Evidence map›Paper›PMID 29502266›Full record

ArticleDiabetologia2018

Loss of angiopoietin-like 4 (ANGPTL4) in mice with diet-induced obesity uncouples visceral obesity from glucose intolerance partly via the gut microbiota.

Aafke W F Janssen, Saeed Katiraei, Barbara Bartosinska, Daniel Eberhard, Ko Willems van Dijk, Sander Kersten

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
8.0field-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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Aafke W F JanssenNutrition, Metabolism and Genomics Group, Division of Human Nutrition and Health, Wageningen University, Stippeneng 4, 6708 WE, Wageningen, the Netherlands.
Saeed KatiraeiDepartment of Human Genetics, Leiden University Medical Center, Leiden, the Netherlands.
Barbara BartosinskaInstitute of Metabolic Physiology, Department of Biology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Daniel EberhardInstitute of Metabolic Physiology, Department of Biology, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
Ko Willems van DijkDepartment of Human Genetics, Leiden University Medical Center, Leiden, the Netherlands.
Sander KerstenNutrition, Metabolism and Genomics Group, Division of Human Nutrition and Health, Wageningen University, Stippeneng 4, 6708 WE, Wageningen, the Netherlands. sander.kersten@wur.nl.
Leiden University Medical Center · NLWageningen University & Research · NLDeutsches Diabetes-Zentrum e.V. · DEGerman Center for Diabetes Research · DE

Funding

Cardiovasculair Onderzoek Nederland (CVON) CVON 2012-03
6 · The paper itself

Abstract

aims/hypothesisAngiopoietin-like 4 (ANGPTL4) is an important regulator of triacylglycerol metabolism, carrying out this role by inhibiting the enzymes lipoprotein lipase and pancreatic lipase. ANGPTL4 is a potential target for ameliorating cardiometabolic diseases. Although ANGPTL4 has been implicated in obesity, the study of the direct role of ANGPTL4 in diet-induced obesity and related metabolic dysfunction is hampered by the massive acute-phase response and development of lethal chylous ascites and peritonitis in Angptl4

methodsWe chronically fed wild-type (WT) and Angptl4

resultsMice lacking ANGPTL4 displayed an increase in body weight gain, visceral adipose tissue mass, visceral adipose tissue lipoprotein lipase activity and visceral adipose tissue inflammation compared with WT mice. However, they also unexpectedly had markedly improved glucose tolerance, which was accompanied by elevated insulin levels. Loss of ANGPTL4 did not affect glucose-stimulated insulin secretion in isolated pancreatic islets. Since the gut microbiota have been suggested to influence insulin secretion, and because ANGPTL4 has been proposed to link the gut microbiota to host metabolism, we hypothesised a potential role of the gut microbiota. Gut microbiota composition was significantly different between Angptl4 CONCLUSIONS/

interpretationDespite increasing visceral fat mass, inactivation of ANGPTL4 improves glucose tolerance, at least partly via a gut microbiota-dependent mechanism.

Indexed as

Gastrointestinal MicrobiomeGlucose IntoleranceAngiopoietin-Like Protein 4AnimalsBody WeightDiet, High-FatFatty AcidsFructoseGlucoseGlucose Tolerance TestHomeostasisInsulinInsulin ResistanceIntra-Abdominal FatMaleMiceAngiopoietin-Like Protein 4Angptl4 protein, mouseFatty AcidsFructoseGlucoseInsulinAngiopoietin-like 4AntibioticsGlucose toleranceGut microbiotaInsulin secretionWhite adipose tissue

Identifiers

PMID29502266
PMCPMC6449003
OpenAlexW2792066403

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LicenceCC BY
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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.