Evidence map›Paper›PMID 32724176›Full record

ArticleActa pharmacologica Sinica2021

AMPK activator C24 inhibits hepatic lipogenesis and ameliorates dyslipidemia in HFHC diet-induced animal models.

Shui-Mei Sun, Zhi-Fu Xie, Yang-Ming Zhang, Xin-Wen Zhang, Chen-Dong Zhou, Jian-Peng Yin, Yan-Yan Yu, Shi-Chao Cui, Hao-Wen Jiang, Teng-Teng Li and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 26 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

13 authors at 3 institutions in 1 country.

Shui-Mei Sun *Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Zhi-Fu Xie *Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Yang-Ming Zhang *Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Xin-Wen ZhangShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Chen-Dong ZhouShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Jian-Peng YinYantai Key Laboratory of Nanomedicine & Advanced Preparations, Yantai Institute of Materia Medica, Yantai, 264000, China.
Yan-Yan YuShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Shi-Chao CuiShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Hao-Wen JiangShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Teng-Teng LiShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Jia LiShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Fa-Jun NanShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. fjnan@simm.ac.cn.
Jing-Ya LiShanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. jyli@simm.ac.cn.
Shanghai Institute of Materia Medica · CNChinese Academy of Sciences · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dyslipidemia is a chronic metabolic disease characterized by elevated levels of lipids in plasma. Recently, various studies demonstrate that the increased activity of adenosine 5'-monophosphate-activated protein kinase (AMPK) causes health benefits in energy regulation. Thus, great efforts have been made to develop AMPK activators as a metabolic syndrome treatment. In the present study, we investigated the effects of the AMPK activator C24 on dyslipidemia and the potential mechanisms. We showed that C24 (5-40 μM) dose-dependently increased the phosphorylation of AMPKα and acetyl-CoA carboxylase (ACC), and inhibited lipogenesis in HepG2 cells. Using compound C, an AMPK inhibitor, or hepatocytes isolated from liver tissue-specific AMPK knockout AMPKα1α2

Indexed as

AMP-Activated Protein KinasesAnimalsDiet, High-FatDyslipidemiasEnzyme ActivatorsHep G2 CellsHumansHypolipidemic AgentsLipogenesisLiverMaleMesocricetusMiceMice, Inbred C57BLOxindolesRabbitsAMP-Activated Protein KinasesEnzyme ActivatorsHypolipidemic AgentsOxindolesadenosine 5′-monophosphate-activated protein kinaseAMPK activatorC24cholesterolhypolipidemic druglivermetabolic syndrometriglyceridesVLDL

Identifiers

PMID32724176
PMCPMC8115652
OpenAlexW3045536090

What OpenQuestion holds

Textmetadata
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.