Evidence map›Paper›PMID 29339400›Full record

ArticleJournal of molecular endocrinology2018

Intact glucose uptake despite deteriorating signaling in adipocytes with high-fat feeding.

Björn Hansson, Sebastian Wasserstrom, Björn Morén, Vipul Periwal, Petter Vikman, Samuel W Cushman, Olga Göransson, Petter Storm, Karin G Stenkula

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  3. Adipocyte traits limiting cellular insulin responsiveness and glucose transport.American journal of physiology. Endocrinology and metabolism · 2023
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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

9 authors at 3 institutions in 2 countries.

Björn HanssonDepartment of Experimental Medical ScienceLund University, Lund, Sweden.
Sebastian WasserstromDepartment of Experimental Medical ScienceLund University, Lund, Sweden.
Björn MorénDepartment of Experimental Medical ScienceLund University, Lund, Sweden.
Vipul PeriwalNational Institute of Diabetes and Digestive and Kidney DiseasesNational Institutes of Health, Bethesda, Maryland, USA.
Petter VikmanDepartment of Clinical SciencesLund University, Malmö, Sweden.
Samuel W CushmanNational Institute of Diabetes and Digestive and Kidney DiseasesNational Institutes of Health, Bethesda, Maryland, USA.
Olga GöranssonDepartment of Experimental Medical ScienceLund University, Lund, Sweden.
Petter StormDepartment of Clinical SciencesLund University, Malmö, Sweden.
Karin G StenkulaDepartment of Experimental Medical ScienceLund University, Lund, Sweden karin.stenkula@med.lu.se.
Lund University · SENational Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Quantitative Estimation of Sensitivity of Lipolysis to InsulinZIADK013030 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI PERIWAL, VIPUL · 2009 to 2025
$2.0M
Adipocyte development and insulin resistanceZIADK013035 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI PERIWAL, VIPUL · 2009 to 2020
$929k
Intramural NIH HHS ZIA DK013030Intramural NIH HHS ZIA DK013035
6 · The paper itself

Abstract

To capture immediate cellular changes during diet-induced expansion of adipocyte cell volume and number, we characterized mature adipocytes during a short-term high-fat diet (HFD) intervention. Male C57BL6/J mice were fed chow diet, and then switched to HFD for 2, 4, 6 or 14 days. Systemic glucose clearance was assessed by glucose tolerance test. Adipose tissue was dissected for RNA-seq and cell size distribution analysis using coulter counting. Insulin response in isolated adipocytes was monitored by glucose uptake assay and Western blotting, and confocal microscopy was used to assess autophagic activity. Switching to HFD was accompanied by an immediate adipocyte size expansion and onset of systemic insulin resistance already after two days, followed by recruitment of new adipocytes. Despite an initially increased non-stimulated and preserved insulin-stimulated glucose uptake, we observed a decreased phosphorylation of insulin receptor substrate-1 (IRS-1) and protein kinase B (PKB). After 14 days of HFD, both the insulin-stimulated phosphorylation of Akt substrate of 160 kDa (AS160) and glucose uptake was blunted. RNA-seq analysis of adipose tissue revealed transient changes in gene expression at day four, including highly significant upregulation of

Indexed as

Diet, High-FatFeeding BehaviorSignal TransductionAdipocytesAdipose TissueAnimalsAutophagyCell ProliferationGlucoseInsulinInsulin ResistanceMaleMice, Inbred C57BLTranscription, GeneticGlucoseInsulinadipocytesautophagyglucose uptakeinsulin signaling

Identifiers

PMID29339400
PMCPMC7459392
OpenAlexW2783055262

What OpenQuestion holds

Textmetadata
LicenceTDM
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.