Evidence map›Paper›PMID 27702832›Full record

ArticleDiabetes2016

Impact of Perturbed Pancreatic β-Cell Cholesterol Homeostasis on Adipose Tissue and Skeletal Muscle Metabolism.

Blake J Cochran, Liming Hou, Anil Paul Chirackal Manavalan, Benjamin M Moore, Fatiha Tabet, Afroza Sultana, Luisa Cuesta Torres, Shudi Tang, Sudichhya Shrestha, Praween Senanayake and 9 more

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. HDL and Diabetes.Advances in experimental medicine and biology · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Macrophage functions in lean and obese adipose tissue.Metabolism: clinical and experimental · 2017
    Review
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 5 institutions in 3 countries.

Blake J CochranLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Liming HouLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Anil Paul Chirackal ManavalanLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Benjamin M MooreDivision of Medicine, Royal Prince Alfred Hospital, Sydney, Australia.
Fatiha TabetLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Afroza SultanaLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Luisa Cuesta TorresLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Shudi TangLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Sudichhya ShresthaLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Praween SenanayakeLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Mili PatelLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
William J RyderLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Andre BongersBiological Resource Imaging Laboratory, Mark Wainwright Analytical Centre, University of New South Wales Australia, Sydney, Australia.
Marie MaraninchiAix-Marseille Université, UMR_S1062, UMR_A1260, Nutrition, Obésité et Risque Thrombotique, Marseille, France.
Valerie C WasingerBioanalytical Mass Spectrometry Facility, Mark Wainwright Analytical Centre, University of New South Wales Australia, Sydney, Australia.
Marit WesterterpDivision of Molecular Medicine, Department of Medicine, Columbia University, New York, NY.
Alan R TallDivision of Molecular Medicine, Department of Medicine, Columbia University, New York, NY.
Philip J BarterLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia.
Kerry-Anne RyeLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales Australia, Sydney, Australia k.rye@unsw.edu.au karye@ozemail.com.au.
UNSW Sydney · AUColumbia University · USAix-Marseille Université · FRRoyal Prince Alfred Hospital · AUUniversity of Sydney · AU

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TALL, ALAN RICHARD · 2007 to 2022
$31.2M
NHLBI NIH HHS P01 HL087123
6 · The paper itself

Abstract

Elevated pancreatic β-cell cholesterol levels impair insulin secretion and reduce plasma insulin levels. This study establishes that low plasma insulin levels have a detrimental effect on two major insulin target tissues: adipose tissue and skeletal muscle. Mice with increased β-cell cholesterol levels were generated by conditional deletion of the ATP-binding cassette transporters, ABCA1 and ABCG1, in β-cells (β-DKO mice). Insulin secretion was impaired in these mice under basal and high-glucose conditions, and glucose disposal was shifted from skeletal muscle to adipose tissue. The β-DKO mice also had increased body fat and adipose tissue macrophage content, elevated plasma interleukin-6 and MCP-1 levels, and decreased skeletal muscle mass. They were not, however, insulin resistant. The adipose tissue expansion and reduced skeletal muscle mass, but not the systemic inflammation or increased adipose tissue macrophage content, were reversed when plasma insulin levels were normalized by insulin supplementation. These studies identify a mechanism by which perturbation of β-cell cholesterol homeostasis and impaired insulin secretion increase adiposity, reduce skeletal muscle mass, and cause systemic inflammation. They further identify β-cell dysfunction as a potential therapeutic target in people at increased risk of developing type 2 diabetes.

Indexed as

Adipose TissueAnimalsATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1Blotting, WesternCholesterolFatty Acid SynthasesGlucoseGlycogenHomeostasisInsulinInsulin-Secreting CellsLactic AcidMagnetic Resonance ImagingMass SpectrometryMiceAbca1 protein, mouseABCG1 protein, mouseATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1CholesterolFatty Acid SynthasesGlucoseGlycogenInsulinLactic Acid

Identifiers

PMID27702832
PMCPMC5132410
OpenAlexW2529433179

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.