Evidence map›Paper›PMID 28771229›Full record

ArticleCell death & disease2017

Autophagy couteracts weight gain, lipotoxicity and pancreatic β-cell death upon hypercaloric pro-diabetic regimens.

Álvaro F Fernández, Clea Bárcena, Gemma G Martínez-García, Isaac Tamargo-Gómez, María F Suárez, Federico Pietrocola, Francesca Castoldi, Lorena Esteban, Elena Sierra-Filardi, Patricia Boya and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% of its field
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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.

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  7. Obesity accelerates cardiovascular ageing.European heart journal · 2025
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6 more citing papers are in PubMed but not listed here.

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

13 authors at 6 institutions in 3 countries.

Álvaro F FernándezInstituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
Clea BárcenaDepartamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología, Universidad de Oviedo, Oviedo, Spain.
Gemma G Martínez-GarcíaInstituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
Isaac Tamargo-GómezInstituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
María F SuárezInstituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
Federico PietrocolaEquipe 11 labellisée par la Ligue Nationale Contre le Cancer, INSERM U1138, Centre de Recherche des Cordeliers, Paris, France.
Francesca CastoldiEquipe 11 labellisée par la Ligue Nationale Contre le Cancer, INSERM U1138, Centre de Recherche des Cordeliers, Paris, France.
Lorena EstebanDepartament of Cellular and Molecular Biology, Centro de Investigaciones Biológicas, CSIC, Madrid, Spain.
Elena Sierra-FilardiDepartament of Cellular and Molecular Biology, Centro de Investigaciones Biológicas, CSIC, Madrid, Spain.
Patricia BoyaDepartament of Cellular and Molecular Biology, Centro de Investigaciones Biológicas, CSIC, Madrid, Spain.
Carlos López-OtínDepartamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología, Universidad de Oviedo, Oviedo, Spain.
Guido KroemerEquipe 11 labellisée par la Ligue Nationale Contre le Cancer, INSERM U1138, Centre de Recherche des Cordeliers, Paris, France.
Guillermo MariñoInstituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain.
Universidad de Oviedo · ESCentro de Investigaciones Biológicas Margarita Salas · ESInstituto de Investigación Sanitaria del Principado de Asturias · ESCentre de Recherche des Cordeliers · FRHôpital Européen Georges-Pompidou · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the last years, autophagy has been revealed as an essential pathway for multiple biological processes and physiological functions. As a catabolic route, autophagy regulation by nutrient availability has been evolutionarily conserved from yeast to mammals. On one hand, autophagy induction by starvation is associated with a significant loss in body weight in mice. Here, we demonstrate that both genetic and pharmacological inhibition of the autophagy process compromise weight loss induced by starvation. Moreover, autophagic potential also impacts on weight gain induced by distinct hypercaloric regimens. Atg4b-deficient mice, which show limited autophagic competence, exhibit a major increase in body weight in response to distinct obesity-associated metabolic challenges. This response is characterized by the presence of larger adipocytes in visceral fat tissue, increased hepatic steatosis, as well as reduced glucose tolerance and attenuated insulin responses. Similarly, autophagy-deficient mice are more vulnerable to experimentally induced type-I diabetes, showing an increased susceptibility to acute streptozotocin administration. Notably, pharmacological stimulation of autophagy in wild-type mice by spermidine reduced both weight gain and obesity-associated alterations upon hypercaloric regimens. Altogether, these results indicate that systemic autophagic activity influences the resilience of the organism to weight gain induced by high-calorie diets, as well as to the obesity-associated features of both type-1 and type-2 diabetes.

Indexed as

AutophagyAdipocytesAnimalsAutophagy-Related ProteinsCell DeathCysteine EndopeptidasesDiabetes Mellitus, ExperimentalDietFatty LiverInsulin-Secreting CellsMiceMice, KnockoutObesityAtg4b protein, mouseAutophagy-Related ProteinsCysteine Endopeptidases

Identifiers

PMID28771229
PMCPMC5596561
OpenAlexW2742757125

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.