Evidence map›Paper›PMID 27340831›Full record

ArticlePloS one2016

Positive Correlation between Enhanced Expression of TLR4/MyD88/NF-κB with Insulin Resistance in Placentae of Gestational Diabetes Mellitus.

Hui Feng, Rina Su, Yilin Song, Chen Wang, Li Lin, Jingmei Ma, Huixia Yang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
6.4field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
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  9. Article
  10. The Placenta as an Immunological Environment.British journal of biomedical science · 2025
    Review
  11. Review
  12. Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  13. Article
  14. Article
  15. Article
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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

7 authors at 2 institutions in 1 country.

Hui FengDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Rina SuDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Yilin SongDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Chen WangDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Li LinDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Jingmei MaDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Huixia YangDepartment of Obstetrics and Gynecology, Peking University First Hospital, Beijing, China.
Peking University · CNPeking University First Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance (IR) is a critical factor of the pathophysiology of Gestational diabetes mellitus (GDM). Studies on key organs involved in IR, such as livers and adipose tissues, showed that Toll-like receptor 4 (TLR4) can regulate insulin sensitivity. As a maternal-fetal interface with multi-functions, placentae could contribute to the development of IR for GDM. Thus, we investigated the expressions of TLR4/Myeloid Differentiation factor 88 (MyD88)/Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) in term placentae from 33 GDM women and 36 healthy pregnant women with normal glucose tolerance, evaluated local and systemic IR and furthermore identified the association between placental TLR4 and IR. TLR4 protein was expressed in various cells of term placenta, particularly in syncytiotrophoblast of villi. Compared with normal pregnancy, the expression of TLR4/MyD88/NF-kB pathway increased in the placenta of GDM (p<0.05), and these differences were more pronounced in the maternal section of the placenta and the syncytiotrophoblast of villi. In addition, more severe IR was observed in the placenta of GDM patients than the control group, evidenced with higher pIRS-1(ser312) (p<0.001) and lower IRS-1 (p<0.05) as well as pAkt proteins (p<0.01). The expression of TLR4 in placentae is positively correlated with local IR (pIRS-1: r = 0.76, p <0.001 and pAkt: r = -0.47, p <0.001) and maternal fasting (r = 0.42, p <0.01), one-hour (r = 0.52, p <0.01) and two-hour glucose (r = 0.54, p <0.01) at OGTT. We found an that enhanced expression of the TLR4-MyD88-NF-kB pathway occurs in GDM placentae, which positively correlates with heightened local IR in placentae and higher maternal hyperglycemia. The TLR4/MyD88/NF-kB pathway may play a potential role in the development of IR in placentae of GDM.

Indexed as

Gene ExpressionInsulin ResistanceAdultBiomarkersBlood GlucoseCase-Control StudiesDiabetes, GestationalFemaleHumansMyeloid Differentiation Factor 88NF-kappa BPlacentaPregnancySignal TransductionToll-Like Receptor 4BiomarkersBlood GlucoseMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptor 4

Identifiers

PMID27340831
PMCPMC4920413
OpenAlexW2468847473

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Registered trials

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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.