Evidence map›Paper›PMID 27121981›Full record

ArticleScientific reports2016

GPR40 agonist ameliorates liver X receptor-induced lipid accumulation in liver by activating AMPK pathway.

Meng Li, Xiangyu Meng, Jie Xu, Xiuqing Huang, Hongxia Li, Guoping Li, Shu Wang, Yong Man, Weiqing Tang, Jian Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 40 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

10 authors at 2 institutions in 1 country.

Meng LiPeking University Fifth School of Clinical Medicine (Beijing Hospital), Beijing, China.
Xiangyu MengPeking University Fifth School of Clinical Medicine (Beijing Hospital), Beijing, China.
Jie XuThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Xiuqing HuangThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Hongxia LiThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Guoping LiThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Shu WangThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Yong ManThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Weiqing TangThe Key Laboratory of Geriatrics, Beijing Institute of Geriatrics &Beijing Hospital, Ministry of Health, Beijing, China.
Jian LiPeking University Fifth School of Clinical Medicine (Beijing Hospital), Beijing, China.
Beijing Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic steatosis is strongly linked to insulin resistance and type 2 diabetes. GPR40 is a G protein-coupled receptor mediating free fatty acid-induced insulin secretion and thus plays a beneficial role in the improvement of diabetes. However, the impact of GPR40 agonist on hepatic steatosis still remains to be elucidated. In the present study, we found that activation of GPR40 by its agonist GW9508 attenuated Liver X receptor (LXR)-induced hepatic lipid accumulation. Activation of LXR in the livers of C57BL/6 mice fed a high-cholesterol diet and in HepG2 cells stimulated by chemical agonist caused increased expression of its target lipogenic genes and subsequent lipid accumulation. All these effects of LXR were dramatically downregulated after GW9508 supplementation. Moreover, GPR40 activation was accompanied by upregulation of AMPK pathway, whereas the inhibitive effect of GPR40 on the lipogenic gene expression was largely abrogated by AMPK knockdown. Taken together, our results demonstrated that GW9508 exerts a beneficial effect to ameliorate LXR-induced hepatic steatosis through regulation of AMPK signaling pathway.

Indexed as

Lipid MetabolismAMP-Activated Protein KinasesAnimalsHep G2 CellsHumansLiverLiver X ReceptorsMethylaminesMice, Inbred C57BLPropionatesReceptors, G-Protein-CoupledAMP-Activated Protein KinasesFfar1 protein, mouseGW9508Liver X ReceptorsMethylaminesPropionatesReceptors, G-Protein-Coupled

Identifiers

PMID27121981
PMCPMC4848522
OpenAlexW2344565744

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.