RapamycinFungusV1, Main, Exploration, bibRecord, 000168

mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.

Identifieur interne : 000168 ( Main/Exploration ); précédent : 000167; suivant : 000169

mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.

Auteurs : Nuria Martinez [États-Unis] ; Catherine Y. Cheng [Singapour] ; Natkunam Ketheesan [Australie] ; Aidan Cullen [États-Unis] ; Yuefeng Tang [États-Unis] ; Josephine Lum [Singapour] ; Kim West [États-Unis] ; Michael Poidinger [Singapour] ; David A. Guertin [États-Unis] ; Amit Singhal [Inde] ; Hardy Kornfeld [États-Unis]

Source :

EBioMedicine [ 2352-3964 ] ; 2019.

RBID : pubmed:31279779

Descripteurs français

KwdFr :
- Adipocytes (métabolisme), Alimentation riche en graisse (MeSH), Animaux (MeSH), Complexe-2 cible mécanistique de la rapamycine (génétique), Humains (MeSH), Inflammation (anatomopathologie), Inflammation (génétique), Inflammation (microbiologie), Inflammation (métabolisme), Insuline (génétique), Insuline (métabolisme), Insulinorésistance (génétique), Modèles animaux de maladie humaine (MeSH), Mycobacterium tuberculosis (métabolisme), Mycobacterium tuberculosis (pathogénicité), Métabolisme lipidique (génétique), Métabolisme énergétique (génétique), Obésité (anatomopathologie), Obésité (génétique), Obésité (microbiologie), Obésité (métabolisme), Protéines proto-oncogènes c-akt (génétique), Souris (MeSH), Souris obèse (MeSH), Tissu adipeux (métabolisme), Tuberculose (anatomopathologie), Tuberculose (génétique), Tuberculose (microbiologie), Tuberculose (métabolisme).
MESH :
- anatomopathologie : Inflammation, Obésité, Tuberculose.
- génétique : Complexe-2 cible mécanistique de la rapamycine, Inflammation, Insuline, Insulinorésistance, Métabolisme lipidique, Métabolisme énergétique, Obésité, Protéines proto-oncogènes c-akt, Tuberculose.
- microbiologie : Inflammation, Obésité, Tuberculose.
- métabolisme : Adipocytes, Inflammation, Insuline, Mycobacterium tuberculosis, Obésité, Tissu adipeux, Tuberculose.
- pathogénicité : Mycobacterium tuberculosis.
- Alimentation riche en graisse, Animaux, Humains, Modèles animaux de maladie humaine, Souris, Souris obèse.

English descriptors

KwdEn :
- Adipocytes (metabolism), Adipose Tissue (metabolism), Animals (MeSH), Diet, High-Fat (MeSH), Disease Models, Animal (MeSH), Energy Metabolism (genetics), Humans (MeSH), Inflammation (genetics), Inflammation (metabolism), Inflammation (microbiology), Inflammation (pathology), Insulin (genetics), Insulin (metabolism), Insulin Resistance (genetics), Lipid Metabolism (genetics), Mechanistic Target of Rapamycin Complex 2 (genetics), Mice (MeSH), Mice, Obese (MeSH), Mycobacterium tuberculosis (metabolism), Mycobacterium tuberculosis (pathogenicity), Obesity (genetics), Obesity (metabolism), Obesity (microbiology), Obesity (pathology), Proto-Oncogene Proteins c-akt (genetics), Tuberculosis (genetics), Tuberculosis (metabolism), Tuberculosis (microbiology), Tuberculosis (pathology).
MESH :
- chemical , genetics : Insulin, Mechanistic Target of Rapamycin Complex 2, Proto-Oncogene Proteins c-akt.
- genetics : Energy Metabolism, Inflammation, Insulin Resistance, Lipid Metabolism, Obesity, Tuberculosis.
- metabolism : Adipocytes, Adipose Tissue, Inflammation, Insulin, Mycobacterium tuberculosis, Obesity, Tuberculosis.
- microbiology : Inflammation, Obesity, Tuberculosis.
- pathogenicity : Mycobacterium tuberculosis.
- pathology : Inflammation, Obesity, Tuberculosis.
- Animals, Diet, High-Fat, Disease Models, Animal, Humans, Mice, Mice, Obese.

