Evidence map›Paper›PMID 25213859›Full record

ArticleThe Journal of biological chemistry2014

Inhibiting monoacylglycerol acyltransferase 1 ameliorates hepatic metabolic abnormalities but not inflammation and injury in mice.

Nisreen Soufi, Angela M Hall, Zhouji Chen, Jun Yoshino, Sara L Collier, James C Mathews, Elizabeth M Brunt, Carolyn J Albert, Mark J Graham, David A Ford and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

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  16. Loss of lipin 1-mediated phosphatidic acid phosphohydrolase activity in muscle leads to skeletal myopathy in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

11 authors at 3 institutions in 1 country.

Nisreen SoufiFrom the Departments of Pediatrics, Medicine, and.
Angela M HallMedicine, and.
Zhouji ChenMedicine, and.
Jun YoshinoMedicine, and.
Sara L CollierMedicine, and.
James C MathewsPathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri 63110.
Elizabeth M BruntPathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri 63110.
Carolyn J Albertthe Edward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, Saint Louis, Missouri 63104, and.
Mark J GrahamISIS Pharmaceuticals Inc., Carlsbad, California 92008.
David A Fordthe Edward A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, Saint Louis, Missouri 63104, and.
Brian N FinckMedicine, and bfinck@dom.wustl.edu.
Washington University in St. Louis · USSaint Louis University · USIonis Pharmaceuticals (United States) · US

Funding

Washington University Institute of Clinical and Translational SciencesUL1TR000448 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$41.4M
Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Irfan J Lodhi · 2013 to 2026
$27.1M
Washington University Institute of Clinical and Translational SciencesKL2TR000450 · NCATS · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2012 to 2016
$8.8M
LIPIN 1 IN THE REGULATION OF HEPATIC LIPID METABOLISMR01DK078187 · NIDDK · WASHINGTON UNIVERSITY · PI FINCK, BRIAN N · 2008 to 2016
$2.8M
Plasmalogen-derived bioactive lipids in atherosclerosisR01HL074214 · NHLBI · SAINT LOUIS UNIVERSITY · PI FORD, DAVID A. · 2004 to 2014
$2.8M
Regulation and Function of MGAT in Hepatic TAG Synthesis and Metabolic DiseaseK01DK087821 · NIDDK · WASHINGTON UNIVERSITY · PI HALL, ANGELA MARIE · 2010 to 2014
$553k
Chlorinated Lipids in Myocardial Ischemia/ReperfusionR21HL111906 · NHLBI · SAINT LOUIS UNIVERSITY · PI FORD, DAVID A. · 2012 to 2013
$404k
NCATS NIH HHS KL2 TR000450NCATS NIH HHS UL1 TR000448NCATS NIH HHS UL1 TR000450NHLBI NIH HHS HL074214NHLBI NIH HHS HL111906NHLBI NIH HHS R01 HL074214NHLBI NIH HHS R21 HL111906NIDDK NIH HHS K01 DK087821NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK052574NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P30 DK52574NIDDK NIH HHS P30 DK56341NIDDK NIH HHS R01 DK078187
6 · The paper itself

Abstract

Abnormalities in hepatic lipid metabolism and insulin action are believed to play a critical role in the etiology of nonalcoholic steatohepatitis. Monoacylglycerol acyltransferase (MGAT) enzymes convert monoacylglycerol to diacylglycerol, which is the penultimate step in one pathway for triacylglycerol synthesis. Hepatic expression of Mogat1, which encodes an MGAT enzyme, is increased in the livers of mice with hepatic steatosis, and knocking down Mogat1 improves glucose metabolism and hepatic insulin signaling, but whether increased MGAT activity plays a role in the etiology of nonalcoholic steatohepatitis is unclear. To examine this issue, mice were placed on a diet containing high levels of trans fatty acids, fructose, and cholesterol (HTF-C diet) or a low fat control diet for 4 weeks. Mice were injected with antisense oligonucleotides (ASOs) to knockdown Mogat1 or a scrambled ASO control for 12 weeks while remaining on diet. The HTF-C diet caused glucose intolerance, hepatic steatosis, and induced hepatic gene expression markers of inflammation, macrophage infiltration, and stellate cell activation. Mogat1 ASO treatment, which suppressed Mogat1 expression in liver and adipose tissue, attenuated weight gain, improved glucose tolerance, improved hepatic insulin signaling, and decreased hepatic triacylglycerol content compared with control ASO-treated mice on HTF-C chow. However, Mogat1 ASO treatment did not reduce hepatic diacylglycerol, cholesterol, or free fatty acid content; improve histologic measures of liver injury; or reduce expression of markers of stellate cell activation, liver inflammation, and injury. In conclusion, inhibition of hepatic Mogat1 in HTF-C diet-fed mice improves hepatic metabolic abnormalities without attenuating liver inflammation and injury.

Indexed as

AcyltransferasesAdipose TissueAdiposityAnimalsBiomarkersDietDiglyceridesFatty AcidsFatty LiverGene Expression RegulationGene Knockdown TechniquesGlucoseGlucose Tolerance TestHepatic Stellate CellsHomeostasisInflammation1,2-diacylglycerolAcyltransferasesBiomarkersDiglyceridesFatty AcidsGlucoseMGAT1 protein, mouseN-AcetylglucosaminyltransferasesOligonucleotides, AntisenseTriglyceridesDiacylglycerolFatty Acid MetabolismInflammationInsulin ResistanceLiverNonalcoholic Steatohepatitis

Identifiers

PMID25213859
PMCPMC4208022
OpenAlexW2088631644

What OpenQuestion holds

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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.