Evidence map›Paper›PMID 33113367›Full record

ArticleCell reports2020

Fat Body p53 Regulates Systemic Insulin Signaling and Autophagy under Nutrient Stress via Drosophila Upd2 Repression.

María Clara Ingaramo, Juan Andrés Sánchez, Norbert Perrimon, Andrés Dekanty

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Adipose Dicer-1 modulates systemic insulin signaling and longevity via a miR-8-Aop-Dilp6 axis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. FOXO-mediated repression of Dicer1 regulates metabolism, stress resistance, and longevity inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
  10. Article
  11. Nutrient Sensing via Gut inInternational journal of molecular sciences · 2022
    Review
  12. Review
  13. 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

4 authors at 3 institutions in 2 countries.

María Clara IngaramoInstituto de Agrobiotecnología del Litoral, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Santa Fe 3000, Argentina.
Juan Andrés SánchezInstituto de Agrobiotecnología del Litoral, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Santa Fe 3000, Argentina.
Norbert PerrimonDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA; Howard Hughes Medical Institute, Boston, MA 02115, USA. Electronic address: perrimon@genetics.med.harvard.edu.
Andrés DekantyInstituto de Agrobiotecnología del Litoral, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Santa Fe 3000, Argentina; Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral (UNL), Santa Fe 3000, Argentina. Electronic address: adekanty@santafe-conicet.gov.ar.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARHarvard University · USInstituto de Agrobiotecnología del Litoral · AR

Funding

Characterization of the Insulin to Autophagy Pathway in MusclesR01AR057352 · NIAMS · HARVARD MEDICAL SCHOOL · PI NORBERT PERRIMON · 2010 to 2026
$8.2M
Howard Hughes Medical InstituteNIAMS NIH HHS R01 AR057352
6 · The paper itself

Abstract

The tumor suppressor p53 regulates multiple metabolic pathways at the cellular level. However, its role in the context of a whole animal response to metabolic stress is poorly understood. Using Drosophila, we show that AMP-activated protein kinase (AMPK)-dependent Dmp53 activation is critical for sensing nutrient stress, maintaining metabolic homeostasis, and extending organismal survival. Under both nutrient deprivation and high-sugar diet, Dmp53 activation in the fat body represses expression of the Drosophila Leptin analog, Unpaired-2 (Upd2), which remotely controls Dilp2 secretion in insulin-producing cells. In starved Dmp53-depleted animals, elevated Upd2 expression in adipose cells and activation of Upd2 receptor Domeless in the brain result in sustained Dilp2 circulating levels and impaired autophagy induction at a systemic level, thereby reducing nutrient stress survival. These findings demonstrate an essential role for the AMPK-Dmp53 axis in nutrient stress responses and expand the concept that adipose tissue acts as a sensing organ that orchestrates systemic adaptation to nutrient status.

Indexed as

AnimalsAutophagyDrosophilaDrosophila melanogasterDrosophila ProteinsFat BodyTumor Suppressor Protein p53Drosophila ProteinsTumor Suppressor Protein p53Upd2 protein, DrosophilaAMPKDrosophilafat bodyinsulin-producing cellsinter-organ communicationLeptinmetabolismp53starvationUpd2

Identifiers

PMID33113367
PMCPMC9036415
OpenAlexW3096016566

What OpenQuestion holds

Textmetadata
LicenceTDM
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.