Evidence map›Paper›PMID 20353583›Full record

ArticleJournal of inflammation (London, England)2010

Elevated endotoxin levels in non-alcoholic fatty liver disease.

Alison L Harte, Nancy F da Silva, Steven J Creely, Kirsty C McGee, Thomas Billyard, Elham M Youssef-Elabd, Gyanendra Tripathi, Esmat Ashour, Mohga S Abdalla, Hayat M Sharada and 5 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of inflammation (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed, 1 pooled it
11.2field-weighted citation impact, top 1% 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

215 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Review
  7. Article
  8. Activation of the noncanonical inflammasome-GSDMD pathway triggers pyroptosis in bone marrow and promotes periosteal bone formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Observational
  19. Review
  20. Article

155 more citing papers are in PubMed but not listed here.

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

15 authors at 4 institutions in 2 countries.

Alison L Harte *University of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Nancy F da Silva *University of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Steven J CreelyUniversity of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Kirsty C McGeeUniversity of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Thomas BillyardUniversity of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Elham M Youssef-ElabdBiochemistry Dept, National Research Center, Dokki, Giza, Egypt.
Gyanendra TripathiUniversity of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Esmat AshourBiochemistry Dept, National Research Center, Dokki, Giza, Egypt.
Mohga S AbdallaChemistry Dept, Faculty of Science, Helwan University, Egypt.
Hayat M SharadaChemistry Dept, Faculty of Science, Helwan University, Egypt.
Ashraf I AminClinical Pathology Dept, National Institute of Diabetes & Endocrinology, Cairo, Egypt.
Alastair D BurtSchool of Clinical Medicine (Hepatology), Floor 4, William Leech Building, The Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
Sudhesh KumarUniversity of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
Christopher P DaySchool of Clinical Medicine (Hepatology), Floor 4, William Leech Building, The Medical School, Framlington Place, Newcastle upon Tyne NE2 4HH, UK.
Philip G McTernanUniversity of Warwick, Unit for Diabetes and Metabolism, Warwick Medical School, Clinical Sciences Research Institute, UHCW, Clifford Bridge Road, Coventry, CV2 2DX, UK.
University of Warwick · GBHelwan University · EGNational Research Centre · EGNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging data indicate that gut-derived endotoxin may contribute to low-grade systemic inflammation in insulin resistant states. This study aimed to examine the importance of serum endotoxin and inflammatory markers in non-alcoholic fatty liver disease (NAFLD) patients, with and without type 2 diabetes mellitus (T2DM), and to explore the effect of treatment with a lipase inhibitor, Orlistat, on their inflammatory status.

methodsFasted serum from 155 patients with biopsy proven NAFLD and 23 control subjects were analysed for endotoxin, soluble CD14 (sCD14), soluble tumour necrosis factor receptor II (sTNFRII) and various metabolic parameters. A subgroup of NAFLD patients were re-assessed 6 and 12 months after treatment with diet alone (n = 6) or diet plus Orlistat (n = 8).

resultsEndotoxin levels were significantly higher in patients with NAFLD compared with controls (NAFLD: 10.6(7.8, 14.8) EU/mL; controls: 3.9(3.2, 5.2) EU/mL, p < 0.001); NAFLD alone produced comparable endotoxin levels to T2DM (NAFLD: T2DM: 10.6(5.6, 14.2) EU/mL; non-diabetic: 10.6(8.5, 15.2) EU/mL), whilst a significant correlation between insulin resistance and serum endotoxin was observed (r = 0.27, p = 0.008). Both sCD14 (p < 0.01) and sTNFRII (p < 0.001) increased with severity of fibrosis. A positive correlation was also noted between sTNFRII and sCD14 in the NAFLD subjects (r = 0.29, p = 0.004).Sub-cohort treatment with Orlistat in patients with NAFLD showed significant decreases in ALT (p = 0.006), weight (p = 0.005) and endotoxin (p = 0.004) compared with the NAFLD, non-Orlistat treated control cohort at 6 and 12 months post therapy, respectively.

conclusionsEndotoxin levels were considerably increased in NAFLD patients, with marked increases noted in early stage fibrosis compared with controls. These results suggest elevated endotoxin may serve as an early indicator of potential liver damage, perhaps negating the need for invasive liver biopsy. As endotoxin may promote insulin resistance and inflammation, interventions aimed at reducing endotoxin levels in NAFLD patients may prove beneficial in reducing inflammatory burden.

Identifiers

PMID20353583
PMCPMC2873499
OpenAlexW2067756762

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.