Evidence map›Paper›PMID 26991836›Full record

ArticleStem cells (Dayton, Ohio)2016

Targeting IκB kinase β in Adipocyte Lineage Cells for Treatment of Obesity and Metabolic Dysfunctions.

Robert N Helsley, Yipeng Sui, Se-Hyung Park, Zun Liu, Richard G Lee, Beibei Zhu, Philip A Kern, Changcheng Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The Genetic Blueprint of Obesity: From Pathogenesis to Novel Therapies.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Adipocyte-Derived PXR Signaling Is Dispensable for Diet-Induced Obesity and Metabolic Disorders in Mice.Drug metabolism and disposition: the biological fate of chemicals · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Anti-CD47 antibody treatment attenuates liver inflammation and fibrosis in experimental non-alcoholic steatohepatitis models.Liver international : official journal of the International Association for the Study of the Liver · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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.

Robert N HelsleyDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.
Yipeng SuiDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.
Se-Hyung ParkDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.
Zun LiuDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.
Richard G LeeCardiovascular Antisense Drug Discovery Group, Ionis Pharmaceuticals, Inc., Carlsbad, California, USA.
Beibei ZhuDepartment of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Philip A KernDepartment of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Changcheng ZhouDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky, USA.
University of Kentucky · USIonis Pharmaceuticals (United States) · US

Funding

The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2012 to 2017
$13.7M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
Endocrine disruptor mediated activation of PXR causes dyslipidemia and atherosclerosisR01ES023470 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2013 to 2022
$2.7M
TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
Mechanisms Underlying Metabolic Syndrome in ObesityR01DK071349 · NIDDK · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A, PETERSON, CHARLOTTE A. · 2005 to 2013
$2.3M
Role of IKKβ in obesity and atherosclerosisR01HL131925 · NHLBI · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2016 to 2019
$1.5M
A novel mechanism for ART-associated dyslipidemia and atherosclerosisR01HL123358 · NHLBI · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2015 to 2018
$1.5M
Mechanisms of atherogenic effects of bisphenol AR21ES022745 · NIEHS · UNIVERSITY OF KENTUCKY · PI ZHOU, CHANGCHENG · 2014 to 2015
$413k
NCATS NIH HHS UL1 TR000117NHLBI NIH HHS R01 HL123358NHLBI NIH HHS R01 HL131925NIDDK NIH HHS R01 DK071349NIDDK NIH HHS T32 DK007778NIEHS NIH HHS R01 ES023470NIEHS NIH HHS R21 ES022745NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

IκB kinase β (IKKβ), a central coordinator of inflammation through activation of nuclear factor-κB, has been identified as a potential therapeutic target for the treatment of obesity-associated metabolic dysfunctions. In this study, we evaluated an antisense oligonucleotide (ASO) inhibitor of IKKβ and found that IKKβ ASO ameliorated diet-induced metabolic dysfunctions in mice. Interestingly, IKKβ ASO also inhibited adipocyte differentiation and reduced adiposity in high-fat (HF)-fed mice, indicating an important role of IKKβ signaling in the regulation of adipocyte differentiation. Indeed, CRISPR/Cas9-mediated genomic deletion of IKKβ in 3T3-L1 preadipocytes blocked these cells differentiating into adipocytes. To further elucidate the role of adipose progenitor IKKβ signaling in diet-induced obesity, we generated mice that selectively lack IKKβ in the white adipose lineage and confirmed the essential role of IKKβ in mediating adipocyte differentiation in vivo. Deficiency of IKKβ decreased HF-elicited adipogenesis in addition to reducing inflammation and protected mice from diet-induced obesity and insulin resistance. Further, pharmacological inhibition of IKKβ also blocked human adipose stem cell differentiation. Our findings establish IKKβ as a pivotal regulator of adipogenesis and suggest that overnutrition-mediated IKKβ activation serves as an initial signal that triggers adipose progenitor cell differentiation in response to HF feeding. Inhibition of IKKβ with antisense therapy may represent as a novel therapeutic approach to combat obesity and metabolic dysfunctions. Stem Cells 2016;34:1883-1895.

Indexed as

Cell LineageMolecular Targeted TherapyAdipocytesAdipogenesisAnimalsDietFatty LiverGene DeletionGene Knockdown TechniquesHumansI-kappa B KinaseInsulinMaleMetabolic SyndromeMice, Inbred C57BLObesityI-kappa B KinaseInsulinOligonucleotides, AntisenseAdipogenesisAdipose stem cellsAntisense oligonucleotideIκB kinase βObesity

Identifiers

PMID26991836
PMCPMC4931966
OpenAlexW2297656649

What OpenQuestion holds

Textmetadata
LicenceTDM
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.