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Autophagy in Obesity and Type 2 Diabetes: Beyond the Protective Paradigm
M Elena Angarita-Plánchez1,2, Paula Sánchez-Rodríguez1, Ana M Múnera-Rodríguez1
1Department of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Current Obesity Reports
|May 8, 2026
Summary
Autophagy dysregulation in obesity and type 2 diabetes mellitus (T2DM) is tissue-specific, not uniformly suppressed. Understanding this context-dependent maladaptation is key for developing precision therapies.
Area of Science:
- Cellular Biology
- Metabolic Disease Research
Background:
- Autophagy plays a crucial role in cellular homeostasis.
- Dysregulation of autophagy is implicated in various metabolic disorders, including obesity and type 2 diabetes mellitus (T2DM).
Purpose of the Study:
- To review current evidence on autophagy dysregulation in obesity and T2DM.
- To emphasize the tissue-specific nature of these autophagic alterations.
- To explore the implications for clinical translation and therapeutic strategies.
Main Methods:
- Review of preclinical and human studies on autophagy markers (LC3, p62, Beclin-1) in metabolic diseases.
- Analysis of signaling pathways involved (mTORC1-AMPK).
- Examination of recent advances in assessing autophagic flux and biomarkers.
Main Results:
- Autophagic alterations in metabolic disease are tissue- and stage-dependent, not uniformly suppressed.
- Dysregulated signaling, mitophagy, and lysosomal function contribute to insulin resistance and metaflammation in key tissues.
- Current human studies often rely on static markers, limiting reliable assessment of autophagic flux.
Conclusions:
- Autophagy in metabolic disease is a context-dependent maladaptation.
- New biomarkers and functional assays are needed for accurate assessment of autophagic flux in humans.
- Integrating these with metabolic phenotyping is crucial for precision therapeutic strategies.
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