Evidence map›Paper›PMID 37111058›Full record

ArticleNutrients2023

Hepatic G Protein-Coupled Receptor 180 Deficiency Ameliorates High Fat Diet-Induced Lipid Accumulation via the Gi-PKA-SREBP Pathway.

Yunhua Zhang, Ziming Zhu, Lijun Sun, Wenzhen Yin, Yuan Liang, Hong Chen, Yanghui Bi, Wenbo Zhai, Yue Yin, Weizhen Zhang

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 7 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.

Yunhua ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Ziming ZhuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.ORCID 0009-0003-0891-5459
Lijun SunDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Wenzhen YinDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Yuan LiangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Hong ChenDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Yanghui BiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Wenbo ZhaiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Yue YinDepartment of Pharmacology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.
Weizhen ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Peking University, Beijing 100191, China.ORCID 0000-0001-8791-2798
Peking University · CNShihezi University · CN

Funding

China Association for Science and Technology YESS20200034National Natural Science Foundation of China 81730020National Natural Science Foundation of China 81930015National Natural Science Foundation of China 82070592National Natural Science Foundation of China 82270610
6 · The paper itself

Abstract

Single-nucleotide polymorphisms in G protein-coupled receptor 180 (GPR180) are associated with hypertriglyceridemia. The aim of this study was to determine whether hepatic GPR180 impacts lipid metabolism. Hepatic GPR180 was knocked down using two approaches:

Indexed as

Diet, High-FatNon-alcoholic Fatty Liver DiseaseAnimalsCholesterolLipid MetabolismLiverMiceMice, Inbred C57BLMice, Inbred StrainsMice, ObeseObesityReceptors, G-Protein-CoupledSterol Regulatory Element Binding Protein 1TriglyceridesCholesterolReceptors, G-Protein-CoupledSterol Regulatory Element Binding Protein 1TriglyceridesGPR180nonalcoholic fatty liver diseaseSREBP1SREBP2

Identifiers

PMID37111058
PMCPMC10144310
OpenAlexW4365148246

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.