Evidence map›Paper›PMID 34211098›Full record

ArticleCommunications biology2021

Deletion of the diabetes candidate gene Slc16a13 in mice attenuates diet-induced ectopic lipid accumulation and insulin resistance.

Tina Schumann, Jörg König, Christian von Loeffelholz, Daniel F Vatner, Dongyan Zhang, Rachel J Perry, Michel Bernier, Jason Chami, Christine Henke, Anica Kurzbach and 9 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

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  14. Dysregulated Liver Metabolism and Polycystic Ovarian Syndrome.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 10 institutions in 4 countries.

Tina SchumannSection of Metabolic and Vascular Medicine, Medical Clinic III, Dresden University School of Medicine, Technische Universität Dresden, Dresden, Germany.
Jörg KönigClinical Pharmacology and Clinical Toxicology, Institute of Experimental and Clinical Pharmacology and Toxicology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Christian von LoeffelholzDepartment of Anaesthesiology and Intensive Care, Jena University Hospital, Jena, Germany.
Daniel F VatnerDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0003-2073-0273
Dongyan ZhangDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.
Rachel J PerryDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0003-0748-8064
Michel BernierExperimental Gerontology Section, Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0002-5948-368X
Jason ChamiHeart Research Institute, Newtown, NSW, Australia.ORCID 0000-0002-1683-2800
Christine HenkeSection of Metabolic and Vascular Medicine, Medical Clinic III, Dresden University School of Medicine, Technische Universität Dresden, Dresden, Germany.
Anica KurzbachSection of Metabolic and Vascular Medicine, Medical Clinic III, Dresden University School of Medicine, Technische Universität Dresden, Dresden, Germany.
Nermeen N El-AgroudySection of Metabolic and Vascular Medicine, Medical Clinic III, Dresden University School of Medicine, Technische Universität Dresden, Dresden, Germany.
Diana M WillmesSection of Metabolic and Vascular Medicine, Medical Clinic III, Dresden University School of Medicine, Technische Universität Dresden, Dresden, Germany.
Dominik PestaGerman Center for Diabetes Research (DZD), Neuherberg, Germany.
Rafael de CaboExperimental Gerontology Section, Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0002-3354-2442
John F O SullivanHeart Research Institute, Newtown, NSW, Australia.
Eric SimonComputational Biology, Boehringer-Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Gerald I ShulmanDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0003-1529-5668
Bradford S HamiltonCardioMetabolic Diseases Research, Boehringer-Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Andreas L BirkenfeldSection of Metabolic and Vascular Medicine, Medical Clinic III, Dresden University School of Medicine, Technische Universität Dresden, Dresden, Germany. Andreas.Birkenfeld@uniklinikum-dresden.de.ORCID 0000-0003-1407-9023
Deutsches Diabetes-Zentrum e.V. · DEYale University · USBoehringer Ingelheim (Germany) · DENational Institutes of Health · USDeutsches Zentrum für Luft- und Raumfahrt e. V. (DLR) · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEJena University Hospital · DEThe Heart Research Institute · AUThe University of Sydney · AUUniversitätsklinikum Tübingen · DE

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Aging Intervention ProgramZIAAG000363 · NIA · NATIONAL INSTITUTE ON AGING · PI DE CABO, RAFAEL · 2009 to 2025
$9.0M
NCATS NIH HHS UL1 TR001863
6 · The paper itself

Abstract

Genome-wide association studies have identified SLC16A13 as a novel susceptibility gene for type 2 diabetes. The SLC16A13 gene encodes SLC16A13/MCT13, a member of the solute carrier 16 family of monocarboxylate transporters. Despite its potential importance to diabetes development, the physiological function of SLC16A13 is unknown. Here, we validate Slc16a13 as a lactate transporter expressed at the plasma membrane and report on the effect of Slc16a13 deletion in a mouse model. We show that Slc16a13 increases mitochondrial respiration in the liver, leading to reduced hepatic lipid accumulation and increased hepatic insulin sensitivity in high-fat diet fed Slc16a13 knockout mice. We propose a mechanism for improved hepatic insulin sensitivity in the context of Slc16a13 deficiency in which reduced intrahepatocellular lactate availability drives increased AMPK activation and increased mitochondrial respiration, while reducing hepatic lipid content. Slc16a13 deficiency thereby attenuates hepatic diacylglycerol-PKCε mediated insulin resistance in obese mice. Together, these data suggest that SLC16A13 is a potential target for the treatment of type 2 diabetes and non-alcoholic fatty liver disease.

Indexed as

AMP-Activated Protein KinasesAnimalsDiabetes Mellitus, Type 2Diet, High-FatGene ExpressionGenetic Predisposition to DiseaseHumansInsulin ResistanceLipid MetabolismLiverMiceMice, Inbred C57BLMice, KnockoutMitochondriaMonocarboxylic Acid TransportersNon-alcoholic Fatty Liver DiseaseAMP-Activated Protein KinasesMct13 protein, mouseMonocarboxylic Acid Transporters

Identifiers

PMID34211098
PMCPMC8249653
OpenAlexW3174193892

What OpenQuestion holds

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LicenceCC BY
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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.