Evidence map›Paper›PMID 35251469›Full record

ArticleOxidative medicine and cellular longevity2022

Farnesoid X Receptor Deficiency Induces Hepatic Lipid and Glucose Metabolism Disorder via Regulation of Pyruvate Dehydrogenase Kinase 4.

Wenyi Deng, Wenjing Fan, Tingting Tang, Hengquan Wan, Simin Zhao, Yao Tan, Kwabena Agyare Oware, Jieqiong Tan, Jiequn Li, Shunlin Qu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.9field-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

9 citing papers in PubMed, 20 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 3 institutions in 1 country.

Wenyi DengInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0003-0616-9993
Wenjing FanEmergency Department, The Second Affiliated Hospital, University of South China, Hengyang City, Hunan, China 421001.ORCID https://orcid.org/0000-0003-0301-9666
Tingting TangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0003-2999-2931
Hengquan WanInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0002-5313-9618
Simin ZhaoInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0001-8195-4540
Yao TanInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0002-3053-4439
Kwabena Agyare OwareInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0002-4738-2224
Jieqiong TanCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, School of Life Science, Central South University, Changsha, Hunan, China 410078.ORCID https://orcid.org/0000-0003-0730-1095
Jiequn LiDepartment of Liver Transplant, Second Xiangya Hospital, Central South University, Changsha, Hunan, China 410011.ORCID https://orcid.org/0000-0002-5285-2403
Shunlin QuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan, China 421001.ORCID https://orcid.org/0000-0003-2229-6140
University of South China · CNCentral South University · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Farnesoid X receptors (FXR) are bile acid receptors that play roles in lipid, glucose, and energy homeostasis. Synthetic FXR-specific agonists have been developed for treating nonalcoholic fatty liver disease (NAFLD) patients. However, the detailed mechanism remains unclear. To investigate the effects of FXR on NAFLD and the possible mechanism, FXR-null mice were fed either a normal or a high-fat diet. The FXR-null mice developed hepatomegaly, steatosis, accumulation of lipid droplets in liver cells, glucose metabolism disorder, and elevated serum lipid levels. Transcriptomic results showed increased expression of key lipid synthesis and glucose metabolism-related proteins. We focused on pyruvate dehydrogenase kinase 4 (PDK4), a key enzyme involved in the regulation of glucose and fatty acid (FA) metabolism and homeostasis. Subsequently, we confirmed an increase in PDK4 expression in FXR knockout cells. Moreover, inhibition of PDK4 expression alleviated lipid accumulation in hepatocytes caused by FXR deficiency

Indexed as

AnimalsDiet, High-FatFatty AcidsGene Knockout TechniquesGlucoseGlucose Metabolism DisordersHEK293 CellsHepatocytesHumansLipid Metabolism DisordersLiverLiver DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutFatty AcidsGlucosePdk4 protein, mousePyruvate Dehydrogenase Acetyl-Transferring KinaseReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearTriglycerides

Identifiers

PMID35251469
PMCPMC8896157
OpenAlexW4214488590

What Socratic 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 Socratic graph.