Evidence map›Paper›PMID 32355674›Full record

ReviewHepatobiliary surgery and nutrition2020

Bile acid-based therapies for non-alcoholic steatohepatitis and alcoholic liver disease.

Tiangang Li, John Y L Chiang

Open access · diamondAbstract readReview
In one paragraph

Review in Hepatobiliary surgery and nutrition, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Unravelling the therapeutic landscape of bile acid-based therapies in gastrointestinal disorders.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Iranian journal of basic medical sciences · 2022
    Review
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

2 authors at 2 institutions in 1 country.

Tiangang LiDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA.
John Y L ChiangDepartment of Integrative Medical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA.
Northeast Ohio Medical University · USUniversity of Kansas Medical Center · US

Funding

MOLECULAR BIOLOGY OF BILE ACID SYNTHESISR01DK044442 · NIDDK · NORTHEAST OHIO MEDICAL UNIVERSITY · PI FERRELL, JESSICA MARIE · 1994 to 2022
$5.9M
Pilot Grants ProgramP30GM118247 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI WEINMAN, STEVEN A · 2016 to 2020
$5.5M
Regulation of Bile Acid Synthesis by Nuclear ReceptorsR37DK058379 · NIDDK · NORTHEAST OHIO MEDICAL UNIVERSITY · PI CHIANG, JOHN Y. L. · 2011 to 2020
$3.6M
Regulation of Bile Acid Metabolism and Signaling in Metabolic DiseasesR01DK117965 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Tiangang Li · 2019 to 2026
$2.7M
Regulation of Bile Acid Synthesis by Nuclear ReceptorsR01DK058379 · NIDDK · NORTHEAST OHIO MEDICAL UNIVERSITY · PI CHIANG, JOHN Y. L. · 2002 to 2010
$2.6M
The role of hepatic Sortlin 1 in diabetic dyslipidemiaR01DK102487 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LI, TIANGANG · 2014 to 2018
$1.6M
Molecular Biology of Bile Acid SynthesisR56DK044442 · NIDDK · NORTHEAST OHIO MEDICAL UNIVERSITY · PI CHIANG, JOHN Y. L. · 2009 to 2009
$379k
NIDDK NIH HHS R01 DK044442NIDDK NIH HHS R01 DK058379NIDDK NIH HHS R01 DK102487NIDDK NIH HHS R01 DK117965NIDDK NIH HHS R37 DK058379NIDDK NIH HHS R56 DK044442NIGMS NIH HHS P30 GM118247
6 · The paper itself

Abstract

Bile acids are synthesized from cholesterol only in hepatocytes. Bile acids circulating in the enterohepatic system act as physiological detergent molecules to help solubilize biliary cholesterol and emulsify dietary lipids and fat-soluble vitamins in small intestine. Bile acids are signaling molecules that activate nuclear receptor farnesoid X receptor (FXR) and cell surface G protein-coupled receptor TGR5. FXR critically regulates bile acid homeostasis by mediating bile acid feedback inhibition of hepatic bile acid synthesis. In addition, bile acid-activated cellular signaling pathways regulate metabolic homeostasis, immunity, and cell proliferation in various metabolically active organs. In the small and large intestine, gut bacterial enzymes modify primary bile acids to generate secondary bile acids to help shape the bile acid pool composition and subsequent biological effects. In turn, bile acids exhibit anti-microbial properties and modulate gut microbiota to influence host metabolism and immunity. Currently, bile acid-based therapies including systemic and intestine-restricted FXR agonists, TGR5 agonists, fibroblast growth factor 19 analogue, intestine FXR antagonists, and intestine apical sodium-bile acid transporter (ASBT) inhibitors have been developed as promising treatments for non-alcoholic steatohepatitis (NASH). These pharmacological agents improved metabolic and inflammatory disorders via distinct mechanisms of action that are subjects of extensive research interest. More recently, human and experimental alcoholic liver disease (ALD) has been associated with disrupted bile acid homeostasis. In additional, new findings showed that targeting bile acid metabolism and signaling may be promising therapeutic approaches for treating ALD.

Indexed as

alcoholic liver disease (ALD)Bile acidfarnesoid X receptor (FXR)microbiotanon-alcoholic steatohepatitis (NASH)

Identifiers

PMID32355674
PMCPMC7188552
OpenAlexW2975622811

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.