Evidence map›Paper›PMID 30516845›Full record

ArticleHepatology (Baltimore, Md.)2019

Thioesterase Superfamily Member 2 Promotes Hepatic VLDL Secretion by Channeling Fatty Acids Into Triglyceride Biosynthesis.

Michele Alves-Bezerra, Yingxia Li, Mariana Acuña, Anna A Ivanova, Kathleen E Corey, Eric A Ortlund, David E Cohen

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Michele Alves-BezerraJoan & Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, NY.
Yingxia LiJoan & Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, NY.
Mariana AcuñaJoan & Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, NY.
Anna A IvanovaEmory Integrated Lipidomics Core, Emory University, Atlanta, GA.
Kathleen E CoreyGastrointestinal Unit, Massachusetts General Hospital, Boston, MA.
Eric A OrtlundDepartment of Biochemistry, Emory University School of Medicine, Atlanta, GA.
David E CohenJoan & Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, NY.
Cornell University · USEmory University · USMassachusetts General Hospital · US

Funding

Implementing a Maternal health and PRegnancy Outcomes Vision for Everyone (IMPROVE)UL1TR002378 · NCATS · EMORY UNIVERSITY · PI Andres J Garcia, Elizabeth O. Ofili · 2017 to 2026
$92.1M
Phospholipid-Mediated Metabolic Control in the Pathogenesis of NAFLDR01DK056626 · NIDDK · YESHIVA UNIVERSITY · PI COHEN, DAVID E. · 2000 to 2024
$10.3M
Regulation of Hepatic Lipid and Glucose Metabolism by Phosphatidylcholine TransfeR01DK048873 · NIDDK · YESHIVA UNIVERSITY · PI DAVID E. COHEN · 2003 to 2026
$5.8M
Regulation of Hepatic Lipid and Glucose Metabolism by PC-TP/StarD2R37DK048873 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI COHEN, DAVID E. · 2012 to 2021
$5.5M
The Impact of Obstructive Sleep Apnea on Non-Alcoholic Fatty Liver DiseaseK23DK099422 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI COREY, KATHLEEN ELIZABETH · 2013 to 2017
$938k
American Heart Association 18POST33990445American Heart Association-American Stroke Association 18POST33990445Emory University School of MedicineNCATS NIH HHS UL1 TR002378NIDDK NIH HHS K23 DK099422NIDDK NIH HHS R01 DK048873NIDDK NIH HHS R01 DK056626NIDDK NIH HHS R37 DK048873Weill Cornell Medical College
6 · The paper itself

Abstract

In nonalcoholic fatty liver disease (NAFLD), triglycerides accumulate within the liver because the rates of fatty acid accrual by uptake from plasma and de novo synthesis exceed elimination by mitochondrial oxidation and secretion as very low-density lipoprotein (VLDL) triglycerides. Thioesterase superfamily member 2 (Them2) is an acyl-coenzyme A (CoA) thioesterase that catalyzes the hydrolysis of fatty acyl-CoAs into free fatty acids plus CoASH. Them2 is highly expressed in the liver, as well as other oxidative tissues. Mice globally lacking Them2 are resistant to diet-induced obesity and hepatic steatosis, and exhibit improved glucose homeostasis. These phenotypes are attributable, at least in part, to roles of Them2 in the suppression of thermogenesis in brown adipose tissue and insulin signaling in skeletal muscle. To elucidate the hepatic function of Them2, we created mice with liver-specific deletion of Them2 (L-Them2

Indexed as

AnimalsFatty AcidsHumansLipoproteins, VLDLLiverMaleMiceNon-alcoholic Fatty Liver DiseaseObesityThiolester HydrolasesTriglyceridesACOT13 protein, humanAcot13 protein, mouseFatty AcidsLipoproteins, VLDLThiolester HydrolasesTriglyceridesvery low density lipoprotein triglyceride

Identifiers

PMID30516845
PMCPMC6551314
OpenAlexW2902023838

What Socratic holds

Textmetadata
LicenceTDM
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.