Evidence map›Paper›PMID 25918168›Full record

ArticleThe Journal of biological chemistry2015

Glycerol-3-phosphate Acyltransferase Isoform-4 (GPAT4) Limits Oxidation of Exogenous Fatty Acids in Brown Adipocytes.

Daniel E Cooper, Trisha J Grevengoed, Eric L Klett, Rosalind A Coleman

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 32 citations in OpenAlex.

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  11. Thermogenesis in Adipose Tissue Activated by Thyroid Hormone.International journal of molecular sciences · 2020
    Review
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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

4 authors at 1 institution in 1 country.

Daniel E CooperFrom the Departments of Nutrition and.
Trisha J GrevengoedFrom the Departments of Nutrition and.
Eric L KlettFrom the Departments of Nutrition and Medicine, University of North Carolina, Chapel Hill, North Carolina 27599.
Rosalind A ColemanFrom the Departments of Nutrition and rcoleman@unc.edu.
University of North Carolina at Chapel Hill · US

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SUSAN M. SMITH · 1999 to 2026
$31.6M
METABOLISM OF GLYCEROLIPIDS IN LIVERR01DK056598 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COLEMAN, ROSALIND ANNE · 1999 to 2016
$5.0M
Role of acyl-CoA synthetases in mouse pancreatic ??-cell functionK08DK090141 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KLETT, ERIC · 2010 to 2014
$775k
Glycerolipid synthesis in liverR56DK056598 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI COLEMAN, ROSALIND ANNE · 2017 to 2017
$228k
NIDDK NIH HHS DK56350NIDDK NIH HHS DK56598NIDDK NIH HHS K08 DK090141NIDDK NIH HHS K08DK090141NIDDK NIH HHS P30 DK056350NIDDK NIH HHS R01 DK056598NIDDK NIH HHS R56 DK056598
6 · The paper itself

Abstract

Glycerol-3-phosphate acyltransferase-4 (GPAT4) null pups grew poorly during the suckling period and, as adults, were protected from high fat diet-induced obesity. To determine why Gpat4(-/-) mice failed to gain weight during these two periods of high fat feeding, we examined energy metabolism. Compared with controls, the metabolic rate of Gpat4(-/-) mice fed a 45% fat diet was 12% higher. Core body temperature was 1 ºC higher after high fat feeding. Food intake, fat absorption, and activity were similar in both genotypes. Impaired weight gain in Gpat4(-/-) mice did not result from increased heat loss, because both cold tolerance and response to a β3-adrenergic agonist were similar in both genotypes. Because GPAT4 comprises 65% of the total GPAT activity in brown adipose tissue (BAT), we characterized BAT function. A 45% fat diet increased the Gpat4(-/-) BAT expression of peroxisome proliferator-activated receptor α (PPAR) target genes, Cpt1α, Pgc1α, and Ucp1, and BAT mitochondria oxidized oleate and pyruvate at higher rates than controls, suggesting that fatty acid signaling and flux through the TCA cycle were enhanced. To assess the role of GPAT4 directly, neonatal BAT preadipocytes were differentiated to adipocytes. Compared with controls, Gpat4(-/-) brown adipocytes incorporated 33% less fatty acid into triacylglycerol and 46% more into the pathway of β-oxidation. The increased oxidation rate was due solely to an increase in the oxidation of exogenous fatty acids. These data suggest that in the absence of cold exposure, GPAT4 limits excessive fatty acid oxidation and the detrimental induction of a hypermetabolic state.

Indexed as

AdipocytesAdipose Tissue, BrownAnimalsDietary FatsFatty AcidsGlycerol-3-Phosphate O-AcyltransferaseMiceMice, Inbred C57BLMice, KnockoutOxidation-ReductionThermogenesisTriglyceridesWeight GainDietary FatsFatty AcidsGlycerol-3-Phosphate O-AcyltransferaseGPAT4 protein, mouseTriglyceridesadipose tissueenergy metabolismfatty acid metabolismlipid dropletlipid signaling

Identifiers

PMID25918168
PMCPMC4463454
OpenAlexW2035376792

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.