Evidence map›Paper›PMID 31427606›Full record

ArticleScientific reports2019

Mechanism of Interleukin-4 Reducing Lipid Deposit by Regulating Hormone-Sensitive Lipase.

Ming-Yuh Shiau, Pei-Hua Chuang, Ching-Ping Yang, Chiao-Wan Hsiao, Shu-Wen Chang, Kai-Yun Chang, Tsung-Ming Liu, Huan-Wen Chen, Cheng-Chieh Chuang, Sheau-Yun Yuan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Ming-Yuh ShiauDepartment of Nursing, College of Nursing, Hungkuang University, Taichung, Taiwan.
Pei-Hua ChuangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Ching-Ping YangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Chiao-Wan HsiaoDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Shu-Wen ChangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Kai-Yun ChangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Tsung-Ming LiuDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Huan-Wen ChenDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Cheng-Chieh ChuangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan.
Sheau-Yun YuanDepartment of Nursing, College of Nursing, Hungkuang University, Taichung, Taiwan.
Yih-Hsin ChangDepartment of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan. cyh@ym.edu.tw.
National Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TWHungkuang University · TWAcademia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence indicates that inflammation participates in the pathophysiological progress from insulin resistance, obesity, metabolic abnormalities, and type 2 diabetes mellitus. Our previous study reveals that interleukin-4 (IL-4) inhibits adipogenesis and promotes lipolysis to decrease lipid deposits by enhancing the activity of hormone sensitive lipase (HSL). The present study further dissects and characterizes the molecular mechanism of IL-4 in regulating HSL expression and lipolytic activity in the terminal differentiated 3T3-L1 mature adipocytes. Our results showed that IL-4 increased cAMP which then enhanced PKA activity and subsequent phosphorylation of HSL and perilipin. The phosphorylated HSL (p-HSL) translocated from cytoplasm to the surface of lipid droplets and exhibited lipolytic function. After being phosphorylated, p-perilipin also facilitated lipolysis through interacting with p-HSL. The in vitro findings were further verified by in vivo study in which IL-4 exhibited pro-lipolytic activity and enhanced HSL activity. In summary, the net outcome of IL-4 treatment is to reduce lipid storage by promoting lipolysis through enhancing HSL activity via cAMP/PKA pathway, the major route leading to lipolysis.

Indexed as

Lipid Metabolism3T3-L1 CellsAdipocytesAnimalsCyclic AMP-Dependent Protein KinasesEnzyme ActivationEnzyme StabilityGene Expression RegulationInterleukin-4LipolysisMiceModels, BiologicalPhosphorylationProteolysisSterol EsteraseCyclic AMP-Dependent Protein KinasesInterleukin-4Sterol Esterase

Identifiers

PMID31427606
PMCPMC6700157
OpenAlexW2969967599

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.