Evidence map›Paper›PMID 31418690›Full record

ArticleeLife2019

Accelerated phosphatidylcholine turnover in macrophages promotes adipose tissue inflammation in obesity.

Kasparas Petkevicius, Sam Virtue, Guillaume Bidault, Benjamin Jenkins, Cankut Çubuk, Cecilia Morgantini, Myriam Aouadi, Joaquin Dopazo, Mireille J Serlie, Albert Koulman and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 75 citations in OpenAlex.

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  17. Deciphering metabolic shifts in Gaucher disease type 1: a multi-omics study.Journal of molecular medicine (Berlin, Germany) · 2025
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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

11 authors at 3 institutions in 3 countries.

Kasparas PetkeviciusUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.ORCID 0000-0003-2295-6065
Sam VirtueUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.ORCID 0000-0002-9545-5432
Guillaume BidaultUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.
Benjamin JenkinsUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.
Cankut ÇubukClinical Bioinformatics Area, Fundación Progreso y Salud, CDCA, Hospital Virgen del Rocio, Sevilla, Spain.ORCID 0000-0003-4646-0849
Cecilia MorgantiniDepartment of Medicine, Integrated Cardio Metabolic Centre, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0003-3142-2508
Myriam AouadiDepartment of Medicine, Integrated Cardio Metabolic Centre, Karolinska Institutet, Huddinge, Sweden.ORCID 0000-0001-6256-7107
Joaquin DopazoClinical Bioinformatics Area, Fundación Progreso y Salud, CDCA, Hospital Virgen del Rocio, Sevilla, Spain.
Mireille J SerlieDepartment of Endocrinology and Metabolism, Amsterdam University Medical Center, Amsterdam, Netherlands.
Albert KoulmanUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.
Antonio Vidal-PuigUniversity of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, MDU MRC, Cambridge, United Kingdom.ORCID 0000-0003-4220-9577
University of Cambridge · GBFundación Progreso y Salud · ESKarolinska Institutet · SE

Funding

British Heart Foundation Programme Grant RG/18/7/33636British Heart Foundation RG/12/13/29853Medical Research Council G0400192Medical Research Council G0600717Medical Research Council G0802051Medical Research Council MC_G0802535Medical Research Council MC_UU_00014/2Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/2Medical Research Council MC_UU_12012/5Medical Research Council MRC_MC_UU_12012/2Medical Research Council MRC_MC_UU_12012/5Wellcome TrustWellcome Trust 4-year PhD programme in Metabolic and Cardiovascular Disease (102354/Z/13/Z​)Wellcome Trust Strategic Award
6 · The paper itself

Abstract

White adipose tissue (WAT) inflammation contributes to the development of insulin resistance in obesity. While the role of adipose tissue macrophage (ATM) pro-inflammatory signalling in the development of insulin resistance has been established, it is less clear how WAT inflammation is initiated. Here, we show that ATMs isolated from obese mice and humans exhibit markers of increased rate of de novo phosphatidylcholine (PC) biosynthesis. Macrophage-specific knockout of phosphocholine cytidylyltransferase A (CCTα), the rate-limiting enzyme of de novo PC biosynthesis pathway, alleviated obesity-induced WAT inflammation and insulin resistance. Mechanistically, CCTα-deficient macrophages showed reduced ER stress and inflammation in response to palmitate. Surprisingly, this was not due to lower exogenous palmitate incorporation into cellular PCs. Instead, CCTα-null macrophages had lower membrane PC turnover, leading to elevated membrane polyunsaturated fatty acid levels that negated the pro-inflammatory effects of palmitate. Our results reveal a causal link between obesity-associated increase in de novo PC synthesis, accelerated PC turnover and pro-inflammatory activation of ATMs.

Indexed as

Adipose TissueAnimalsCholine-Phosphate CytidylyltransferaseDisease Models, AnimalGene DeletionHumansInflammationInsulin ResistanceMacrophagesMice, ObeseObesityPhosphatidylcholinesCholine-Phosphate CytidylyltransferasePhosphatidylcholinesadipose tissuecell biologyER stressfatty acidhumanhuman biologyimmunometabolismmacrophagemedicinemembrane lipidmouse

Identifiers

PMID31418690
PMCPMC6748830
OpenAlexW2967265235

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.