Evidence map›Paper›PMID 37076885›Full record

ArticleBMC medicine2023

The impact of metabolic endotoxaemia on the browning process in human adipocytes.

Farah Omran, Alice M Murphy, Awais Z Younis, Ioannis Kyrou, Jana Vrbikova, Vojtech Hainer, Petra Sramkova, Martin Fried, Graham Ball, Gyanendra Tripathi and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.3field-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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Propionate Induces Energy Expenditure via Browning in Mesenteric Adipose Tissue.The Journal of clinical endocrinology and metabolism · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. The Effect of Enteric-Derived Lipopolysaccharides on Obesity.International journal of molecular sciences · 2024
    Review
  12. Review
  13. Article
  14. Nutrients · 2023
    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 7 institutions in 2 countries.

Farah Omran *Division of Biomedical Sciences, Warwick Medical School, University of Warwick, Coventry, CV2 2DX, UK.
Alice M Murphy *Department of Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham, NG11 8NS, UK.
Awais Z YounisDepartment of Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham, NG11 8NS, UK.
Ioannis KyrouWarwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry, CV2 2DX, UK.
Jana VrbikovaInstitute of Endocrinology, Prague, Czech Republic.
Vojtech HainerInstitute of Endocrinology, Prague, Czech Republic.
Petra SramkovaOB Clinic, Prague, Czech Republic.
Martin FriedOB Clinic, Prague, Czech Republic.
Graham BallMedical Technology Research Centre, Anglia Ruskin University, Cambridge, UK.
Gyanendra TripathiHuman Sciences Research Centre, College of Life and Natural Sciences, University of Derby, Derby, DE22 1GB, UK.
Sudhesh KumarWarwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry, CV2 2DX, UK.
Philip G McTernanDepartment of Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham, NG11 8NS, UK. philip.mcternan@ntu.ac.uk.
Mark ChristianDepartment of Biosciences, School of Science and Technology, Nottingham Trent University, Nottingham, NG11 8NS, UK. mark.christian@ntu.ac.uk.
Nottingham Trent University · GBInstitute of Endocrinology · CZAnglia Ruskin University · GBAston University · GBUniversity Hospitals Coventry and Warwickshire NHS Trust · GBUniversity of Derby · GBUniversity of Warwick · GB

Funding

Biotechnology and Biological Sciences Research Council BB/P008879/2
6 · The paper itself

Abstract

backgroundDysfunctional adipose tissue (AT) is known to contribute to the pathophysiology of metabolic disease, including type 2 diabetes mellitus (T2DM). This dysfunction may occur, in part, as a consequence of gut-derived endotoxaemia inducing changes in adipocyte mitochondrial function and reducing the proportion of BRITE (brown-in-white) adipocytes. Therefore, the present study investigated whether endotoxin (lipopolysaccharide; LPS) directly contributes to impaired human adipocyte mitochondrial function and browning in human adipocytes, and the relevant impact of obesity status pre and post bariatric surgery.

methodsHuman differentiated abdominal subcutaneous (AbdSc) adipocytes from participants with obesity and normal-weight participants were treated with endotoxin to assess in vitro changes in mitochondrial function and BRITE phenotype. Ex vivo human AbdSc AT from different groups of participants (normal-weight, obesity, pre- and 6 months post-bariatric surgery) were assessed for similar analyses including circulating endotoxin levels.

resultsEx vivo AT analysis (lean & obese, weight loss post-bariatric surgery) identified that systemic endotoxin negatively correlated with BAT gene expression (p < 0.05). In vitro endotoxin treatment of AbdSc adipocytes (lean & obese) reduced mitochondrial dynamics (74.6% reduction; p < 0.0001), biogenesis (81.2% reduction; p < 0.0001) and the BRITE phenotype (93.8% reduction; p < 0.0001). Lean AbdSc adipocytes were more responsive to adrenergic signalling than obese AbdSc adipocytes; although endotoxin mitigated this response (92.6% reduction; p < 0.0001).

conclusionsTaken together, these data suggest that systemic gut-derived endotoxaemia contributes to both individual adipocyte dysfunction and reduced browning capacity of the adipocyte cell population, exacerbating metabolic consequences. As bariatric surgery reduces endotoxin levels and is associated with improving adipocyte functionality, this may provide further evidence regarding the metabolic benefits of such surgical interventions.

Indexed as

Diabetes Mellitus, Type 2EndotoxemiaAdipocytesEndotoxinsHumansLipopolysaccharidesObesityEndotoxinsLipopolysaccharidesAdipocyte browningBariatric surgeryEndotoxinHuman adipocytesLipopolysaccharideMitochondriaObesity

Identifiers

PMID37076885
PMCPMC10116789
OpenAlexW4366581008

What Socratic 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 Socratic graph.