Evidence map›Paper›PMID 17404808›Full record

ReviewPharmaceutical research2007

Bile acid transporters: structure, function, regulation and pathophysiological implications.

Waddah A Alrefai, Ravinder K Gill

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pharmaceutical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed, 2 pooled it
12.5field-weighted citation impact, top 1% 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

173 citing papers in PubMed, 2 syntheses or guidelines pooled it, 489 citations in OpenAlex.

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113 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Waddah A AlrefaiSection of Digestive Diseases and Nutrition, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612, USA. walrefai@uic.edu
Ravinder K Gill
University of Illinois Chicago · US

Funding

Regulation of Intestinal Bile Acid TransportR01DK071596 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALREFAI, WADDAH A. · 2005 to 2014
$2.3M
Regulation of Intestinal Bile Acid TransportR56DK071596 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALREFAI, WADDAH A. · 2010 to 2010
$196k
NIDDK NIH HHS DK71596
6 · The paper itself

Abstract

Specific transporters expressed in the liver and the intestine, play a critical role in driving the enterohepatic circulation of bile acids. By preserving a circulating pool of bile acids, an important factor influencing bile flow, these transporters are involved in maintaining bile acid and cholesterol homeostasis. Enterohepatic circulation of bile acids is fundamentally composed of two major processes: secretion from the liver and absorption from the intestine. In the hepatocytes, the vectorial transport of bile acids from blood to bile is ensured by Na+ taurocholate co-transporting peptide (NTCP) and organic anion transport polypeptides (OATPs). After binding to a cytosolic bile acid binding protein, bile acids are secreted into the canaliculus via ATP-dependent bile salt excretory pump (BSEP) and multi drug resistant proteins (MRPs). Bile acids are then delivered to the intestinal lumen through bile ducts where they emulsify dietary lipids and cholesterol to facilitate their absorption. Intestinal epithelial cells reabsorb the majority of the secreted bile acids through the apical sodium dependent bile acid transporter (ASBT) and sodium independent organic anion transporting peptide (OATPs). Cytosolic ileal bile acid binding protein (IBABP) mediates the transcellular movement of bile acids to the basolateral membrane across which they exit the cells via organic solute transporters (OST). An essential role of bile acid transporters is evident from the pathology associated with their genetic disruption or dysregulation of their function. Malfunctioning of hepatic and intestinal bile acid transporters is implicated in the pathophysiology of cholestatic liver disease and the depletion of circulating pool of bile acids, respectively. Extensive efforts have been recently made to enhance our understanding of the structure, function and regulation of the bile acid transporters and exploring new potential therapeutics to treat bile acid or cholesterol related diseases. This review will highlight current knowledge about structure, function and molecular characterization of bile acid transporters and discuss the implications of their defects in various hepatic and intestinal disorders.

Indexed as

Enterohepatic CirculationAnimalsATP-Binding Cassette TransportersBile Acids and SaltsBile CanaliculiBile DuctsCarrier ProteinsCell PolarityCholestasisEnterocytesEpithelial CellsHepatocytesHumansIntestinal MucosaKidney Tubules, ProximalLiverATP-Binding Cassette Transportersbile acid binding proteinsBile Acids and SaltsCarrier ProteinsMembrane GlycoproteinsOrganic Anion Transporters, Sodium-DependentOrganic Anion Transporters, Sodium-Independentsodium-bile acid cotransporterSymporters

Identifiers

PMID17404808
OpenAlexW2071450296

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.