Evidence map›Paper›PMID 27257600›Full record

ArticleMolecular metabolism2016

A comprehensive lipidomic screen of pancreatic β-cells using mass spectroscopy defines novel features of glucose-stimulated turnover of neutral lipids, sphingolipids and plasmalogens.

Gemma L Pearson, Natalie Mellett, Kwan Yi Chu, Ebru Boslem, Peter J Meikle, Trevor J Biden

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Article
  3. Contribution of specific ceramides to obesity-associated metabolic diseases.Cellular and molecular life sciences : CMLS · 2022
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Plasma lipid species at type 1 diabetes onset predict residual beta-cell function after 6 months.Metabolomics : Official journal of the Metabolomic Society · 2018
    Observational
  16. Article
  17. Review
  18. Article
  19. Article
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

6 authors at 4 institutions in 1 country.

Gemma L PearsonDiabetes and Metabolism Division, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, NSW, 2010, Australia; St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Australia.
Natalie MellettBaker IDI Heart and Diabetes Institute, Melbourne, Australia.
Kwan Yi ChuDiabetes and Metabolism Division, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, NSW, 2010, Australia.
Ebru BoslemDiabetes and Metabolism Division, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, NSW, 2010, Australia; St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Australia.
Peter J MeikleBaker IDI Heart and Diabetes Institute, Melbourne, Australia. Electronic address: peter.meikle@bakeridi.edu.au.
Trevor J BidenDiabetes and Metabolism Division, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, NSW, 2010, Australia; St. Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Australia. Electronic address: t.biden@garvan.org.au.
Baker Heart and Diabetes Institute · AUGarvan Institute of Medical Research · AUSt Vincent's Clinic · AUUNSW Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGlucose promotes lipid remodelling in pancreatic β-cells, and this is thought to contribute to the regulation of insulin secretion, but the metabolic pathways and potential signalling intermediates have not been fully elaborated.

methodsUsing mass spectrometry (MS) we quantified changes in approximately 300 lipid metabolites in MIN6 β-cells and isolated mouse islets following 1 h stimulation with glucose. Flux through sphingolipid pathways was also assessed in (3)H-sphinganine-labelled cells using TLC.

resultsGlucose specifically activates the conversion of triacylglycerol (TAG) to diacylglycerol (DAG). This leads indirectly to the formation of 18:1 monoacylglycerol (MAG), via degradation of saturated/monounsaturated DAG species, such as 16:0_18:1 DAG, which are the most abundant, immediate products of glucose-stimulated TAG hydrolysis. However, 16:0-containing, di-saturated DAG species are a better direct marker of TAG hydrolysis since, unlike the 18:1-containing DAGs, they are predominately formed via this route. Using multiple reaction monitoring, we confirmed that in islets under basal conditions, 18:1 MAG is the most abundant species. We further demonstrated a novel site of glucose to enhance the conversion of ceramide to sphingomyelin (SM) and galactosylceramide (GalCer). Flux and product:precursor analyses suggest regulation of the enzyme SM synthase, which would constitute a separate mechanism for localized generation of DAG in response to glucose. Phosphatidylcholine (PC) plasmalogen (P) species, specifically those containing 20:4, 22:5 and 22:6 side chains, were also diminished in the presence of glucose, whereas the more abundant phosphatidylethanolamine plasmalogens were unchanged.

conclusionOur results highlight 18:1 MAG, GalCer, PC(P) and DAG/SM as potential contributors to metabolic stimulus-secretion coupling.

Indexed as

ATGL, adipose tissue glycerolipaseCE, cholesterol esterCeramideCOH, free cholesterolDAG, diacylglycerolDiacylglycerolFA, fatty acidGalCer, galactosylceramideGluCer, glucosylceramideGSIS, glucose-stimulated insulin secretionHSL, hormone sensitive lipaseInsulin secretionKRHB, Krebs Ringer Hepes BufferMAG, monacylglycerolMHC, monohexosylceramideMonacylglycerolMS, mass spectrometry(O), ether lipidPancreatic β-cellPC, phosphatidylcholinePE, phosphatidylethanolaminePI, phosphatidylinositolPKD, protein kinase DPLA2, phospholipase A2Plasmalogen(P), plasmalogenSM, sphingomyelinTAG, triacylglycerol

Identifiers

PMID27257600
PMCPMC4877660
OpenAlexW2340621143

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.