Evidence map›Paper›PMID 31391467›Full record

ArticleNature communications2019

S100A9 extends lifespan in insulin deficiency.

Giorgio Ramadori, Sanda Ljubicic, Serena Ricci, Despoina Mikropoulou, Xavier Brenachot, Christelle Veyrat-Durebex, Ebru Aras, Rafael M Ioris, Jordi Altirriba, Elisabeth Malle and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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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 2 institutions in 3 countries.

Giorgio RamadoriDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland. giorgio.ramadori@unige.ch.ORCID http://orcid.org/0000-0003-0194-3257
Sanda LjubicicDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Serena RicciDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Despoina MikropoulouDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Xavier BrenachotDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Christelle Veyrat-DurebexDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Ebru ArasDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Rafael M IorisDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Jordi AltirribaDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.ORCID http://orcid.org/0000-0002-8922-2333
Elisabeth MalleDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland.
Dirk FoellDepartment of Pediatric Rheumatology and Immunology, University of Munster, 48149, Munster, Germany.
Thomas VoglInstitute of Immunology, University of Munster, 48149, Munster, Germany.
Roberto CoppariDiabetes Center of the Faculty of Medicine, University of Geneva, 1211 Geneva 4, Geneva, Switzerland. roberto.coppari@unige.ch.
University of Geneva · CHUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tens of millions suffer from insulin deficiency (ID); a defect leading to severe metabolic imbalance and death. The only means for management of ID is insulin therapy; yet, this approach is sub-optimal and causes life-threatening hypoglycemia. Hence, ID represents a great medical and societal challenge. Here we report that S100A9, also known as Calgranulin B or Myeloid-Related Protein 14 (MRP14), is a leptin-induced circulating cue exerting beneficial anti-diabetic action. In murine models of ID, enhanced expression of S100A9 alone (i.e. without administered insulin and/or leptin) slightly improves hyperglycemia, and normalizes key metabolic defects (e.g. hyperketonemia, hypertriglyceridemia, and increased hepatic fatty acid oxidation; FAO), and extends lifespan by at least a factor of two. Mechanistically, we report that Toll-Like Receptor 4 (TLR4) is required, at least in part, for the metabolic-improving and pro-survival effects of S100A9. Thus, our data identify the S100A9/TLR4 axis as a putative target for ID care.

Indexed as

AnimalsCalgranulin BDiabetes Mellitus, ExperimentalDiphtheria ToxinFatty AcidsHumansHyperglycemiaInsulinLeptinLiverLongevityMaleMiceMice, KnockoutOxidation-ReductionSignal TransductionCalgranulin BDiphtheria ToxinFatty AcidsInsulinLeptinS100A9 protein, mouseStreptozocinTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID31391467
PMCPMC6686003
OpenAlexW2965516552

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.