Evidence map›Paper›PMID 33893772›Full record

ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2021

Leptin Influence Cholelithiasis Formation by Regulating Bile Acid Metabolism.

Jian Wen, Yu Jiang, Zhengming Lei, Jingyu He, Mingxin Ye, Wenguang Fu

Open access · greenAbstract read
In one paragraph

Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Is hyperleptinemia associated with gallstone disease? A systematic review and meta-analysis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2023
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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

6 authors at 2 institutions in 1 country.

Jian WenDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Yu JiangDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Zhengming LeiDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Jingyu HeDepartment of Hepatobiliary Surgery, Mianyang No.3 People's Hospital, Sichuan, China.
Mingxin YeDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Wenguang FuDepartment of Hepatobiliary Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
Affiliated Hospital of Southwest Medical University · CNSichuan Mianyang 404 Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBile acid metabolism is a contributing factor that promotes cholelithiasis. Recent studies have suggested novel roles of leptin in the formation of gallbladder stones (GS); however, no evidence confirmed the function of leptin in the formation of primary intrahepatic bile duct stones (PIBDS) . In the current study, the liver tissues of patients with GS and PIBDS were collected to check the mRNA and protein expression levels of BSEP.

methodsL02 cells stimulated with leptin were served for the expression of OB-Rb, AMPKα2, and BSEP by quantitative-polymerase chain reaction (q-PCR), Western blot, and immunohistochemistry, respectively.

resultsThe results showed that the level of serum leptin was higher in the GS group than in the control and PIBDS groups. Compared with the control group, the expression levels of OB-Rb, p-AMPKa2, and BSEP decreased significantly in the GS and PIBDS groups. In vitro, compared with the control cells, the protein levels of OB-Rb, p-AMPKa2, and BSEP increased in the L02 cells cultured with leptin. However, these enhancements disappeared when the cells were co-cultured with leptin plus Compound C.

conclusionThe present results suggest that cholelithiasis, especially the formation of PIBDS, was connected with leptin, which could regulate bile acid metabolism through the OB-Rb/AMPKa2/BSEP signaling pathway.

Indexed as

AMP-Activated Protein KinasesATP Binding Cassette Transporter, Subfamily B, Member 11Bile Acids and SaltsCholelithiasisLeptinReceptors, LeptinAdultAgedBile Ducts, IntrahepaticCell LineCross-Sectional StudiesEnergy MetabolismFemaleGallstonesHepatocytesHumansABCB11 protein, humanAMP-Activated Protein KinasesATP Binding Cassette Transporter, Subfamily B, Member 11Bile Acids and SaltsLeptinPRKAA2 protein, humanReceptors, LeptinRNA, Messenger

Identifiers

PMID33893772
PMCPMC8975486
OpenAlexW3023451953

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.