Evidence map›Paper›PMID 30635917›Full record

ArticleBritish journal of pharmacology2019

Betulinic acid alleviates endoplasmic reticulum stress-mediated nonalcoholic fatty liver disease through activation of farnesoid X receptors in mice.

Ming Gu, Ping Zhao, Shiying Zhang, Shengjie Fan, Li Yang, Qingchun Tong, Guang Ji, Cheng Huang

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. mSystems · 2026
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  10. Nuclear Receptor-Targeted Therapy for Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of drug discovery and pharmacology · 2025
    Article
  11. Betulinic acid and obesity-related disorders.Frontiers in pharmacology · 2025
    Review
  12. Review
  13. Review
  14. Review
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  16. Review
  17. Article
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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

8 authors at 3 institutions in 2 countries.

Ming GuInstitute of Digestive Disease, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Ping ZhaoSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Shiying ZhangSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Shengjie FanSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Li YangResearch Center for Traditional Chinese Medicine of Complexity Systems, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Qingchun TongBrown Foundation Institute of Molecular Medicine and Program in Neuroscience, Graduate School of Biological Sciences, University of Texas McGovern Medical School, Houston, Texas, USA.
Guang JiInstitute of Digestive Disease, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Cheng HuangSchool of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, China.ORCID 0000-0003-0704-2943
Shanghai University of Traditional Chinese Medicine · CNShanghai University · CNBrown Foundation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe molecular mechanism for the pathogenesis of nonalcoholic fatty liver disease (NAFLD) remains elusive. Both farnesoid X receptor (FXR) signalling and endoplasmic reticulum (ER) stress contribute to the progression of NAFLD; however, it is not clear whether the actions of these two pathways are dependent on each other. Moreover, the pharmacological benefits and mechanism of betulinic acid (BA) in controlling metabolic syndrome and NAFLD are largely unknown. EXPERIMENTAL APPROACH: A reporter assay and a time-resolved FRET assay were used to identify BA as an agonist of the FXR. NAFLD was induced by a methionine and choline-deficient L-amino acid diet (MCD) and high-fat diet (HFD). The pharmacological effects of BA (100 mg·kg KEY

resultsActivation of the FXR inhibited intracellular PERK/EIF2α/ATF4 and CHOP signalling, thereby alleviating hepatic ER stress, whereas FXR silencing resulted in an opposite effect. Furthermore, we identified BA as an FXR agonist that effectively attenuated the progression of NAFLD and metabolic disorders in both HFD- and MCD diet-fed mice and restored the hepatocellular ER homeostasis by stimulating the FXR signalling pathway and blocking PERK/EIF2α signalling. In contrast, the effects of BA were attenuated in FXR CONCLUSIONS AND IMPLICATIONS: Our data demonstrate that pharmacological activation of the FXR by BA reduces hepatocellular ER stress and attenuates NAFLD in an animal model of hepatic steatosis.

Indexed as

AnimalsBetulinic AcidEndoplasmic Reticulum StressFemaleHep G2 CellsHumansLiverMice, Inbred C57BLNon-alcoholic Fatty Liver DiseasePentacyclic TriterpenesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, Small InterferingTriterpenesBetulinic AcidPentacyclic TriterpenesReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearRNA, Small InterferingTriterpenes

Identifiers

PMID30635917
PMCPMC6433649
OpenAlexW2911129444

What OpenQuestion holds

Textmetadata
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.