Evidence map›Paper›PMID 17180352›Full record

ArticleDiabetologia2007

Role of inflammatory mediators in the suppression of insulin receptor phosphorylation in circulating mononuclear cells of obese subjects.

H Ghanim, A Aljada, N Daoud, R Deopurkar, A Chaudhuri, P Dandona

Registry-linked trialOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01722266 (Liraglutide in the Treatment of Type 1 Diabetes Mellitus), which is not on this map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.1field-weighted citation impact, top 5% 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.

NCT01722266 phase3completedstarted 2012, after this paper: background citation

Liraglutide in the Treatment of Type 1 Diabetes Mellitus

Ran2012Enrolled72Registered outcomes7Posted comparisons0ConditionsType 1 DiabetesArmsliraglutide, Placebo
Open the trial in the graph
3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 95 citations in OpenAlex.

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  11. The effect ofFrontiers in endocrinology · 2023
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  19. How much does obesity affect the male reproductive function?International journal of obesity supplements · 2019
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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

6 authors at 2 institutions in 1 country.

H GhanimDivision of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo, Buffalo, NY, USA.
A Aljada
N Daoud
R Deopurkar
A Chaudhuri
P Dandona
University at Buffalo, State University of New York · USKaleida Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisObesity is associated with insulin resistance and inflammation. The circulating human mononuclear cell (MNC) has been shown to respond to low-dose insulin infusion. We have now investigated whether in obesity: (1) phosphorylated insulin receptor beta subunit (p-INSR-beta) is reduced in the MNC; (2) pro-inflammatory mediators including inhibitor of kappa light polypeptide gene enhancer in B cells-kinase beta (IKBKB), suppressor of cytokine signalling-3 (SOCS) and protein kinase C-beta 2 (PRKCB2) are increased and related to p-INSR-beta; and (3) the reduction in MNC p-INSR-beta is related to the reduction in insulin sensitivity. MATERIALS AND

methodsMNCs were prepared from fasting blood samples of 16 normal weight and 16 obese female subjects.

resultsOur data show that p-INSR-beta is reduced significantly in MNCs from obese subjects compared with that of normal controls. MNCs from obese subjects have higher IKBKB expression, increased nuclear factor kappa B (NFkappaB) binding and higher mRNA expression of TNFAIP1 and IL6 genes. NFkappaB binding, TNFAIP1 mRNA and plasma C-reactive protein are inversely related to p-INSR-beta. PRKCB2 mRNA and protein expression were significantly higher in the obese subjects and were related significantly to pro-inflammatory mediators but not to p-INSR-beta. SOCS3 mRNA expression was markedly elevated and positively related to pro-inflammatory mediators including IKBKB and PRKCB2 on the one hand and inversely related to p-INSR-beta on the other. CONCLUSIONS/

interpretationWe conclude that in obesity the MNC is characterised by reduced p-INSR-beta and increased inflammatory mediators including IKBKB, PRKCB2 and SOCS3. The increase in SOCS3 but not IKBKB or PRKCB2 is related inversely to p-INSR-beta and might mediate the inhibition of p-INSR-beta. These data elucidate the relationship between inflammation and insulin resistance using the MNC as a model.

Indexed as

AdultBlood PressureCholesterolFatty Acids, NonesterifiedFemaleHumansInflammationInsulinLeukocytes, MononuclearMiddle AgedObesityPhosphorylationReceptor, InsulinReference ValuesTriglyceridesCholesterolFatty Acids, NonesterifiedInsulinReceptor, InsulinTriglycerides

Identifiers

PMID17180352
OpenAlexW2016991304

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.