Evidence map›Paper›PMID 25402228›Full record

ArticlePloS one2014

Enhanced gastrointestinal expression of cytosolic malic enzyme (ME1) induces intestinal and liver lipogenic gene expression and intestinal cell proliferation in mice.

Ahmed Al-Dwairi, Adam R Brown, John Mark P Pabona, Trang H Van, Hamdan Hamdan, Charles P Mercado, Charles M Quick, Patricia A Wight, Rosalia C M Simmen, Frank A Simmen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. A cryptic allosteric pocket shapes isoform-selective inhibition of human malic enzymes.Protein science : a publication of the Protein Society · 2026
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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

10 authors at 2 institutions in 1 country.

Ahmed Al-DwairiDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Adam R BrownDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America; Interdisciplinary Biomedical Sciences Program, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
John Mark P PabonaDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Trang H VanDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Hamdan HamdanDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Charles P MercadoDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Charles M QuickDepartment of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Patricia A WightDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Rosalia C M SimmenDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America; Interdisciplinary Biomedical Sciences Program, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America; The Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
Frank A SimmenDepartment of Physiology & Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America; Interdisciplinary Biomedical Sciences Program, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America; The Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, Little Rock, AR, United States of America.
University of Arkansas for Medical Sciences · USWinthrop Rockefeller Foundation · US

Funding

Arkansas Center for Clinical and Translational ResearchUL1TR000039 · NCATS · UNIV OF ARKANSAS FOR MED SCIS · PI BECK, CORNELIA MARIE, JAMES, LAURA P · 2012 to 2014
$10.0M
Dietary Factors in Colon Cancer PreventionR01CA136493 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI SIMMEN, FRANK ALBERT · 2010 to 2014
$1.4M
Colorectal Cancer Prevention Through Thyroid Hormone TargetsF31CA165665 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI BROWN, ADAM ROBERT · 2012 to 2014
$91k
NCATS NIH HHS UL1 TR000039NCATS NIH HHS UL1TR000039NCI NIH HHS F31 CA165665NCI NIH HHS F31CA165665NCI NIH HHS R01 CA136493NCI NIH HHS R01CA136493
6 · The paper itself

Abstract

The small intestine participates in lipid digestion, metabolism and transport. Cytosolic malic enzyme 1 (ME1) is an enzyme that generates NADPH used in fatty acid and cholesterol biosynthesis. Previous work has correlated liver and adipose ME1 expression with susceptibility to obesity and diabetes; however, the contributions of intestine-expressed ME1 to these conditions are unknown. We generated transgenic (Tg) mice expressing rat ME1 in the gastrointestinal epithelium under the control of the murine villin1 promoter/enhancer. Levels of intestinal ME1 protein (endogenous plus transgene) were greater in Tg than wildtype (WT) littermates. Effects of elevated intestinal ME1 on body weight, circulating insulin, select adipocytokines, blood glucose, and metabolism-related genes were examined. Male Tg mice fed a high-fat (HF) diet gained significantly more body weight than WT male littermates and had heavier livers. ME1-Tg mice had deeper intestinal and colon crypts, a greater intestinal 5-bromodeoxyuridine labeling index, and increased expression of intestinal lipogenic (Fasn, Srebf1) and cholesterol biosynthetic (Hmgcsr, Hmgcs1), genes. The livers from HF diet-fed Tg mice also exhibited an induction of cholesterol and lipogenic pathway genes and altered measures (Irs1, Irs2, Prkce) of insulin sensitivity. Results indicate that gastrointestinal ME1 via its influence on intestinal epithelial proliferation, and lipogenic and cholesterologenic genes may concomitantly impact signaling in liver to modify this tissue's metabolic state. Our work highlights a new mouse model to address the role of intestine-expressed ME1 in whole body metabolism, hepatomegaly, and crypt cell proliferation. Intestinal ME1 may thus constitute a therapeutic target to reduce obesity-associated pathologies.

Indexed as

Cell ProliferationAdiposityAnimalsCells, CulturedCytosolDiet, High-FatGastrointestinal TractGene Expression RegulationImmunoenzyme TechniquesInsulin ResistanceIntestinal MucosaIntestinesLipid MetabolismLipogenesisLiverMalate DehydrogenaseMalate DehydrogenaseRNA, Messenger

Identifiers

PMID25402228
PMCPMC4234650
OpenAlexW2044494885

What OpenQuestion holds

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LicenceCC BY
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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.