Evidence map›Paper›PMID 32937117›Full record

ArticleCell reports2020

Adipocyte Reprogramming by the Transcriptional Coregulator GPS2 Impacts Beta Cell Insulin Secretion.

Karima Drareni, Raphaëlle Ballaire, Fawaz Alzaid, Andreia Goncalves, Catherine Chollet, Serena Barilla, Jean-Louis Nguewa, Karine Dias, Sophie Lemoine, Jean-Pierre Riveline and 6 more

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 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

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  7. Nuclear Receptors in Energy Metabolism.Advances in experimental medicine and biology · 2022
    Article
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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

16 authors at 9 institutions in 2 countries.

Karima DrareniCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France. Electronic address: karimadrareni@gmail.com.
Raphaëlle BallaireInovarion, Paris, France.
Fawaz AlzaidCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France.
Andreia GoncalvesCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France.
Catherine CholletCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France.
Serena BarillaDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge 14157, Sweden.
Jean-Louis NguewaDepartment of Diabetes, Clinical Investigation Centre (CIC-9504), Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
Karine DiasÉcole Normale Supérieure, PSL Research University, Centre National de la Recherche Scientifique (CNRS), INSERM, Institut de Biologie de l'École Normale Supérieure (IBENS), Plateforme Génomique, Paris, France.
Sophie LemoineÉcole Normale Supérieure, PSL Research University, Centre National de la Recherche Scientifique (CNRS), INSERM, Institut de Biologie de l'École Normale Supérieure (IBENS), Plateforme Génomique, Paris, France.
Jean-Pierre RivelineCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France; Department of Diabetes, Clinical Investigation Centre (CIC-9504), Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
Ronan RousselCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France; Department of Diabetology, Endocrinology and Nutrition, DHU FIRE, Bichat Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
Elise DalmasCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France.
Gilberto VelhoCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France.
Eckardt TreuterDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge 14157, Sweden.
Jean-François GautierCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France; Department of Diabetes, Clinical Investigation Centre (CIC-9504), Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France.
Nicolas VenteclefCordeliers Research Centre, INSERM, Immunity and Metabolism in Diabetes Laboratory, Sorbonne Université, Université de Paris, 75006 Paris, France. Electronic address: nicolas.venteclef@inserm.fr.
Université Paris Cité · FRInserm · FRKarolinska Institutet · SESorbonne Université · FRAssistance Publique – Hôpitaux de Paris · FRCentre de Recherche des Cordeliers · FRCentre National de la Recherche Scientifique · FRHôpital Lariboisière · FRUniversité Paris Sciences et Lettres · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose homeostasis is maintained through organ crosstalk that regulates secretion of insulin to keep blood glucose levels within a physiological range. In type 2 diabetes, this coordinated response is altered, leading to a deregulation of beta cell function and inadequate insulin secretion. Reprogramming of white adipose tissue has a central role in this deregulation, but the critical regulatory components remain unclear. Here, we demonstrate that expression of the transcriptional coregulator GPS2 in white adipose tissue is correlated with insulin secretion rate in humans. The causality of this relationship is confirmed using adipocyte-specific GPS2 knockout mice, in which inappropriate secretion of insulin promotes glucose intolerance. This phenotype is driven by adipose-tissue-secreted factors, which cause increased pancreatic islet inflammation and impaired beta cell function. Thus, our study suggests that, in mice and in humans, GPS2 controls the reprogramming of white adipocytes to influence pancreatic islet function and insulin secretion.

Indexed as

Adipocytes, WhiteAdipose TissueAdipose Tissue, WhiteAnimalsDiabetes Mellitus, Type 2FemaleGlucoseGlucose IntoleranceInflammationInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionIntracellular Signaling Peptides and ProteinsMaleMiceGlucoseGPS2 protein, mouseInsulinIntracellular Signaling Peptides and Proteinsadipose tissuebeta cellsG protein pathway suppressor 2GPS2insulinorgan crosstalkpancreastranscriptional coregulatortype 2 diabetes

Identifiers

PMID32937117
PMCPMC7495095
OpenAlexW3085483771

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.