Evidence map›Paper›PMID 24490657›Full record

ArticleBMC complementary and alternative medicine2014

Isoquercitrin activates the AMP-activated protein kinase (AMPK) signal pathway in rat H4IIE cells.

Jingxin Zhou, Hisae Yoshitomi, Tonghua Liu, Boxin Zhou, Wen Sun, Lingling Qin, Xiangyu Guo, Liansha Huang, Lili Wu, Ming Gao

Open access · goldAbstract read
In one paragraph

Article in BMC complementary and alternative medicine, 2014. 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
1.1field-weighted citation impact, top 23% 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, 35 citations in OpenAlex.

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  13. Isoquercitrin, ingredients inCell adhesion & migration · 2018
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  14. Article
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  16. Effect ofFrontiers in physiology · 2017
    Article
  17. Article
  18. Review
  19. Article
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

10 authors at 4 institutions in 3 countries.

Jingxin Zhou
Hisae Yoshitomi
Tonghua LiuBeijing University of Chinese Medicine, 11 North 3rd-ring East Road, Beijing, Chaoyang District 100029, People's Republic of China. thliu@vip.163.com.
Boxin Zhou
Wen Sun
Lingling Qin
Xiangyu Guo
Liansha Huang
Lili Wu
Ming Gao
Beijing University of Chinese Medicine · CNMukogawa Women's University · JPCM Hospital · KRGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIsoquercitrin, a flavonoid compound that is widely distributed in medicinal and dietary plants, possesses many biological activities, including inhibition of adipocyte differentiation. In this study, we investigated the effect of isoquercitrin on lipid accumulation and its molecular mechanisms in rat hepatoma H4IIE cells.

methodsTo investigate the effect of isoquercitrin on lipid accumulation, H4IIE cells were induced by FFA and the total lipid levels were detected by Oil Red O staining. Furthermore, The protein levels of AMPK and acetyl-CoA carboxylase (ACC), the gene expressions of transcriptional factor, lipogenic genes, and adiponectin receptor 1 (AdipoR1) were analyzed by Western blotting and quantitative real-time PCR. To further confirm the pathway of isoquercitrin-mediated hepatic lipid metabolism, H4IIE cells were treated with an AMPK inhibitor and AdipoR1 siRNA.

resultsIsoquercitrin significantly enhances AMPK phosphorylation, downregulates sterol regulatory element binding protein transcription factor 1 (SREBP-1) and fatty acid synthase (FAS) gene expressions. Pretreatment with AMPK inhibitor, significantly decreased the AMPK phosphorylation and increased FAS expression stimulated by isoquercitrin. Isoquercitrin might also upregulate the expression of AdipoR1 dose-dependently via AMPK in the presence of an AMPK inhibitor and AdipoR1 siRNA.

conclusionsIsoquercitrin appears to regulate AMPK activation, thereby enhancing AdipoR1 expression, suppressing SREBP-1 and FAS expressions, and resulting in the regulation of lipid accumulation. These results suggest that isoquercitrin is a novel dietary compound that can be potentially be used to prevent lipid metabolic disorder and nonalcoholic fatty liver disease.

Indexed as

AMP-Activated Protein KinasesAnimalsDown-RegulationFatty Acid SynthasesHepatocytesLipid MetabolismLiverPhosphorylationPlant ExtractsPlants, EdibleQuercetinRatsReceptors, AdiponectinSignal TransductionSterol Regulatory Element Binding Protein 1adiponectin receptor 1, ratAMP-Activated Protein KinasesFatty Acid SynthasesisoquercitrinPlant ExtractsQuercetinReceptors, AdiponectinSterol Regulatory Element Binding Protein 1

Identifiers

PMID24490657
PMCPMC3914011
OpenAlexW1975301598

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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.