Abstract

BACKGROUND

Mycobacterium tuberculosis has co-evolved with the human host, adapting to exploit the immune system for persistence and transmission. While immunity to tuberculosis (TB) has been intensively studied in the lung and lymphoid system, little is known about the participation of adipose tissues and non-immune cells in the host-pathogen interaction during this systemic disease.

METHODS

C57BL/6J mice were aerosol infected with M. tuberculosis Erdman and presence of the bacteria and the fitness of the white and brown adipose tissues, liver and skeletal muscle were studied compared to uninfected mice.

FINDINGS

M. tuberculosis infection in mice stimulated immune cell infiltration in visceral, and brown adipose tissue. Despite the absence of detectable bacterial dissemination to fat tissues, adipocytes produced localized pro-inflammatory signals that disrupted adipocyte lipid metabolism, resulting in adipocyte hypertrophy. Paradoxically, this resulted in increased insulin sensitivity and systemic glucose tolerance. Adipose tissue inflammation and enhanced glucose tolerance also developed in obese mice after aerosol M. tuberculosis infection. We found that infection induced adipose tissue Akt signaling, while inhibition of the Akt activator mTORC2 in adipocytes reversed TB-associated adipose tissue inflammation and cell hypertrophy.

INTERPRETATION

Our study reveals a systemic response to aerosol M. tuberculosis infection that regulates adipose tissue lipid homeostasis through mTORC2/Akt signaling in adipocytes. Adipose tissue inflammation in TB is not simply a passive infiltration with leukocytes but requires the mechanistic participation of adipocyte signals.

