Evidence map›Paper›PMID 24695116›Full record

Trial reportPloS one2014

Metabolic signatures of cultured human adipocytes from metabolically healthy versus unhealthy obese individuals.

Anja Böhm, Anna Halama, Tobias Meile, Marty Zdichavsky, Rainer Lehmann, Cora Weigert, Andreas Fritsche, Norbert Stefan, Alfred Königsrainer, Hans-Ulrich Häring and 3 more

Open access · goldAbstract readClinical TrialComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Fibroblast Growth Factor 21 Is Elevated in HIV and Associated With Interleukin-6.Journal of acquired immune deficiency syndromes (1999) · 2020
    Article
  16. Observational
  17. Article
  18. Article
  19. Article
  20. 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

13 authors at 4 institutions in 1 country.

Anja BöhmHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
Anna HalamaHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany.
Tobias MeileDepartment of General, Visceral and Transplant Surgery, University Hospital, Eberhard Karls University, Tübingen, Germany.
Marty ZdichavskyDepartment of General, Visceral and Transplant Surgery, University Hospital, Eberhard Karls University, Tübingen, Germany.
Rainer LehmannDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
Cora WeigertHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
Andreas FritscheDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
Norbert StefanDepartment of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
Alfred KönigsrainerDepartment of General, Visceral and Transplant Surgery, University Hospital, Eberhard Karls University, Tübingen, Germany.
Hans-Ulrich HäringHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
Martin Hrabě de AngelisHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany; German Center for Diabetes Research, Neuherberg, Germany; Chair of Experimental Genetics, Technical University München, Freising-Weihenstephan, Germany.
Jerzy AdamskiHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany; German Center for Diabetes Research, Neuherberg, Germany; Chair of Experimental Genetics, Technical University München, Freising-Weihenstephan, Germany.
Harald StaigerHelmholtz Zentrum München, German Research Center for Environmental Health, Institute of Experimental Genetics, Genome Analysis Center, Neuherberg, Germany; Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology, and Clinical Chemistry, University Hospital, Eberhard Karls University, Tübingen, Germany; German Center for Diabetes Research, Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center München at the Eberhard Karls University of Tübingen, Tübingen, Germany.
University of Tübingen · DEDeutsches Diabetes-Zentrum e.V. · DEHelmholtz Zentrum München · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsAmong obese subjects, metabolically healthy and unhealthy obesity (MHO/MUHO) can be differentiated: the latter is characterized by whole-body insulin resistance, hepatic steatosis, and subclinical inflammation. Aim of this study was, to identify adipocyte-specific metabolic signatures and functional biomarkers for MHO versus MUHO.

methods10 insulin-resistant (IR) vs. 10 insulin-sensitive (IS) non-diabetic morbidly obese (BMI >40 kg/m2) Caucasians were matched for gender, age, BMI, and percentage of body fat. From subcutaneous fat biopsies, primary preadipocytes were isolated and differentiated to adipocytes in vitro. About 280 metabolites were investigated by a targeted metabolomic approach intracellularly, extracellularly, and in plasma. RESULTS/

interpretationAmong others, aspartate was reduced intracellularly to one third (p = 0.0039) in IR adipocytes, pointing to a relative depletion of citric acid cycle metabolites or reduced aspartate uptake in MUHO. Other amino acids, already known to correlate with diabetes and/or obesity, were identified to differ between MUHO's and MHO's adipocytes, namely glutamine, histidine, and spermidine. Most species of phosphatidylcholines (PCs) were lower in MUHO's extracellular milieu, though simultaneously elevated intracellularly, e.g., PC aa C32∶3, pointing to increased PC synthesis and/or reduced PC release. Furthermore, altered arachidonic acid (AA) metabolism was found: 15(S)-HETE (15-hydroxy-eicosatetraenoic acid; 0 vs. 120pM; p = 0.0014), AA (1.5-fold; p = 0.0055) and docosahexaenoic acid (DHA, C22∶6; 2-fold; p = 0.0033) were higher in MUHO. This emphasizes a direct contribution of adipocytes to local adipose tissue inflammation. Elevated DHA, as an inhibitor of prostaglandin synthesis, might be a hint for counter-regulatory mechanisms in MUHO. CONCLUSION/

interpretationWe identified adipocyte-inherent metabolic alterations discriminating between MHO and MUHO.

Indexed as

Insulin ResistanceAdipocytesAdultArachidonic AcidsCells, CulturedFemaleHumansMaleMiddle AgedObesity, MorbidArachidonic Acids

Identifiers

PMID24695116
PMCPMC3973696
OpenAlexW2036273215

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.