Evidence map›Paper›PMID 42101776›Full record

ReviewCurrent obesity reports2026

Autophagy in Obesity and Type 2 Diabetes: Beyond the Protective Paradigm.

M Elena Angarita-Plánchez, Paula Sánchez-Rodríguez, Ana M Múnera-Rodríguez, Camila Leiva-Castro, Juan Manuel Benítez-Márquez, Icíar Reina-Pérez, Francisca Palomares, Soledad López-Enríquez

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current obesity reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

M Elena Angarita-PlánchezDepartment of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Paula Sánchez-RodríguezDepartment of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Ana M Múnera-RodríguezDepartment of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Camila Leiva-CastroDepartment of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Juan Manuel Benítez-Márquez *Department of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Icíar Reina-Pérez *Department of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain.
Francisca PalomaresDepartment of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain. fpalomares1@us.es.
Soledad López-EnríquezDepartment of Medical Biochemistry, Molecular Biology and Immunology, Faculty of Medicine, University of Seville. Av. Sánchez Pizjuan S/N, 41009, Seville, Spain. slopez9@us.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThis review examines the current evidence on autophagy dysregulation in obesity and type 2 diabetes mellitus (T2DM), with particular emphasis on its tissue-specific nature and implications for clinical translation. RECENT

findingsRecent human and preclinical evidence indicates that autophagic alterations in metabolic disease are not uniformly suppressed but vary according to tissue type and disease stage. In adipose tissue, liver, skeletal muscle, pancreatic β cells, and immune cells, dysregulated mTORC1-AMPK signaling, defective mitophagy, and impaired lysosomal function contribute to insulin resistance, ectopic lipid accumulation, and metaflammation. However, most human studies rely on static markers such as LC3, p62, and Beclin-1, which do not reliably reflect dynamic autophagic flux. Recent advances, including organelle-specific biomarkers, ex vivo functional assays, and circulating exosomal cargo, offer new translational opportunities, although standardization remains limited. Autophagy in metabolic disease represents a context-dependent maladaptation rather than a uniformly protective pathway. Future progress will depend on harmonized biomarker panels, functional assessment of autophagic flux in humans, and integration with metabolic phenotyping to enable precision-based therapeutic strategies.

Indexed as

AutophagyDiabetes Mellitus, Type 2ObesityAdipose TissueAnimalsBiomarkersHumansInsulin ResistanceMitophagyMuscle, SkeletalSignal TransductionBiomarkersAutophagy fluxBiomarkersMitophagyObesityTherapeutic targetsType 2 diabetes

Identifiers

PMID42101776
PMCPMC13156086

What Socratic holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.