DOI: 10.1016/j.ebiom.2019.06.052
PubMed: 31279779
PubMed Central: PMC6642333

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<author><name sortKey="Guertin, David A" sort="Guertin, David A" uniqKey="Guertin D" first="David A" last="Guertin">David A. Guertin</name>
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<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Singhal, Amit" sort="Singhal, Amit" uniqKey="Singhal A" first="Amit" last="Singhal">Amit Singhal</name>
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<country xml:lang="fr">Inde</country>
<wicri:regionArea>Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore; Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore; Vaccine and Infectious Disease Research Centre (VIDRC), Translational Health Science and Technology Institute (THSTI), Faridabad, Haryana</wicri:regionArea>
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<author><name sortKey="Kornfeld, Hardy" sort="Kornfeld, Hardy" uniqKey="Kornfeld H" first="Hardy" last="Kornfeld">Hardy Kornfeld</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Medicine, University of Massachusetts Medical School, Worcester, MA</wicri:regionArea>
<placeName><region type="state">Massachusetts</region>
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<term>Adipose Tissue (metabolism)</term>
<term>Animals (MeSH)</term>
<term>Diet, High-Fat (MeSH)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Energy Metabolism (genetics)</term>
<term>Humans (MeSH)</term>
<term>Inflammation (genetics)</term>
<term>Inflammation (metabolism)</term>
<term>Inflammation (microbiology)</term>
<term>Inflammation (pathology)</term>
<term>Insulin (genetics)</term>
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<term>Insulin Resistance (genetics)</term>
<term>Lipid Metabolism (genetics)</term>
<term>Mechanistic Target of Rapamycin Complex 2 (genetics)</term>
<term>Mice (MeSH)</term>
<term>Mice, Obese (MeSH)</term>
<term>Mycobacterium tuberculosis (metabolism)</term>
<term>Mycobacterium tuberculosis (pathogenicity)</term>
<term>Obesity (genetics)</term>
<term>Obesity (metabolism)</term>
<term>Obesity (microbiology)</term>
<term>Obesity (pathology)</term>
<term>Proto-Oncogene Proteins c-akt (genetics)</term>
<term>Tuberculosis (genetics)</term>
<term>Tuberculosis (metabolism)</term>
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<term>Tuberculosis (pathology)</term>
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<term>Alimentation riche en graisse (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Complexe-2 cible mécanistique de la rapamycine (génétique)</term>
<term>Humains (MeSH)</term>
<term>Inflammation (anatomopathologie)</term>
<term>Inflammation (génétique)</term>
<term>Inflammation (microbiologie)</term>
<term>Inflammation (métabolisme)</term>
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<term>Insuline (métabolisme)</term>
<term>Insulinorésistance (génétique)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
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<term>Obésité (métabolisme)</term>
<term>Protéines proto-oncogènes c-akt (génétique)</term>
<term>Souris (MeSH)</term>
<term>Souris obèse (MeSH)</term>
<term>Tissu adipeux (métabolisme)</term>
<term>Tuberculose (anatomopathologie)</term>
<term>Tuberculose (génétique)</term>
<term>Tuberculose (microbiologie)</term>
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<term>Proto-Oncogene Proteins c-akt</term>
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<term>Obésité</term>
<term>Tuberculose</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Energy Metabolism</term>
<term>Inflammation</term>
<term>Insulin Resistance</term>
<term>Lipid Metabolism</term>
<term>Obesity</term>
<term>Tuberculosis</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Complexe-2 cible mécanistique de la rapamycine</term>
<term>Inflammation</term>
<term>Insuline</term>
<term>Insulinorésistance</term>
<term>Métabolisme lipidique</term>
<term>Métabolisme énergétique</term>
<term>Obésité</term>
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<term>Tuberculose</term>
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<term>Adipose Tissue</term>
<term>Inflammation</term>
<term>Insulin</term>
<term>Mycobacterium tuberculosis</term>
<term>Obesity</term>
<term>Tuberculosis</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Inflammation</term>
<term>Obésité</term>
<term>Tuberculose</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Inflammation</term>
<term>Obesity</term>
<term>Tuberculosis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adipocytes</term>
<term>Inflammation</term>
<term>Insuline</term>
<term>Mycobacterium tuberculosis</term>
<term>Obésité</term>
<term>Tissu adipeux</term>
<term>Tuberculose</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Mycobacterium tuberculosis</term>
</keywords>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term>
<term>Obesity</term>
<term>Tuberculosis</term>
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<term>Diet, High-Fat</term>
<term>Disease Models, Animal</term>
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<term>Mice</term>
<term>Mice, Obese</term>
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<term>Animaux</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Souris</term>
<term>Souris obèse</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Mycobacterium tuberculosis has co-evolved with the human host, adapting to exploit the immune system for persistence and transmission. While immunity to tuberculosis (TB) has been intensively studied in the lung and lymphoid system, little is known about the participation of adipose tissues and non-immune cells in the host-pathogen interaction during this systemic disease.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>C57BL/6J mice were aerosol infected with M. tuberculosis Erdman and presence of the bacteria and the fitness of the white and brown adipose tissues, liver and skeletal muscle were studied compared to uninfected mice.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>FINDINGS</b>
</p>
<p>M. tuberculosis infection in mice stimulated immune cell infiltration in visceral, and brown adipose tissue. Despite the absence of detectable bacterial dissemination to fat tissues, adipocytes produced localized pro-inflammatory signals that disrupted adipocyte lipid metabolism, resulting in adipocyte hypertrophy. Paradoxically, this resulted in increased insulin sensitivity and systemic glucose tolerance. Adipose tissue inflammation and enhanced glucose tolerance also developed in obese mice after aerosol M. tuberculosis infection. We found that infection induced adipose tissue Akt signaling, while inhibition of the Akt activator mTORC2 in adipocytes reversed TB-associated adipose tissue inflammation and cell hypertrophy.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>INTERPRETATION</b>
</p>
