Evidence map›Paper›PMID 26833058›Full record

ArticleCardiovascular diabetology2016

Polydatin ameliorates lipid and glucose metabolism in type 2 diabetes mellitus by downregulating proprotein convertase subtilisin/kexin type 9 (PCSK9).

Yu Wang, Jiantao Ye, Jie Li, Cheng Chen, Junying Huang, Peiqing Liu, Heqing Huang

Open access · goldFull text read
In one paragraph

Article in Cardiovascular diabetology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 78 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

7 authors at 2 institutions in 1 country.

Yu WangLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, 132 WaiHuan East Road, Guangzhou Higher Education Mega Center, Guangzhou, 510006, China. wangyuyaoxue@163.com.
Jiantao YeLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, 132 WaiHuan East Road, Guangzhou Higher Education Mega Center, Guangzhou, 510006, China. yejt@mail.sysu.edu.cn.
Jie LiLaboratory Animal Center, Sun Yat-sen University, Guangzhou, 510080, China. celiagz@163.com.
Cheng ChenLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, 132 WaiHuan East Road, Guangzhou Higher Education Mega Center, Guangzhou, 510006, China. chencheng4610@163.com.
Junying HuangLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, 132 WaiHuan East Road, Guangzhou Higher Education Mega Center, Guangzhou, 510006, China. 919808259@qq.com.
Peiqing LiuLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, 132 WaiHuan East Road, Guangzhou Higher Education Mega Center, Guangzhou, 510006, China. liupq@mail.sysu.edu.cn.
Heqing HuangLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, 132 WaiHuan East Road, Guangzhou Higher Education Mega Center, Guangzhou, 510006, China. huangheq@mail.sysu.edu.cn.
Sun Yat-sen University · CNNational Medical Products Administration · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbnormalities in lipid and glucose metabolism are constantly observed in type 2 diabetes. However, these abnormalities can be ameliorated by polydatin. Considering the important role of proprotein convertase subtilisin/kexin type 9 (PCSK9) in metabolic diseases, we explore the possible mechanism of polydatin on lipid and glucose metabolism through its effects on PCSK9.

methodsAn insulin-resistant HepG2 cell model induced by palmitic acid (PA) and a db/db mice model were used to clarify the role of polydatin on lipid and glucose metabolism.

resultsIn insulin-resistant HepG2 cells, polydatin upregulated the protein levels of LDLR and GCK but repressed PCSK9 protein expression, besides, polydatin also inhibited the combination between PCSK9 and LDLR. Knockdown and overexpression experiments indicated that polydatin regulated LDLR and GCK expressions through PCSK9. In the db/db mice model, we found that polydatin markedly enhanced GCK and LDLR protein levels, and inhibited PCSK9 expression in the liver. Molecular docking assay was further performed to analyze the possible binding mode between polydatin and the PCSK9 crystal structure (PDB code: 2p4e), which indicated that steady hydrogen bonds formed between polydatin and PCSK9.

conclusionsOur study indicates that polydatin ameliorates lipid and glucose metabolism in type 2 diabetes mellitus by downregulating PCSK9.

Indexed as

Insulin ResistanceAnimalsBiomarkersBlood GlucoseDiabetes Mellitus, Type 2Disease Models, AnimalDown-RegulationDrugs, Chinese HerbalFemaleGerminal Center KinasesGlucosidesHepatocytesHep G2 CellsHumansHydrogen BondingHypoglycemic AgentsBiomarkersBlood GlucoseDrugs, Chinese HerbalGerminal Center KinasesGlucosidesHypoglycemic AgentsLDLR protein, humanLipidsPalmitic AcidPCSK9 protein, humanPcsk9 protein, mousepolydatinProprotein Convertase 9Proprotein ConvertasesProtein Serine-Threonine KinasesReceptors, LDLSerine EndopeptidasesStilbenes

Identifiers

PMID26833058
PMCPMC4736185
OpenAlexW2271500264

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LicenceCC BY
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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.