Evidence map›Paper›PMID 21357625›Full record

ArticleThe Journal of biological chemistry2011

Regulator of G protein signaling (RGS16) inhibits hepatic fatty acid oxidation in a carbohydrate response element-binding protein (ChREBP)-dependent manner.

Victor Pashkov, Jie Huang, Vinay K Parameswara, Wojciech Kedzierski, Deborah M Kurrasch, Gregory G Tall, Victoria Esser, Robert D Gerard, Kosaku Uyeda, Howard C Towle and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed, 59 citations in OpenAlex.

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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 2 institutions in 1 country.

Victor PashkovDepartment of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9041, USA.
Jie Huang
Vinay K Parameswara
Wojciech Kedzierski
Deborah M Kurrasch
Gregory G Tall
Victoria Esser
Robert D Gerard
Kosaku Uyeda
Howard C Towle
Thomas M Wilkie
The University of Texas Southwestern Medical Center · USUniversity of Minnesota · US

Funding

Regulation of Heterotrimeric G proteins by non-receptor activatorsR01GM088242 · NIGMS · UNIVERSITY OF ROCHESTER · PI TALL, GREGORY GORDON · 2009 to 2022
$4.2M
GQ/RGS MEDIATED SIGNALINGR01GM061395 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI WILKIE, THOMAS M · 2000 to 2009
$2.3M
Characterizing RGS Mutations in CardiomyopathyF32HL072551 · NHLBI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI KURRASCH-ORBAUGH, DEBORAH M · 2003 to 2005
$124k
NHLBI NIH HHS F32 HL072551NHLBI NIH HHS HL072551NIGMS NIH HHS GM61395NIGMS NIH HHS R01 GM061395NIGMS NIH HHS R01 GM088242
6 · The paper itself

Abstract

G protein-coupled receptor (GPCR) pathways control glucose and fatty acid metabolism and the onset of obesity and diabetes. Regulators of G protein signaling (RGS) are GTPase-activating proteins (GAPs) for G(i) and G(q) α-subunits that control the intensity and duration of GPCR signaling. Herein we determined the role of Rgs16 in GPCR regulation of liver metabolism. Rgs16 is expressed during the last few hours of the daily fast in periportal hepatocytes, the oxygen-rich zone of the liver where lipolysis and gluconeogenesis predominate. Rgs16 knock-out mice had elevated expression of fatty acid oxidation genes in liver, higher rates of fatty acid oxidation in liver extracts, and higher plasma β-ketone levels compared with wild type mice. By contrast, transgenic mice that overexpressed RGS16 protein specifically in liver exhibited reciprocal phenotypes as well as low blood glucose levels compared with wild type littermates and fatty liver after overnight fasting. The transcription factor carbohydrate response element-binding protein (ChREBP), which induces fatty acid synthesis genes in response to high carbohydrate feeding, was unexpectedly required during fasting for maximal Rgs16 transcription in liver and in cultured primary hepatocytes during gluconeogenesis. Thus, RGS16 provides a signaling mechanism for glucose production to inhibit GPCR-stimulated fatty acid oxidation in hepatocytes.

Indexed as

AnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsFatty AcidsGluconeogenesisGlucoseHepatocytesLiverMiceMice, KnockoutMice, TransgenicNuclear ProteinsOxidation-ReductionReceptors, G-Protein-CoupledRGS ProteinsTranscription FactorsTranscription, GeneticBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsFatty AcidsGlucoseMlxipl protein, mouseNuclear ProteinsReceptors, G-Protein-CoupledRGS16 proteinRGS ProteinsTranscription Factors

Identifiers

PMID21357625
PMCPMC3083217
OpenAlexW2049489442

What OpenQuestion holds

Textmetadata
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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.