Evidence map›Paper›PMID 24854430›Full record

ArticleInternational journal of obesity (2005)2015

Phosphorylation of glycogen synthase kinase-3β in metabolically abnormal obesity affects immune stimulation-induced cytokine production.

C-L Yen, W-C Chao, C-H Wu, Y-F Huang, C-S Chang, Y-S Tsai, C-F Lin, C-C Shieh

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Article in International journal of obesity (2005), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

C-L YenInstitute of Basic Medical Science, National Cheng Kung University Medical College, Tainan, Taiwan.
W-C Chao1] Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan [2] Department of Internal Medicine, Taichung Veteran General Hospital, Chiayi Branch, Chiayi, Taiwan.
C-H WuDepartment of Family Medicine, National Cheng Kung University Hospital, Tainan, Taiwan.
Y-F HuangInstitute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan.
C-S ChangDepartment of Family Medicine, National Cheng Kung University Hospital, Tainan, Taiwan.
Y-S TsaiInstitute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan.
C-F LinInstitute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan.
C-C Shieh1] Institute of Basic Medical Science, National Cheng Kung University Medical College, Tainan, Taiwan [2] Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan, Taiwan [3] Department of Pediatrics, National Cheng Kung University Hospital, Tainan, Taiwan.
National Cheng Kung University · TWNational Cheng Kung University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is a severe health problem worldwide, which leads to multiple comorbidities including type 2 diabetes mellitus and cardiovascular diseases. Inflammation has been found to be an important characteristic of adipose tissue in obese subjects. However, obesity is also associated with compromised immune responses to infections and the impact of obesity on immune function has not been fully understood. SUBJECTS/

methodsTo clarify the role of obesity in the immune responses, we investigated the Toll-like receptor (TLR)-induced cytokine secretion by leukocytes from obese and lean subjects. We also investigated the relationship between insulin-induced intracellular signaling and cytokine production using peripheral blood mononuclear cells (PBMCs) and a monocytic cell line THP-1.

resultsWe found decreased TLR-induced interferon-γ, interleukin-6 (IL-6) and tumor necrosis factor-α secretions and elevated IL-10 secretion by leukocytes from obese subjects when compared with lean controls. PBMCs from obese subjects showed enhanced basal Akt and glycogen synthase kinase-3β (GSK-3β) phosphorylation, which did not further increase with insulin and lipopolysaccharide (LPS) stimulation. We also found that LPS-induced IκBα degradation was inhibited in PBMCs from obese subjects. By using THP-1 cells with GSK-3β knockdown or cells treated with hyperinsulinemic and high-fatty acid conditions, we found that LPS-induced nuclear factor κB (NF-κB) activation was inhibited and cyclic adenosine monophosphate response element-binding protein (CREB) activation was enhanced.

conclusionsThese findings indicate that GSK-3β is important in the regulation of NF-κB and CREB activation in leukocytes under the metabolic condition of obesity. Our study revealed a key mechanism through which metabolic abnormalities compromise leukocyte functions in people with obesity.

Indexed as

Glycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansHyperinsulinismHyperlipidemiasI-kappa B ProteinsInflammationInterleukin-10Leukocytes, MononuclearNF-kappa BNF-KappaB Inhibitor alphaObesityPhosphorylationSignal TransductionTumor Necrosis Factor-alphaGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanI-kappa B ProteinsIL10 protein, humanInterleukin-10NF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID24854430
OpenAlexW2022745993

What OpenQuestion holds

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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.