Evidence map›Paper›PMID 43000678›Full record

ArticleActa physiologica (Oxford, England)2026

Intermittent Fasting Remodels Mitochondrial Morphology and Bioenergetic Capacity in Brown Adipose Tissue of Obese Mice.

Fernanda Silva Carneiro, Larissa Moreira Dias, Scylas José de Andrade Junior, Matheus Biscaro Rocha, Mariana Lima Ribeiro, Ana Paula Morelli, Gabriel Calheiros Antunes, Adelino Sanchez Ramos Da Silva, Dennys Esper Cintra, José Rodrigo Pauli and 1 more

Abstract read
In one paragraph

Article in Acta physiologica (Oxford, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Fernanda Silva CarneiroLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.ORCID https://orcid.org/0000-0003-3142-2743
Larissa Moreira DiasLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.ORCID https://orcid.org/0000-0002-3104-3711
Scylas José de Andrade JuniorLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.
Matheus Biscaro RochaLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.ORCID https://orcid.org/0000-0002-8766-2984
Mariana Lima RibeiroLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.
Ana Paula MorelliLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.
Gabriel Calheiros AntunesLaboratory of Cell Signaling (LabSinCel), Faculty of Medical Sciences, University of Campinas, Campinas, Brazil.ORCID https://orcid.org/0000-0002-2400-8475
Adelino Sanchez Ramos Da SilvaPostgraduate Program in Rehabilitation and Functional Performance, Ribeirão Preto Medical School, and School of Physical Education and Sport of Ribeirão Preto, University of São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.ORCID https://orcid.org/0000-0002-9679-8357
Dennys Esper CintraLaboratory of Nutritional Genomics, School of Applied Sciences, University of Campinas (UNICAMP), Limeira, Sao Paulo, Brazil.ORCID https://orcid.org/0000-0002-7954-5630
José Rodrigo PauliLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.ORCID https://orcid.org/0000-0002-6129-1521
Eduardo Rochete RopelleLaboratory of Molecular Biology of Exercise (LaBMEx), School of Applied Sciences, University of Campinas, Limeira, Sao Paulo, Brazil.ORCID https://orcid.org/0000-0003-1655-9557

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 304123/2023-4Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 88887.142758/2025-00Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 88887.204283/2025-00Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 88887.238630/2025-00Fundação de Amparo à Pesquisa do Estado de São Paulo 2019/21709-4Fundação de Amparo à Pesquisa do Estado de São Paulo 2022/02350-8Fundação de Amparo à Pesquisa do Estado de São Paulo 2023/02751-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2023/13629-6Fundação de Amparo à Pesquisa do Estado de São Paulo 2024/05542-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2024/21229-0
6 · The paper itself

Abstract

Brown adipose tissue (BAT) is a specialized adipose tissue that is associated with thermogenesis, endocrine function, and energy expenditure, characterized by a high mitochondrial density. However, obesity induces profound structural and functional remodeling of mitochondria in BAT, compromising their thermogenic and oxidative capacities. On the other hand, intermittent fasting is a non-pharmacological approach that can enhance mitochondrial function, thereby contributing to weight loss. Despite this, the effects of intermittent fasting on the morphofunctional aspects of BAT mitochondria are not yet well understood. Thus, we investigated the effects of a chronic 16:8 daily intermittent fasting protocol over 8 weeks on the BAT mitochondria of obese mice. Diet-induced obesity reduced energy expenditure, increased body weight gain, and adiposity within the BAT. Obesity altered BAT mitochondrial morphology, resulting in smaller, more rounded organelles with disrupted cristae. Conversely, intermittent fasting increased energy expenditure, reduced body weight gain and adiposity within the BAT, increased the UCP1 protein content, and restored browning in the BAT. Remarkably, intermittent fasting promoted extensive remodeling of mitochondrial dynamics protein markers and structural profile in BAT, increasing mitochondrial elongation, total cristae length, and cristae alignment. In addition, intermittent fasting increased the maximum intrinsic capacity of respiratory mitochondrial complexes and the content of proteins related to oxidative phosphorylation. These findings demonstrate that intermittent fasting is a potential strategy for regulating mitochondrial dysfunction in BAT during metabolic disorders.

Indexed as

Adipose Tissue, BrownEnergy MetabolismFastingIntermittent FastingMitochondriaObesityAnimalsMaleMiceMice, Inbred C57BLMice, ObeseThermogenesisbrown adipose tissueintermittent fastingmitochondrial dynamicsmitochondrial metabolism

Identifiers

PMID43000678
PMCPMC13745782

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.