Evidence map›Paper›PMID 29796244›Full record

ArticleTherapeutic advances in endocrinology and metabolism2018

9- and 13-HODE regulate fatty acid binding protein-4 in human macrophages, but does not involve HODE/GPR132 axis in PPAR-γ regulation of FABP4.

Venkat Vangaveti, Venkatesh Shashidhar, Fiona Collier, Jason Hodge, Catherine Rush, Usman Malabu, Bernhard Baune, Richard Lee Kennedy

Open access · bronzeAbstract read
In one paragraph

Article in Therapeutic advances in endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

23 citing papers in PubMed, 29 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

8 authors at 3 institutions in 1 country.

Venkat VangavetiRoom 114, Building 47, College of Medicine and Dentistry, James Cook University, Townsville, Queensland, Australia 4814, Australia.ORCID https://orcid.org/0000-0002-4363-309X
Venkatesh ShashidharCollege of Medicine and Dentistry, James Cook University, Queensland, Australia.
Fiona CollierSchool of Medicine, Deakin University, Victoria, Australia.
Jason HodgeSchool of Medicine, Deakin University, Victoria, Australia.
Catherine RushCollege of Public Health, Medical & Vet Sciences, James Cook University, Queensland, Australia.
Usman MalabuCollege of Medicine and Dentistry, James Cook University, Queensland, Australia.
Bernhard BauneDepartment of Psychiatry, University of Adelaide, South Australia.
Richard Lee KennedySchool of Medicine, Deakin University, Victoria, Australia.
James Cook University · AUDeakin University · AUThe University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBoth activation of monocytes and increased serum fatty acid binding protein-4 (FABP4) occur in diabetes and are associated with increased atherosclerosis. The oxidized lipid, 9-hydroxyoctadecadienoic acid (9-HODE) increases FABP4 in macrophages, and is a ligand for G protein-coupled receptor 132 (GPR132). We investigated the involvement of GPR132 in mediating the 9-, 13-HODE stimulation of FABP4 secretion, and whether GPR132 expression is increased in monocytes from patients with type 2 diabetes.

methodsThe effects of siRNA silencing of GPR132 gene and of the PPAR-γ antagonist T0070907 were studied in THP-1 cells. Serum levels of FABP4 and other adipokines were measured in patients with diabetes, and monocyte subpopulations were analyzed using flow cytometry. GPR132 mRNA was quantified in isolated CD14

results9-HODE and 13-HODE increased FABP4 expression in THP-1 monocytes and macrophages, and also increased GPR132 expression. Silencing of GPR132 did not influence the increase in FABP4 with 9-HODE, 13-HODE, or rosiglitazone (ROSI). By contrast, T0070907 inhibited the effect of all three ligands on FABP4 expression. Diabetic subjects had increased serum FABP4, and activated monocytes. They also expressed higher levels of GPR132 mRNA in CD14

conclusionsWe conclude that GPR132 is an independent monocyte activation marker in diabetes, but does not contribute to PPAR-γ-mediated induction of FABP4 by HODEs.

Indexed as

FABP4HODEsmacrophages

Identifiers

PMID29796244
PMCPMC5958425
OpenAlexW2791598282

What OpenQuestion holds

Textmetadata
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.