Evidence map›Paper›PMID 30705117›Full record

ReviewJournal of lipid research2019

Adipokine FABP4 integrates energy stores and counterregulatory metabolic responses.

Kacey J Prentice, Jani Saksi, Gökhan S Hotamisligil

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of lipid research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 2 pooled it
7.6field-weighted citation impact, top 2% 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

112 citing papers in PubMed, 2 syntheses or guidelines pooled it, 208 citations in OpenAlex.

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52 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Kacey J PrenticeSabri Ülker Center for Metabolic Research Harvard T. H. Chan School of Public Health, Boston, MA; Department of Genetics and Complex Diseases Harvard T. H. Chan School of Public Health, Boston, MA.
Jani SaksiSabri Ülker Center for Metabolic Research Harvard T. H. Chan School of Public Health, Boston, MA; Department of Genetics and Complex Diseases Harvard T. H. Chan School of Public Health, Boston, MA.
Gökhan S HotamisligilSabri Ülker Center for Metabolic Research Harvard T. H. Chan School of Public Health, Boston, MA; Department of Genetics and Complex Diseases Harvard T. H. Chan School of Public Health, Boston, MA; Broad Institute of Harvard and MIT Cambridge, MA. Electronic address: ghotamis@hsph.harvard.edu.
Harvard University · US

Funding

The role of fatty acid binding protein aP2 in the pathogenesis and treatment of asthmaR01AI116901 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI HOTAMISLIGIL, GOKHAN S · 2015 to 2018
$1.6M
NIAID NIH HHS R01 AI116901
6 · The paper itself

Abstract

Although counterregulatory hormones and mediators of the fight-or-flight responses are well defined at many levels, how energy stores per se are integrated into this system remains an enigmatic question. Recent years have seen the adipose tissue become a central focus for mediating intracellular signaling and communication through the release of a variety of bioactive lipids and substrates, as well as various adipokines. A critical integration node among these mediators and responses is controlled by FA binding protein 4 (FABP4), also known as adipocyte protein 2 (aP2), which is highly expressed in adipose tissue and functions as a lipid chaperone protein. Recently, it was demonstrated that FABP4 is a secreted hormone that has roles in maintaining glucose homeostasis, representing a key juncture facilitating communication between energy-storage systems and distant organs to respond to life-threatening situations. However, chronic engagement of FABP4 under conditions of immunometabolic stress, such as obesity, exacerbates a number of immunometabolic diseases, including diabetes, asthma, cancer, and atherosclerosis. In both preclinical mouse models and humans, levels of circulating FABP4 have been correlated with metabolic disease incidence, and reducing FABP4 levels or activity is associated with improved metabolic health. In this review, we will discuss the intriguing emerging biology of this protein, including potential therapeutic options for targeting circulating FABP4.

Indexed as

AnimalsEnergy MetabolismFatty Acid-Binding ProteinsHumansMiceFABP4 protein, humanFabp4 protein, mouseFatty Acid-Binding Proteinsimmunometabolismmetabolismobesity

Identifiers

PMID30705117
PMCPMC6446704
OpenAlexW2913186709

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.