<p>Our study reveals a systemic response to aerosol M. tuberculosis infection that regulates adipose tissue lipid homeostasis through mTORC2/Akt signaling in adipocytes. Adipose tissue inflammation in TB is not simply a passive infiltration with leukocytes but requires the mechanistic participation of adipocyte signals.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31279779</PMID>
<DateCompleted><Year>2019</Year>
<Month>12</Month>
<Day>17</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>25</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">2352-3964</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>45</Volume>
<PubDate><Year>2019</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>EBioMedicine</Title>
<ISOAbbreviation>EBioMedicine</ISOAbbreviation>
</Journal>
<ArticleTitle>mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.</ArticleTitle>
<Pagination><MedlinePgn>314-327</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S2352-3964(19)30433-5</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ebiom.2019.06.052</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Mycobacterium tuberculosis has co-evolved with the human host, adapting to exploit the immune system for persistence and transmission. While immunity to tuberculosis (TB) has been intensively studied in the lung and lymphoid system, little is known about the participation of adipose tissues and non-immune cells in the host-pathogen interaction during this systemic disease.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">C57BL/6J mice were aerosol infected with M. tuberculosis Erdman and presence of the bacteria and the fitness of the white and brown adipose tissues, liver and skeletal muscle were studied compared to uninfected mice.</AbstractText>
<AbstractText Label="FINDINGS" NlmCategory="RESULTS">M. tuberculosis infection in mice stimulated immune cell infiltration in visceral, and brown adipose tissue. Despite the absence of detectable bacterial dissemination to fat tissues, adipocytes produced localized pro-inflammatory signals that disrupted adipocyte lipid metabolism, resulting in adipocyte hypertrophy. Paradoxically, this resulted in increased insulin sensitivity and systemic glucose tolerance. Adipose tissue inflammation and enhanced glucose tolerance also developed in obese mice after aerosol M. tuberculosis infection. We found that infection induced adipose tissue Akt signaling, while inhibition of the Akt activator mTORC2 in adipocytes reversed TB-associated adipose tissue inflammation and cell hypertrophy.</AbstractText>
<AbstractText Label="INTERPRETATION" NlmCategory="CONCLUSIONS">Our study reveals a systemic response to aerosol M. tuberculosis infection that regulates adipose tissue lipid homeostasis through mTORC2/Akt signaling in adipocytes. Adipose tissue inflammation in TB is not simply a passive infiltration with leukocytes but requires the mechanistic participation of adipocyte signals.</AbstractText>
<CopyrightInformation>Copyright © 2019. Published by Elsevier B.V.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Martinez</LastName>
<ForeName>Nuria</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cheng</LastName>
<ForeName>Catherine Y</ForeName>
<Initials>CY</Initials>
<AffiliationInfo><Affiliation>Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ketheesan</LastName>
<ForeName>Natkunam</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA; School of Science and Technology, University of New England, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cullen</LastName>
<ForeName>Aidan</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tang</LastName>
<ForeName>Yuefeng</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lum</LastName>
<ForeName>Josephine</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>West</LastName>
<ForeName>Kim</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Poidinger</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Guertin</LastName>
<ForeName>David A</ForeName>
<Initials>DA</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Singhal</LastName>
<ForeName>Amit</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore; Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore; Vaccine and Infectious Disease Research Centre (VIDRC), Translational Health Science and Technology Institute (THSTI), Faridabad, Haryana, India.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kornfeld</LastName>
<ForeName>Hardy</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA. Electronic address: Hardy.Kornfeld@umassmed.edu.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 DK094004</GrantID>
<Acronym>DK</Acronym>
<Agency>NIDDK NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2019</Year>
<Month>07</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>EBioMedicine</MedlineTA>
<NlmUniqueID>101647039</NlmUniqueID>
<ISSNLinking>2352-3964</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007328">Insulin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D000076225">Mechanistic Target of Rapamycin Complex 2</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D017667" MajorTopicYN="N">Adipocytes</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000273" MajorTopicYN="N">Adipose Tissue</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004734" MajorTopicYN="N">Energy Metabolism</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007328" MajorTopicYN="N">Insulin</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007333" MajorTopicYN="N">Insulin Resistance</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050356" MajorTopicYN="N">Lipid Metabolism</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000076225" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 2</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008820" MajorTopicYN="N">Mice, Obese</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009169" MajorTopicYN="N">Mycobacterium tuberculosis</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051057" MajorTopicYN="N">Proto-Oncogene Proteins c-akt</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014376" MajorTopicYN="N">Tuberculosis</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adipose tissue</Keyword>
<Keyword MajorTopicYN="N">Akt</Keyword>
<Keyword MajorTopicYN="N">Inflammation</Keyword>
<Keyword MajorTopicYN="N">Insulin resistance</Keyword>
<Keyword MajorTopicYN="N">Tuberculosis</Keyword>
<Keyword MajorTopicYN="N">mTORC2</Keyword>
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<Day>27</Day>
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<Month>06</Month>
<Day>26</Day>
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<Day>27</Day>
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   |clé=     pubmed:31279779
   |texte=   mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.
}}

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mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.

mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.

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