Evidence map›Paper›PMID 22982338›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012

A novel nutrient sensing mechanism underlies substrate-induced regulation of monocarboxylate transporter-1.

Alip Borthakur, Shubha Priyamvada, Anoop Kumar, Arivarasu A Natarajan, Ravinder K Gill, Waddah A Alrefai, Pradeep K Dudeja

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 100 citations in OpenAlex.

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  15. Short chain fatty acids and monocarboxylate transporters in irritable bowel syndrome.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020
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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

7 authors at 2 institutions in 1 country.

Alip BorthakurSection of Digestive Diseases & Nutrition, Dept. of Medicine, Univ. of Illinois at Chicago, Chicago, IL 60612, USA. alipb@uic.edu
Shubha Priyamvada
Anoop Kumar
Arivarasu A Natarajan
Ravinder K Gill
Waddah A Alrefai
Pradeep K Dudeja
Jesse Brown VA Medical Center · USUniversity of Illinois Chicago · US

Funding

Intestinal Anion Transporters: Function and RegulationR01DK054016 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEJA, PRADEEP K · 1998 to 2022
$7.0M
Transcriptional Regulation of NHE-3 Isoform in Human IntestineP01DK067887 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HECHT, GAIL A · 2006 to 2011
$4.9M
Transporter Trafficking Mechanisms in Infectious DiarrheaR01DK092441 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEJA, PRADEEP K · 2011 to 2020
$3.0M
Probiotics:Potential Therapeutic Roles in DiarrheaR01DK081858 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUDEJA, PRADEEP K · 2008 to 2017
$2.5M
Regulation of Intestinal Bile Acid TransportR01DK071596 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALREFAI, WADDAH A. · 2005 to 2014
$2.3M
Anion Transport in EPEC Induced DiarrheaK01DK074458 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GILL, RAVINDER K · 2007 to 2011
$680k
Regulation of Intestinal Bile Acid TransportR56DK071596 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALREFAI, WADDAH A. · 2010 to 2010
$196k
BLRD VA I01 BX000152BLRD VA IK6 BX005243NIDDK NIH HHS DK-067887NIDDK NIH HHS DK-54016NIDDK NIH HHS DK-71596NIDDK NIH HHS DK-74458NIDDK NIH HHS DK-81858NIDDK NIH HHS DK-92441NIDDK NIH HHS R01 DK054016NIDDK NIH HHS R01 DK071596NIDDK NIH HHS R01 DK092441
6 · The paper itself

Abstract

Monocarboxylate transporter isoform-1 (MCT1) plays an important role in the absorption of short-chain fatty acids (SCFAs) in the colon. Butyrate, a major SCFA, serves as the primary energy source for the colonic mucosa, maintains epithelial integrity, and ameliorates intestinal inflammation. Previous studies have shown substrate (butyrate)-induced upregulation of MCT1 expression and function via transcriptional mechanisms. The present studies provide evidence that short-term MCT1 regulation by substrates could be mediated via a novel nutrient sensing mechanism. Short-term regulation of MCT1 by butyrate was examined in vitro in human intestinal C2BBe1 and rat intestinal IEC-6 cells and ex vivo in rat intestinal mucosa. Effects of pectin feeding on MCT1, in vivo, were determined in rat model. Butyrate treatment (30-120 min) of C2BBe1 cells increased MCT1 function {p-(chloromercuri) benzene sulfonate (PCMBS)-sensitive [(14)C]butyrate uptake} in a pertussis toxin-sensitive manner. The effects were associated with decreased intracellular cAMP levels, increased V(max) of butyrate uptake, and GPR109A-dependent increase in apical membrane MCT1 level. Nicotinic acid, an agonist for the SCFA receptor GPR109A, also increased MCT1 function and decreased intracellular cAMP. Pectin feeding increased apical membrane MCT1 levels and nicotinate-induced transepithelial butyrate flux in rat colon. Our data provide strong evidence for substrate-induced enhancement of MCT1 surface expression and function via a novel nutrient sensing mechanism involving GPR109A as a SCFA sensor.

Indexed as

AnimalsButyratesCaco-2 CellsCell LineColforsinColonCyclic AMPHumansIntestinal MucosaMaleMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersNiacinPectinsPertussis ToxinRatsButyratesColforsinCyclic AMPHcar2 protein, ratMonocarboxylate Transport Protein 1Monocarboxylic Acid TransportersNiacinPectinsPertussis ToxinReceptors, G-Protein-CoupledReceptors, NicotinicSymporters

Identifiers

PMID22982338
PMCPMC3517653
OpenAlexW2150780140

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.