Evidence map›Paper›PMID 18029454›Full record

ArticleThe Journal of clinical endocrinology and metabolism2008

Increased toll-like receptor (TLR) 2 and TLR4 expression in monocytes from patients with type 1 diabetes: further evidence of a proinflammatory state.

Sridevi Devaraj, Mohan R Dasu, Jason Rockwood, William Winter, Steven C Griffen, Ishwarlal Jialal

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed, 1 pooled it
10.7field-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

184 citing papers in PubMed, 1 synthesis or guideline pooled it, 370 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Elevated Markers of Intestinal Barrier Dysfunction and TLR2 Ligands in Individuals with Type 1 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The advantages ofFuture microbiology · 2025
    Review
  13. Review
  14. Article
  15. Sigma-1 Receptor as a Novel Therapeutic Target in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

124 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

6 authors at 2 institutions in 1 country.

Sridevi DevarajLaboratory for Atherosclerosis and Metabolic Research, University of California Davis Medical Center, Sacramento, California 95817, USA.
Mohan R Dasu
Jason Rockwood
William Winter
Steven C Griffen
Ishwarlal Jialal
University of California Davis Medical Center · USUniversity of Florida · US

Funding

Cellular pathways of inflammation in type 1 diabetesR33DK069801 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DEVARAJ, SRIDEVI · 2007 to 2008
$1.3M
CLINICAL STUDIES IN NUTRITION AND METABOLISMK24AT000596 · NCCIH · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI JIALAL, ISHWARLAL · 2000 to 2009
$1.3M
Cellular pathways of inflammation in type 1 diabetesR21DK069801 · NIDDK · UNIVERSITY OF CALIFORNIA DAVIS · PI DEVARAJ, SRIDEVI · 2004 to 2005
$747k
NCCIH NIH HHS K24 AT000596NCCIH NIH HHS K24 AT 00596NIDDK NIH HHS DK69801NIDDK NIH HHS R21 DK069801NIDDK NIH HHS R33 DK069801
6 · The paper itself

Abstract

contextType 1 diabetes (T1DM) is associated with increased cardiovascular mortality. It is a pro-inflammatory state as evidenced by increased circulating biomarkers and monocyte activity. The toll-like receptors (TLRs) are pattern recognition receptors, expressed abundantly on monocytes. TLR2 and TLR4 are important in atherosclerosis. However, there is a paucity of data examining TLR2 and TLR4 expression in T1DM and examining its contribution to the proinflammatory state.

objectiveThus, we examined TLR2 and TLR4 expression in monocytes from T1DM patients compared with controls (n = 31 per group).

settingThe study was performed at the University of California Davis Medical Center. PATIENTS: Healthy controls (n = 31) and T1DM patients (n = 31) were included in the study.

resultsTLR2 and TLR4 surface expression and mRNA were significantly increased in T1DM monocytes compared with controls. Downstream targets of TLR, nuclear factor kappaB, myeloid differentiation factor 88, Trif, and phosphorylated IL-1 receptor-associated kinase were significantly up-regulated in T1DM. Finally, the release of IL-1beta and TNF-alpha was significantly increased in monocytes from T1DM compared with controls and correlated with TLR2 and TLR4 expression (P < 0.005). In addition, TLR2 and TLR4 expression was significantly correlated to glycosylated hemoglobin, carboxymethyllysine, and nuclear factor kappaB (P < 0.02).

conclusionThus, we make the novel observation that TLR2 and TLR4 expression and signaling are increased in T1DM and contribute to the proinflammatory state.

Indexed as

AdultBlotting, WesternDiabetes Mellitus, Type 1FemaleHumansInterleukin-1betaInterleukin-1 Receptor-Associated KinasesLeukocytes, MononuclearMaleMyeloid Differentiation Factor 88NF-kappa BReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionStatistics, NonparametricToll-Like Receptor 2Interleukin-1betaInterleukin-1 Receptor-Associated KinasesMYD88 protein, humanMyeloid Differentiation Factor 88NF-kappa BRNA, MessengerTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID18029454
PMCPMC2243229
OpenAlexW2035717904

What OpenQuestion holds

Textmetadata
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.