fed a control or HFD for 16 weeks, with some receiving FO supplementation in the last 8 weeks.
  • Analysis of WAT included RNA and protein extraction, functional genomics (PCR-array, RT-PCR), and Western Blot.
  • ASCs were isolated, cultured, and treated with leptin to assess signaling pathways.

Main Results

  • HFD led to increased body mass, fat accumulation, and altered gene expression in WAT, indicating inflammation and dysfunction.
  • FO supplementation attenuated HFD-induced obesity markers and partially reversed H3K27 histone modifications in WAT.
  • Leptin signaling in ASCs suggested a mechanism for their dysfunction in the obesogenic environment.

Conclusions

  • FO supplementation demonstrates efficacy in mitigating HFD-induced obesity.
  • FO influences epigenetic and molecular pathways in WAT, offering a protective role against obesity.
  • The study highlights the involvement of ASCs and leptin signaling in WAT dysfunction associated with obesity.

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