Evidence map›Paper›PMID 31401979›Full record

ArticleBMB reports2020

Sinapic acid induces the expression of thermogenic signature genes and lipolysis through activation of PKA/CREB signaling in brown adipocytes.

Monir Hossain, Khan Mohammad Imran, Md Shamim Rahman, Dahyeon Yoon, Vignesh Marimuthu, Yong-Sik Kim

Open access · goldAbstract readNews
In one paragraph

Article in BMB reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  7. Nutrients · 2023
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  8. Journal of microbiology and biotechnology · 2023
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  13. TheFood chemistry. Molecular sciences · 2021
    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

6 authors at 1 institution in 1 country.

Monir HossainInstitute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Chenan 31151; Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea.
Khan Mohammad ImranInstitute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Chenan 31151; Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea.
Md Shamim RahmanInstitute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Chenan 31151; Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea.
Dahyeon YoonInstitute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Chenan 31151; Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea.
Vignesh MarimuthuInstitute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Chenan 31151; Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea.
Yong-Sik KimInstitute of Tissue Regeneration, College of Medicine, Soonchunhyang University, Chenan 31151; Department of Microbiology, College of Medicine, Soonchunhyang University, Cheonan 31151, Korea.
Soonchunhyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid accumulation in white adipose tissue is the key contributor to the obesity and orchestrates numerous metabolic health problems such as type 2 diabetes, hypertension, atherosclerosis, and cancer. Nonetheless, the prevention and treatment of obesity are still inadequate. Recently, scientists found that brown adipose tissue (BAT) in adult humans has functions that are diametrically opposite to those of white adipose tissue and that BAT holds promise for a new strategy to counteract obesity. In this study, we evaluated the potential of sinapic acid (SA) to promote the thermogenic program and lipolysis in BAT. SA treatment of brown adipocytes induced the expression of brown-adipocyte activation-related genes such as Ucp1, Pgc-1α, and Prdm16. Furthermore, structural analysis and western blot revealed that SA upregulates protein kinase A (PKA) phosphorylation with competitive inhibition by a pan-PKA inhibitor, H89. SA binds to the adenosine triphosphate (ATP) site on the PKA catalytic subunit where H89 binds specifically. PKA-cat-α1 gene-silencing experiments confirmed that SA activates the thermogenic program via a mechanism involving PKA and cyclic AMP response element-binding protein (CREB) signaling. Moreover, SA treatment promoted lipolysis via a PKA/p38-mediated pathway. Our findings may allow us to open a new avenue of strategies against obesity and need further investigation. [BMB Reports 2020; 53(3): 142-147].

Indexed as

Adipocytes, BrownAdipose Tissue, BrownCell LineCoumaric AcidsCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinCyclic AMP Response Element-Binding Protein AGene Expression RegulationHumansLipolysisPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphorylationSignal TransductionThermogenesisUncoupling Protein 1Coumaric AcidsCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinCyclic AMP Response Element-Binding Protein APeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humansinapinic acidUCP1 protein, humanUncoupling Protein 1

Identifiers

PMID31401979
PMCPMC7118353
OpenAlexW2992919401

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.