Evidence map›Paper›PMID 30309776›Full record

ArticleMolecular metabolism2018

Glucose tolerance and insulin sensitivity define adipocyte transcriptional programs in human obesity.

R Gerlini, L Berti, J Darr, M Lassi, S Brandmaier, L Fritsche, F Scheid, A Böhm, A Königsrainer, H Grallert and 4 more

Abstract read
In one paragraph

Article in Molecular metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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  8. Non-coding variants in MYH11, FZD3, and SORCS3 are associated with dementia in women.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021
    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

14 authors.

R GerliniInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research center for Environmental Health - Neuherberg, Germany; German Center for Diabetes Research (DZD) - Neuherberg, Germany.
L BertiGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Tübingen, Germany.
J DarrInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research center for Environmental Health - Neuherberg, Germany; German Center for Diabetes Research (DZD) - Neuherberg, Germany.
M LassiInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research center for Environmental Health - Neuherberg, Germany; German Center for Diabetes Research (DZD) - Neuherberg, Germany.
S BrandmaierGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Research Unit Molecular Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany; Institute of Epidemiology 2, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany.
L FritscheGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Tübingen, Germany.
F ScheidInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research center for Environmental Health - Neuherberg, Germany; German Center for Diabetes Research (DZD) - Neuherberg, Germany.
A BöhmGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University of Tübingen, Tübingen, Germany.
A KönigsrainerDepartment of General, Visceral and Transplant Surgery, University of Tübingen, Tübingen, Germany.
H GrallertGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Research Unit Molecular Epidemiology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany; Institute of Epidemiology 2, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany.
H U HäringGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Tübingen, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University of Tübingen, Tübingen, Germany.
M Hrabě de AngelisInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research center for Environmental Health - Neuherberg, Germany; German Center for Diabetes Research (DZD) - Neuherberg, Germany; Experimental Genetics, Faculty of Life and Food Sciences Weihenstephan, Technische Universität München, Freising-Weihenstephan, Germany.
H StaigerGerman Center for Diabetes Research (DZD) - Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the Eberhard-Karls-University of Tübingen, Tübingen, Germany; Institute of Pharmaceutical Sciences, Department of Pharmacy and Biochemistry, University of Tübingen, Tübingen, Germany. Electronic address: Harald.Staiger@med.uni-tuebingen.de.
R TeperinoInstitute of Experimental Genetics, Helmholtz Zentrum München, German Research center for Environmental Health - Neuherberg, Germany; German Center for Diabetes Research (DZD) - Neuherberg, Germany. Electronic address: Raffaele.teperino@helmholtz-muenchen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAlthough debated, metabolic health characterizes 10-25% of obese individuals and reduces risk of developing life-threatening co-morbidities. Adipose tissue is a recognized endocrine organ important for the maintenance of whole-body metabolic health. Adipocyte transcriptional signatures of healthy and unhealthy obesity are largely unknown.

methodsHere, we used a small cohort of highly characterized obese individuals discordant for metabolic health, characterized their adipocytes transcriptional signatures, and cross-referenced them to mouse phenotypic and human GWAs databases. RESULTS AND

conclusionsOur study showed that glucose intolerance and insulin resistance co-operate to remodel adipocyte transcriptome. We also identified the Nuclear Export Mediator Factor (NEMF) and the Ectoderm-Neural Cortex 1 (ENC1) as novel potential targets in the management of metabolic health in human obesity.

Indexed as

Glucose IntoleranceInsulin ResistanceTranscriptomeAdipocytesAdultAntigens, NeoplasmCells, CulturedFemaleHumansMaleMicrofilament ProteinsMiddle AgedNeuropeptidesNuclear ProteinsNucleocytoplasmic Transport ProteinsObesityAntigens, Neoplasmectodermal-neural cortex 1 proteinMicrofilament ProteinsNEMF protein, humanNeuropeptidesNuclear ProteinsNucleocytoplasmic Transport ProteinsGlucose toleranceInsulin sensitivityMouse geneticsObesitySystemic phenotypingTranscriptomics

Identifiers

PMID30309776
PMCPMC6308911

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.