Evidence map›Paper›PMID 31037987›Full record

ArticleAdipocyte2019

Adipocyte abundances of CES1, CRYAB, ENO1 and GANAB are modified in-vitro by glucose restriction and are associated with cellular remodelling during weight regain.

Qi Qiao, Freek G Bouwman, Marleen A van Baak, Nadia J T Roumans, Roel G Vink, Susan L M Coort, Johan W Renes, Edwin C M Mariman

Open access · goldAbstract read
In one paragraph

Article in Adipocyte, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 33% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Phenolic Compounds Reduce the Fat Content inPharmaceuticals (Basel, Switzerland) · 2020
    Article
  6. Article
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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 1 institution in 1 country.

Qi Qiaoa Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.
Freek G Bouwmana Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.ORCID 0000-0002-5582-1370
Marleen A van Baaka Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.
Nadia J T Roumansb Institute for Technology-Inspired Regenerative Medicine, MERLN , Maastricht University Medical Centre , Maastricht , The Netherlands.
Roel G Vinka Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.
Susan L M Coortc Department of Bioinformatics, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.ORCID 0000-0003-1224-9690
Johan W Renesa Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.
Edwin C M Marimana Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism , Maastricht University Medical Centre , Maastricht , The Netherlands.ORCID 0000-0002-5691-8633
Maastricht University Medical Centre · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term weight loss maintenance is a problem of overweight and obesity. Changes of gene expression during weight loss (WL) by calorie restriction (CR) are linked to the risk of weight regain (WR). However, detailed information on genes/proteins involved in the mechanism is still lacking. Therefore, we developed an in-vitro model system for glucose restriction (GR) and refeeding (RF) to uncover proteome differences between GR with RF vs normal feeding, of which we explored the relation with WR after WL. Human Simpson-Golabi-Behmel Syndrome cells were subjected to changing levels of glucose to mimic the condition of CR and RF. Proteome profiling was performed by liquid chromatography tandem mass spectrometry. This in-vitro model revealed 44 proteins differentially expressed after GR and RF versus feeding including proteins of the focal adhesions. Four proteins showed a persistent up- or down-regulation: liver carboxylesterase (CES1), mitochondrial superoxide dismutase [Mn] (SOD2), alpha-crystallin B-chain (CRYAB), alpha-enolase (ENO1). In-vivo weight loss-induced RNA expression changes linked CES1, CRYAB and ENO1 to WR. Moreover, of these 44 proteins, CES1 and glucosidase II alpha subunit (GANAB) during follow up correlated with WR. Correlation clustering of in-vivo protein expression data indicated an interaction of these proteins with structural components of the focal adhesions and cytoplasmic filaments in the adipocytes.

Indexed as

Weight GainAdipocytesalpha-Crystallin B ChainBiomarkers, TumorCarboxylic Ester HydrolasesCells, CulturedDNA-Binding ProteinsGlucoseGlucosidasesHumansPhosphopyruvate HydrataseTumor Suppressor Proteinsalpha-Crystallin B ChainBiomarkers, TumorCarboxylic Ester HydrolasesCES1 protein, humanCRYAB protein, humanDNA-Binding ProteinsENO1 protein, humanGANAB protein, humanGlucoseGlucosidasesPhosphopyruvate HydrataseTumor Suppressor Proteinsfat-regainfocal adhesionproteomicsSGBS adipocytesweight regain

Identifiers

PMID31037987
PMCPMC6768247
OpenAlexW2942557900

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.