Evidence map›Paper›PMID 27858140›Full record

ArticleDiabetologia2017

Adipocyte STAT5 deficiency promotes adiposity and impairs lipid mobilisation in mice.

Doris Kaltenecker, Kristina M Mueller, Pia Benedikt, Ursula Feiler, Madeleine Themanns, Michaela Schlederer, Lukas Kenner, Martina Schweiger, Guenter Haemmerle, Richard Moriggl

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

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  15. Adipose tissue lipid metabolism: lipolysis.Current opinion in genetics & development · 2023
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  20. Important Hormones Regulating Lipid Metabolism.Molecules (Basel, Switzerland) · 2022
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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

10 authors at 3 institutions in 1 country.

Doris KalteneckerLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Kristina M MuellerLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Pia BenediktInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Ursula FeilerInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Madeleine ThemannsLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Michaela SchledererLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Lukas KennerLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Martina SchweigerInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Guenter HaemmerleInstitute of Molecular Biosciences, University of Graz, Graz, Austria.
Richard MorigglLudwig Boltzmann Institute for Cancer Research, Vienna, Austria. richard.moriggl@lbicr.lbg.ac.at.
University of Veterinary Medicine Vienna · ATUniversity of Graz · ATMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisDysfunction of lipid metabolism in white adipose tissue can substantially interfere with health and quality of life, for example in obesity and associated metabolic diseases. Therefore, it is important to characterise pathways that regulate lipid handling in adipocytes and determine how they affect metabolic homeostasis. Components of the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway are involved in adipocyte physiology and pathophysiology. However, the exact physiological importance of the STAT family member STAT5 in white adipose tissue is yet to be determined. Here, we aimed to delineate adipocyte STAT5 functions in the context of lipid metabolism in white adipose tissue.

methodsWe generated an adipocyte specific knockout of Stat5 in mice using the Adipoq-Cre recombinase transgene followed by in vivo and in vitro biochemical and molecular studies.

resultsAdipocyte-specific deletion of Stat5 resulted in increased adiposity, while insulin resistance and gluconeogenic capacity was decreased, indicating that glucose metabolism can be improved by interfering with adipose STAT5 function. Basal lipolysis and fasting-induced lipid mobilisation were diminished upon STAT5 deficiency, which coincided with reduced levels of the rate-limiting lipase of triacylglycerol hydrolysis, adipose triglyceride lipase (ATGL, encoded by Pnpla2) and its coactivator comparative gene identification 58 (CGI-58). In a mechanistic analysis, we identified a functional STAT5 response element within the Pnpla2 promoter, indicating that Pnpla2 is transcriptionally regulated by STAT5. CONCLUSIONS/

interpretationOur findings reveal an essential role for STAT5 in maintaining lipid homeostasis in white adipose tissue and provide a rationale for future studies into the potential of STAT5 manipulation to improve outcomes in metabolic diseases.

Indexed as

3T3-L1 CellsAdipocytesAdiposityAnimalsBlotting, WesternChromatin ImmunoprecipitationElectrophoretic Mobility Shift AssayFemaleGlucoseInsulin ResistanceLipid MetabolismLipid MobilizationLipolysisMaleMiceQuality of LifeGlucoseSTAT5 Transcription FactorAdipose tissueEnergy metabolismLipolysisSTAT5

Identifiers

PMID27858140
PMCPMC6518368
OpenAlexW2554875477

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.