Evidence map›Paper›PMID 28627510›Full record

ArticleNature communications2017

Glycogen controls Caenorhabditis elegans lifespan and resistance to oxidative stress.

Ivan Gusarov, Bibhusita Pani, Laurent Gautier, Olga Smolentseva, Svetlana Eremina, Ilya Shamovsky, Olga Katkova-Zhukotskaya, Alexander Mironov, Evgeny Nudler

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 138 citations in OpenAlex.

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  13. A comprehensive approach, based on the use ofCurrent research in food science · 2025
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  15. Anti-aging effect of glycerophosphocholine inFrontiers in physiology · 2024
    Article
  16. Article
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  18. Lysosomal glucose sensing and glycophagy in metabolism.Trends in endocrinology and metabolism: TEM · 2023
    Review
  19. Article
  20. Article

7 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

9 authors at 3 institutions in 2 countries.

Ivan GusarovDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
Bibhusita PaniDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
Laurent GautierDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
Olga SmolentsevaDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
Svetlana EreminaEngelhardt Institute of Molecular Biology, Russian Academy of Science, Moscow 119991, Russia.
Ilya ShamovskyDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
Olga Katkova-ZhukotskayaEngelhardt Institute of Molecular Biology, Russian Academy of Science, Moscow 119991, Russia.
Alexander MironovEngelhardt Institute of Molecular Biology, Russian Academy of Science, Moscow 119991, Russia.
Evgeny NudlerDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA.
New York University · USEngelhardt Institute of Molecular Biology · RUHoward Hughes Medical Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A high-sugar diet has been associated with reduced lifespan in organisms ranging from worms to mammals. However, the mechanisms underlying the harmful effects of glucose are poorly understood. Here we establish a causative relationship between endogenous glucose storage in the form of glycogen, resistance to oxidative stress and organismal aging in Caenorhabditis elegans. We find that glycogen accumulated on high dietary glucose limits C. elegans longevity. Glucose released from glycogen and used for NADPH/glutathione reduction renders nematodes and human hepatocytes more resistant against oxidative stress. Exposure to low levels of oxidants or genetic inhibition of glycogen synthase depletes glycogen stores and extends the lifespan of animals fed a high glucose diet in an AMPK-dependent manner. Moreover, glycogen interferes with low insulin signalling and accelerates aging of long-lived daf-2 worms fed a high glucose diet. Considering its extensive evolutionary conservation, our results suggest that glycogen metabolism might also have a role in mammalian aging.

Indexed as

AMP-Activated Protein KinasesAnimalsAnimals, Genetically ModifiedAntioxidantsCaenorhabditis elegansCaenorhabditis elegans ProteinsDiamideGlucoseGlutathioneGlycogenGlycogen SynthaseHep G2 CellsHumansLongevityNADPOxidantsAMP-Activated Protein KinasesAntioxidantsCaenorhabditis elegans ProteinsDAF-2 protein, C elegansDiamideGlucoseGlutathioneGlycogenGlycogen SynthaseNADPOxidantsReceptor, InsulinSod-3 protein, C elegansSuperoxide Dismutase

Identifiers

PMID28627510
PMCPMC5481799
OpenAlexW2626036901

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.