Evidence map›Paper›PMID 30038292›Full record

ArticleScientific reports2018

PAS Kinase deficiency alters the glucokinase function and hepatic metabolism.

A Pérez-García, P Dongil, V Hurtado-Carneiro, E Blazquez, C Sanz, E Alvarez

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.8field-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

11 citing papers in PubMed, 18 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

6 authors at 1 institution in 1 country.

A Pérez-GarcíaDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University of Madrid, Institute of Medical Research at the Hospital Clínico San Carlos (IdISSC), Ciudad Universitaria, s/n, 28040, Madrid, Spain.
P DongilDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University of Madrid, Institute of Medical Research at the Hospital Clínico San Carlos (IdISSC), Ciudad Universitaria, s/n, 28040, Madrid, Spain.
V Hurtado-CarneiroDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University of Madrid, Institute of Medical Research at the Hospital Clínico San Carlos (IdISSC), Ciudad Universitaria, s/n, 28040, Madrid, Spain.
E BlazquezDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University of Madrid, Institute of Medical Research at the Hospital Clínico San Carlos (IdISSC), Ciudad Universitaria, s/n, 28040, Madrid, Spain.
C SanzSpanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), Madrid, Spain. mcsanz@med.ucm.es.ORCID 0000-0001-7025-6667
E AlvarezDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, Complutense University of Madrid, Institute of Medical Research at the Hospital Clínico San Carlos (IdISSC), Ciudad Universitaria, s/n, 28040, Madrid, Spain.
Universidad Complutense de Madrid · ES

Funding

Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) RTC-2016-4823-1
6 · The paper itself

Abstract

The liver controls metabolic homeostasis in response to fasting and refeeding periods. Glucokinase (GCK) adjusts hepatic glucose phosphorylation to blood glucose levels, acting as a glucose sensor. Our objective was to determine whether PAS kinase (PASK), a nutrient sensor, could be affecting the expression or activity of liver GCK and the response to fasting and refeeding states of key hepatic metabolic pathways. PASK-deficient mice have impaired insulin signaling (AKT overactivation). Furthermore, PASK deficiency modified the expression of several transcription factors involved in the adjustment to fasting and refeeding. Foxo1 decreased under fasting conditions, while Ppara and Pparg were overexpressed in PASK-deficient mice. However, PEPCK protein levels were similar or higher, while the expression of Cpt1a decreased in PASK-deficient mice. By contrast, Lxra and Chrebp were overexpressed after refeeding, while the expression of Acc and Fas decreased in PASK-deficient mice. Likewise, with a decreased expression of Gck and increased nuclear location of the complex GCK-GCKR, GCK activity decreased in PASK-deficient mice. Therefore, PASK regulated some of the genes and proteins responsible for glucose sensing, such as glucokinase, and for insulin signalling, affecting glucose and lipid metabolism and consequently certain critical hepatic functions.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarrier ProteinsFastingFeeding BehaviorGene Expression RegulationGlucokinaseInsulinIntracellular Signaling Peptides and ProteinsLiverMice, Inbred C57BLPhosphoenolpyruvate Carboxykinase (ATP)Protein Serine-Threonine KinasesRNA, MessengerSignal TransductionSterol Regulatory Element Binding Protein 1Adaptor Proteins, Signal TransducingCarrier ProteinsGckr protein, mouseGlucokinaseInsulinIntracellular Signaling Peptides and ProteinsPAS domain kinasesPhosphoenolpyruvate Carboxykinase (ATP)Protein Serine-Threonine KinasesRNA, MessengerSrebf1 protein, mouseSterol Regulatory Element Binding Protein 1

Identifiers

PMID30038292
PMCPMC6056484
OpenAlexW2884745721

What OpenQuestion holds

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Registered trials

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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.