Evidence map›Paper›PMID 32615989›Full record

ArticleLipids in health and disease2020

The effect of ursodeoxycholic acid on the relative expression of the lipid metabolism genes in mouse cholesterol gallstone models.

Ning Fan, Ke Meng, Yuqing Zhang, Yong Hu, Donghua Li, Qiaoying Gao, Jianhua Wang, Yanning Li, Shangwei Wu, Yunfeng Cui

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

8 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 4 institutions in 1 country.

Ning FanBeichen Chinese Medicine Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, 436 Jingjin Road, Beichen District, Tianjin, 300400, China.
Ke MengDepartment of Obstetrics and Gynecology, General Hospital of Tianjin Medical University, 154 AnShan Road, HePing District, Tianjin, 300052, China.
Yuqing ZhangDepartment of Surgery, Tianjin Nankai Hospital, Nankai Clinical School of Medicine, Tianjin Medical University, 122 Sanwei Road Nankai District, Tianjin, 300100, China.
Yong HuTianjin Medical University, 22 Qixiangtai Road, Heping District, Tianjin, 300070, China.
Donghua LiInstitute of Acute Abdomen in Integrative Medicine, Tianjin Nankai Hospital, Nankai Clinical School of Medicine, Tianjin Medical University, 122 Sanwei Road Nankai District, Tianjin, 300100, China.
Qiaoying GaoInstitute of Acute Abdomen in Integrative Medicine, Tianjin Nankai Hospital, Nankai Clinical School of Medicine, Tianjin Medical University, 122 Sanwei Road Nankai District, Tianjin, 300100, China.
Jianhua WangBeichen Chinese Medicine Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, 436 Jingjin Road, Beichen District, Tianjin, 300400, China.
Yanning LiBeichen Chinese Medicine Hospital Affiliated to Tianjin University of Traditional Chinese Medicine, 436 Jingjin Road, Beichen District, Tianjin, 300400, China.
Shangwei WuInstitute of Acute Abdomen in Integrative Medicine, Tianjin Nankai Hospital, Nankai Clinical School of Medicine, Tianjin Medical University, 122 Sanwei Road Nankai District, Tianjin, 300100, China.
Yunfeng CuiDepartment of Surgery, Tianjin Nankai Hospital, Nankai Clinical School of Medicine, Tianjin Medical University, 122 Sanwei Road Nankai District, Tianjin, 300100, China. yfcuink@hotmail.com.ORCID http://orcid.org/0000-0001-6415-0321
Tianjin Nankai Hospital · CNTianjin University of Traditional Chinese Medicine · CNTianjin Medical University · CNTianjin Medical University General Hospital · CN

Funding

Foundation of Tianjin Clinical Medical Research Center of Acute Abdomen with integrated Chinese and Western medicine 15ZXLCSY00030Key project of Tianjin science and technology support plan 14ZCZDSY00021Natural Science Foundation of Tianjin Bureau of traditional Chinese Medicine 13040Project of the national science and technology program of Ministry of human resources and social security -Project of Tianjin thousands of people plan -
6 · The paper itself

Abstract

backgroundMany studies indicate that gallstone formation has genetic components. The abnormal expression of lipid-related genes could be the basis for particular forms of cholesterol gallstone disease. The aim of this study was to obtain insight into lipid metabolism disorder during cholesterol gallstone formation and to evaluate the effect of ursodeoxycholic acid (UDCA) on the improvement of bile lithogenicity and its potential influence on the transcription of lipid-related genes.

methodsGallstone-susceptible mouse models were induced by feeding with a lithogenic diet (LD) for 8 weeks. Bile and liver tissues were obtained from these mouse models after 0, 4 and 8 weeks. Bile lipids were measured enzymatically, and the cholesterol saturation index (CSI) was calculated to evaluate the bile lithogenicity by using Carey's critical tables. Real-time polymerase chain reaction (RT-PCR) was used to detect the mRNA expression levels of farnesoid X receptor (FXR), liver X receptor (LXR), adenosine triphosphate-binding cassette subfamily G member 5/8 (ABCG5/8), cholesterol 7-α hydroxylase (CYP7A1), oxysterol 7-α hydroxylase (CYP7B1), sterol 27-α hydroxylase (CYP27A1), peroxisome proliferator-activated receptor alpha (PPAR-α) and adenosine triphosphate-binding cassette subfamily B member 11 (ABCB11).

resultsThe rate of gallstone formation was 100% in the 4-week group but only 30% in the UDCA-treated group. The UDCA-treated group had a significantly lower CSI compared with other groups. Of special note, the data on the effects of UDCA showed higher expression levels of ABCG8, ABCB11 and CYP27A1, as well as lower expression levels of LXR and PPAR-α, compared to the model control group.

conclusionsUDCA exhibits tremendously potent activity in restraining lipid accumulation, thus reversing the lithogenic effect and protecting hepatocytes from serious pathological damage. The abnormal expression of ABCG8, CYP7A1, CYP27A1, LXR and PPAR-α might lead to high lithogenicity of bile. These results are helpful in exploring new lipid metabolism pathways and potential targets for the treatment of cholesterol stones and for providing some basis for the study of the pathogenesis and genetic characteristics of cholelithiasis. Research on the mechanism of UDCA in improving lipid metabolism and bile lithogenicity may be helpful for clinical treatment and for reducing the incidence of gallstones.

Indexed as

AnimalsATP Binding Cassette Transporter, Subfamily G, Member 8BileBile Acids and SaltsCholestanetriol 26-MonooxygenaseCholesterol 7-alpha-HydroxylaseDietDisease Models, AnimalGallstonesGene Expression RegulationLipid MetabolismLipoproteinsLiverMaleMice, Inbred C57BLPPAR alphaABCG8 protein, mouseATP Binding Cassette Transporter, Subfamily G, Member 8Bile Acids and SaltsCholestanetriol 26-MonooxygenaseCholesterol 7-alpha-HydroxylaseCyp27a1 protein, mouseCyp7a1 protein, mouseLipoproteinsPPAR alphaPpara protein, mouseUrsodeoxycholic AcidABCB11ABCG8Cholesterol gallstoneCYP27A1CYP7A1Lipid metabolismLXRPPAR-αUrsodeoxycholic acid

Identifiers

PMID32615989
PMCPMC7333299
OpenAlexW3039481628

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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.