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Purpose of Review <p>This review provides a comprehensive analysis of <i>trans</i> fatty acids (TFAs) and their impact on human health, examining the molecular mechanisms underlying TFA-induced pathogenesis of chronic diseases. We combine current evidence on TFA metabolism, cellular effects, and associated health outcomes to inform public health strategies.</p> Recent Findings <p>TFAs are mainly derived from two sources: industrial processes and natural biohydrogenation. Following dietary intake, TFAs are absorbed in the gastrointestinal tract and enter systemic circulation. Recent epidemiological and experimental evidence has shown that TFAs disrupt lipid metabolism, elevate oxidative stress, and activate inflammatory signaling pathways, including NF-κB. Additionally, TFAs induce endoplasmic reticulum stress and impair autophagy, contributing to insulin resistance, hepatic steatosis, and adipose tissue dysfunction. These processes impair systemic metabolic dysfunction.</p> Summary <p>TFAs exert multiple adverse effects on metabolic and cellular processes, supporting their role in the progression of chronic diseases. Understanding the mechanistic basis of TFA-induced dysfunction underscores the importance of reducing dietary intake through regulatory policies and public health interventions.</p> Graphical Abstract <p></p>

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Trans Fatty Acids and Chronic Metabolic Diseases: Molecular Mechanisms and Public Health Strategies for Risk Mitigation

  • 期刊论文

  • 发表日期：

    2025年8月4日

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  • Nageena Qayyum,
  • Ya Wang,
  • Tingyi Mo,
  • Zhixin Li,
  • Shan Wang,
  • Ruijie Liu,
  • Bingquan Mo,
  • Honghui Guo

摘要

Purpose of Review

This review provides a comprehensive analysis of trans fatty acids (TFAs) and their impact on human health, examining the molecular mechanisms underlying TFA-induced pathogenesis of chronic diseases. We combine current evidence on TFA metabolism, cellular effects, and associated health outcomes to inform public health strategies.

Recent Findings

TFAs are mainly derived from two sources: industrial processes and natural biohydrogenation. Following dietary intake, TFAs are absorbed in the gastrointestinal tract and enter systemic circulation. Recent epidemiological and experimental evidence has shown that TFAs disrupt lipid metabolism, elevate oxidative stress, and activate inflammatory signaling pathways, including NF-κB. Additionally, TFAs induce endoplasmic reticulum stress and impair autophagy, contributing to insulin resistance, hepatic steatosis, and adipose tissue dysfunction. These processes impair systemic metabolic dysfunction.

Summary

TFAs exert multiple adverse effects on metabolic and cellular processes, supporting their role in the progression of chronic diseases. Understanding the mechanistic basis of TFA-induced dysfunction underscores the importance of reducing dietary intake through regulatory policies and public health interventions.

Graphical Abstract