Evidence map›Paper›PMID 21569294›Full record

ArticleDiagnostic pathology2011

The CEACAM1 expression is decreased in the liver of severely obese patients with or without diabetes.

Wonae Lee

Abstract read
In one paragraph

Article in Diagnostic pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

42 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. CEACAM1: Shielding the liver against fibrosis.European journal of clinical investigation · 2024
    Article
  11. Review
  12. Loss of CEACAM1 in endothelial cells causes hepatic fibrosis.Metabolism: clinical and experimental · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Insulin Clearance in Obesity and Type 2 Diabetes.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Review
  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

1 author.

Wonae LeeDepartment of Pathology, Dankook University College of Medicine, Cheonan, Korea. walee@dankook.ac.kr

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes is mainly caused by insulin resistance. The carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is an important candidate for causing insulin resistance.

methodsThe CEACAM1 expression was evaluated immunohistochemically in the liver tissues of 99 severely obese or non-obese subjects with or without diabetes. The CEACAM1 expression was classified into two categories: a normal expression or a decreased expression.

resultsThe CEACAM1 expression was markedly decreased in the hepatocytes with macrovesicular steatosis. A decreased CEACAM1 expression was noted in 29 (29%) of 99 cases. The incidence of a decreased CEACAM1 expression was significantly higher in high grade fatty liver as well as severe obesity with or without diabetes (p < 0.05). The incidence of a decreased CEACAM1 expression was not different between the diabetic and non-diabetic groups.

conclusionsThis data supports that a decreased CEACAM1 expression is related to obesity and a fatty liver.

Indexed as

AdultAgedAged, 80 and overAntigens, CDBiomarkersBiopsyCell Adhesion MoleculesDiabetes Mellitus, Type 2Fatty LiverHepatocytesHumansMiddle AgedObesity, MorbidAntigens, CDBiomarkersCD66 antigensCell Adhesion Molecules

Identifiers

PMID21569294
PMCPMC3104481

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.