Evidence map›Paper›PMID 33079450›Full record

ArticleMolecular nutrition & food research2020

The Beneficial Effects of Apical Sodium-Dependent Bile Acid Transporter Inactivation Depend on Dietary Fat Composition.

Ivo P van de Peppel, Anuradha Rao, Marleen B Dommerholt, Laura Bongiovanni, Rachel Thomas, Alain de Bruin, Saul J Karpen, Paul A Dawson, Henkjan J Verkade, Johan W Jonker

Open access · hybridAbstract read
In one paragraph

Article in Molecular nutrition & food research, 2020. 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
0.8field-weighted citation impact, top 24% 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, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Nutrients · 2024
    Article
  5. Article
  6. Loss of apical sodium bile acid transporter alters bile acid circulation and reduces biliary damage in cholangitis.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  7. Article
  8. Article
  9. Article
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 2 countries.

Ivo P van de PeppelSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.ORCID https://orcid.org/0000-0002-6268-3404
Anuradha RaoDepartment of Pediatrics, Emory University School of Medicine, 1760 Haygood Drive Northeast, Atlanta, GA 30322, USA.
Marleen B DommerholtSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.
Laura BongiovanniDutch Molecular Pathology Centre, Department of Pathobiology, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 1, Utrecht, 3584 CL, The Netherlands.
Rachel ThomasDutch Molecular Pathology Centre, Department of Pathobiology, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 1, Utrecht, 3584 CL, The Netherlands.
Alain de BruinDutch Molecular Pathology Centre, Department of Pathobiology, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 1, Utrecht, 3584 CL, The Netherlands.
Saul J KarpenDepartment of Pediatrics, Emory University School of Medicine, 1760 Haygood Drive Northeast, Atlanta, GA 30322, USA.
Paul A DawsonDepartment of Pediatrics, Emory University School of Medicine, 1760 Haygood Drive Northeast, Atlanta, GA 30322, USA.
Henkjan J VerkadeSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.
Johan W JonkerSection of Molecular Metabolism and Nutrition, Department of Pediatrics, University of Groningen, University Medical Center Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.
University Medical Center Groningen · NLEmory University · USUtrecht University · NL

Funding

ILEAL BILE ACID TRANSPORTER METABOLISM AND REGULATIONR01DK047987 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI DAWSON, PAUL A · 2000 to 2021
$6.8M
MOLECULAR REGULATION OF HEPATIC TRANSPORTERSR01DK056239 · NIDDK · YALE UNIVERSITY · PI KARPEN, SAUL J. · 1999 to 2017
$4.8M
NIDDK NIH HHS R01 DK047987NIDDK NIH HHS R01 DK056239
6 · The paper itself

Abstract

scopeThe apical sodium-dependent bile acid transporter (ASBT, SLC10A2) is important in the enterohepatic cycling of bile acids and thereby in the intestinal absorption of lipids. ASBT inhibition has been shown to improve aspects of the metabolic syndrome, but the underlying mechanisms have remained unclear. Here, the effect of ASBT inhibition on the uptake of specific fatty acids and its consequences for diet-induced obesity and non-alcoholic fatty liver disease (NAFLD) are investigated.

methodsIntestinal fat absorption is determined in mice receiving an ASBT inhibitor and in Asbt

resultsBoth ASBT inhibition and Asbt gene inactivation reduce total fat absorption, particularly of SFAs. Asbt gene inactivation lowers bodyweight gain, improves insulin sensitivity, and decreases the NAFLD activity score upon feeding a HFD rich in SFAs, but not in PUFAs.

conclusionsThe beneficial metabolic effects of ASBT inactivation on diet-induced obesity depend on decreased intestinal absorption of SFAs, and thus on the dietary fatty acid composition. These findings highlight the importance of dietary fatty acid composition in the therapeutic effects of ASBT inhibition.

Indexed as

bile acidenterohepatic circulationfat absorptionobesitysteatosis

Identifiers

PMID33079450
PMCPMC7757219
OpenAlexW3092819530

What Socratic holds

Textmetadata
LicenceCC BY-NC
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.