Evidence map›Paper›PMID 25915184›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

ACSL1 Is Associated With Fetal Programming of Insulin Sensitivity and Cellular Lipid Content.

Roy Joseph, Jeremie Poschmann, Rami Sukarieh, Peh Gek Too, Sofi G Julien, Feng Xu, Ai Ling Teh, Joanna D Holbrook, Kai Lyn Ng, Yap Seng Chong and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

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  14. The Combined Partial Knockdown ofAntioxidants (Basel, Switzerland) · 2022
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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

13 authors at 4 institutions in 2 countries.

Roy JosephSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Jeremie PoschmannSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Rami SukariehSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Peh Gek TooSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Sofi G JulienSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Feng XuSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Ai Ling TehSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Joanna D HolbrookSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Kai Lyn NgSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Yap Seng ChongSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Peter D GluckmanSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Shyam PrabhakarSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Walter StünkelSingapore Institute for Clinical Sciences (R.J., R.S., P.G.T., S.G.J., F.X., A.L.T., J.D.H., Y.S.C., P.D.G., W.S.), Agency for Science, Technology and Research, Singapore 117609; Genome Institute of Singapore (J.P., S.P.), Agency for Science, Technology and Research, Singapore 138672; Department of Obstetrics and Gynaecology (K.L.N., Y.S.C.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119228; and Liggins Institute (P.D.G.), University of Auckland, Auckland 1142, New Zealand.
Agency for Science, Technology and Research · SGSingapore Institute for Clinical Sciences · SGNational University of Singapore · SGGenome Institute of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Individuals who are born small for gestational age (SGA) have a risk to develop various metabolic diseases during their life course. The biological memory of the prenatal state of growth restricted individuals may be reflected in epigenetic alterations in stem cell populations. Mesenchymal stem cells (MSCs) from the Wharton's jelly of umbilical cord tissue are multipotent, and we generated primary umbilical cord MSC isolates from SGA and normal neonates, which were subsequently differentiated into adipocytes. We established chromatin state maps for histone marks H3K27 acetylation and H3K27 trimethylation and tested whether enrichment of these marks was associated with gene expression changes. After validating gene expression levels for 10 significant chromatin immunoprecipitation sequencing candidate genes, we selected acyl-coenzyme A synthetase 1 (ACSL1) for further investigations due to its key roles in lipid metabolism. The ACSL1 gene was found to be highly associated with histone acetylation in adipocytes differentiated from MSCs with SGA background. In SGA-derived adipocytes, the ACSL1 expression level was also found to be associated with increased lipid loading as well as higher insulin sensitivity. ACSL1 depletion led to changes in expression of candidate genes such as proinflammatory chemokines and down-regulated both, the amount of cellular lipids and glucose uptake. Increased ACSL1, as well as modulated downstream candidate gene expression, may reflect the obese state, as detected in mice fed a high-fat diet. In summary, we believe that ACSL1 is a programmable mediator of insulin sensitivity and cellular lipid content and adipocytes differentiated from Wharton's jelly MSCs recapitulate important physiological characteristics of SGA individuals.

Indexed as

Fetal DevelopmentLipid MetabolismAcetylationAdipocytesAdipogenesisAnimalsCell DifferentiationCells, CulturedChromatin ImmunoprecipitationCoenzyme A LigasesCytokinesEpigenesis, GeneticGene Knockdown TechniquesGenetic Association StudiesGlucoseHistonesACSL1 protein, humanACSL1 protein, mouseCoenzyme A LigasesCytokinesGlucoseHistonesInsulinLysine

Identifiers

PMID25915184
PMCPMC5414735
OpenAlexW2055098534

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.