Evidence map›Paper›PMID 23223024›Full record

ArticleDiabetes2013

Inverse regulation of inflammation and mitochondrial function in adipose tissue defines extreme insulin sensitivity in morbidly obese patients.

Mohammed Qatanani, Yejun Tan, Radu Dobrin, Danielle M Greenawalt, Guanghui Hu, Wenqing Zhao, Jerrold M Olefsky, Dorothy D Sears, Lee M Kaplan, Daniel M Kemp

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.9field-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

36 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. White adipose tissue mitochondrial bioenergetics in metabolic diseases.Reviews in endocrine & metabolic disorders · 2023
    Review
  4. Review
  5. Article
  6. LMO3 reprograms visceral adipocyte metabolism during obesity.Journal of molecular medicine (Berlin, Germany) · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Sex-Specific Regulation of Inflammation and Metabolic Syndrome in Obesity.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Observational
  11. Review
  12. Article
  13. Review
  14. Review
  15. Metabolically healthy obesity: facts and fantasies.The Journal of clinical investigation · 2019
    Review
  16. Review
  17. Review
  18. Article
  19. Genes that make you fat, but keep you healthy.Journal of internal medicine · 2018
    Review
  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

10 authors at 3 institutions in 1 country.

Mohammed QatananiDiscovery and Preclinical Sciences, Merck Research Laboratories, Rahway, New Jersey, USA.
Yejun Tan
Radu Dobrin
Danielle M Greenawalt
Guanghui Hu
Wenqing Zhao
Jerrold M Olefsky
Dorothy D Sears
Lee M Kaplan
Daniel M Kemp
Merck & Co., Inc., Rahway, NJ, USA (United States) · USUniversity of California, San Diego · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is associated with insulin resistance, a major risk factor for type 2 diabetes and cardiovascular disease. However, not all obese individuals are insulin resistant, which confounds our understanding of the mechanistic link between these conditions. We conducted transcriptome analyses on 835 obese subjects with mean BMI of 48.8, on which we have previously reported genetic associations of gene expression. Here, we selected ~320 nondiabetic (HbA(1c) <7.0) subjects and further stratified the cohort into insulin-resistant versus insulin-sensitive subgroups based on homeostasis model assessment-insulin resistance. An unsupervised informatics analysis revealed that immune response and inflammation-related genes were significantly downregulated in the omental adipose tissue of obese individuals with extreme insulin sensitivity and, to a much lesser extent, in subcutaneous adipose tissue. In contrast, genes related to β-oxidation and the citric acid cycle were relatively overexpressed in adipose of insulin-sensitive patients. These observations were verified by querying an independent cohort of our published dataset of 37 subjects whose subcutaneous adipose tissue was sampled before and after treatment with thiazolidinediones. Whereas the immune response and inflammation pathway genes were downregulated by thiazolidinedione treatment, β-oxidation and citric acid cycle genes were upregulated. This work highlights the critical role that omental adipose inflammatory pathways might play in the pathophysiology of insulin resistance, independent of body weight.

Indexed as

Gene Expression Regulation, EnzymologicInsulin ResistanceAdultBiopsyBody Mass IndexCitric Acid CycleCohort StudiesDiabetes Mellitus, Type 2Gene Expression ProfilingHumansHypoglycemic AgentsIntra-Abdominal FatMitochondriaMitochondrial ProteinsObesity, MorbidOligonucleotide Array Sequence AnalysisHypoglycemic AgentsMitochondrial ProteinsRNA, MessengerThiazolidinediones

Identifiers

PMID23223024
PMCPMC3581230
OpenAlexW2123923369

What OpenQuestion holds

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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.