Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet‐Induced Obesity

Scope To test whether myeloid cells Tsc1 deletion and therefore constitutive activation of the nutrient sensor mTORC1 protects from high‐fat diet (HFD)‐induced obesity, glucose intolerance, and adipose tissue inflammation. Methods and results Mice with Tsc1 deletion in myeloid cells (MTsc1KO) and li...

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Veröffentlicht in:Molecular nutrition & food research 2018-09, Vol.62 (17), p.e1800283-n/a
Hauptverfasser: Paschoal, Vivian A., Belchior, Thiago, Amano, Mariane T., Burgos‐Silva, Marina, Peixoto, Albert S., Magdalon, Juliana, Vieira, Thayna S., Andrade, Maynara L., Moreno, Mayara F., Chimin, Patricia, Câmara, Niels O., Festuccia, William T.
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container_issue 17
container_start_page e1800283
container_title Molecular nutrition & food research
container_volume 62
creator Paschoal, Vivian A.
Belchior, Thiago
Amano, Mariane T.
Burgos‐Silva, Marina
Peixoto, Albert S.
Magdalon, Juliana
Vieira, Thayna S.
Andrade, Maynara L.
Moreno, Mayara F.
Chimin, Patricia
Câmara, Niels O.
Festuccia, William T.
description Scope To test whether myeloid cells Tsc1 deletion and therefore constitutive activation of the nutrient sensor mTORC1 protects from high‐fat diet (HFD)‐induced obesity, glucose intolerance, and adipose tissue inflammation. Methods and results Mice with Tsc1 deletion in myeloid cells (MTsc1KO) and littermate controls (MTsc1WT) were fed with HFD for 8 weeks and evaluated for body weight, glucose homeostasis, and adipose tissue inflammation. MTsc1KO mice were protected from HFD‐induced obesity and glucose intolerance. MTsc1KO, however, displayed, independently of the diet, abnormal behavior, episodes of intense movement, and muscle spasms followed by temporary paralysis. To investigate whether obesity protection was due to myeloid cells Tsc1 deletion, bone marrow was transplanted from MTsc1WT and MTsc1KO into irradiated C57BL6/J mice. Mice transplanted with MTsc1KO bone marrow displayed reduced body weight gain, adiposity, and inflammation, and enhanced energy expenditure, glucose tolerance and adipose tissue M2 macrophage content upon HFD feeding, in the absence of abnormal behavior. In vitro, Tsc1 deletion increased in a mTORC1‐dependent manner macrophage polarization to M2 profile and mRNA levels of fatty acid binding protein 4 and PPARγ. Conclusion Constitutive mTORC1 activation in myeloid cells protects mice from HFD‐induced obesity, adipose tissue inflammation, and glucose intolerance by promoting macrophage polarization to M2 pro‐resolution profile and increasing energy expenditure. Mice transplanted with Tsc1‐deficient bone marrow are protected from high‐fat‐diet‐induced obesity, adipose tissue inflammation, and glucose intolerance through a mechanism that involves macrophage polarization to the pro‐resolution M2 profile and an increase in whole‐body energy expenditure. These findings support the important role of macrophages and the nutrient sensor mTORC1 as major modulators of energy balance, metabolism, and inflammation.
doi_str_mv 10.1002/mnfr.201800283
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Methods and results Mice with Tsc1 deletion in myeloid cells (MTsc1KO) and littermate controls (MTsc1WT) were fed with HFD for 8 weeks and evaluated for body weight, glucose homeostasis, and adipose tissue inflammation. MTsc1KO mice were protected from HFD‐induced obesity and glucose intolerance. MTsc1KO, however, displayed, independently of the diet, abnormal behavior, episodes of intense movement, and muscle spasms followed by temporary paralysis. To investigate whether obesity protection was due to myeloid cells Tsc1 deletion, bone marrow was transplanted from MTsc1WT and MTsc1KO into irradiated C57BL6/J mice. Mice transplanted with MTsc1KO bone marrow displayed reduced body weight gain, adiposity, and inflammation, and enhanced energy expenditure, glucose tolerance and adipose tissue M2 macrophage content upon HFD feeding, in the absence of abnormal behavior. In vitro, Tsc1 deletion increased in a mTORC1‐dependent manner macrophage polarization to M2 profile and mRNA levels of fatty acid binding protein 4 and PPARγ. Conclusion Constitutive mTORC1 activation in myeloid cells protects mice from HFD‐induced obesity, adipose tissue inflammation, and glucose intolerance by promoting macrophage polarization to M2 pro‐resolution profile and increasing energy expenditure. Mice transplanted with Tsc1‐deficient bone marrow are protected from high‐fat‐diet‐induced obesity, adipose tissue inflammation, and glucose intolerance through a mechanism that involves macrophage polarization to the pro‐resolution M2 profile and an increase in whole‐body energy expenditure. These findings support the important role of macrophages and the nutrient sensor mTORC1 as major modulators of energy balance, metabolism, and inflammation.</description><identifier>ISSN: 1613-4125</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.201800283</identifier><identifier>PMID: 30001482</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Activation ; Adipose tissue ; Adipose Tissue - pathology ; Adipose Tissue - physiology ; adipose tissue inflammation ; Animal tissues ; Animals ; Body weight ; Body weight gain ; Bone marrow ; Bone marrow transplantation ; Clonal deletion ; Cytokines - metabolism ; Diet ; Diet, High-Fat - adverse effects ; Energy expenditure ; Fatty acid-binding protein ; Fatty acids ; Feeding behavior ; Gene Expression Regulation ; Glucose ; Glucose tolerance ; High fat diet ; Homeostasis ; Immunological tolerance ; Inflammation ; Intolerance ; Macrophages ; Macrophages - pathology ; Male ; Mechanistic Target of Rapamycin Complex 1 - genetics ; Mechanistic Target of Rapamycin Complex 1 - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; mRNA ; mTORC1 ; Muscles ; Myeloid cells ; Myeloid Cells - metabolism ; Nutrients ; Obesity ; Obesity - etiology ; Obesity - genetics ; Panniculitis - metabolism ; Panniculitis - pathology ; Paralysis ; Polarization ; Proteins ; Spasms ; Tsc1 deletion ; Tuberous Sclerosis Complex 1 ; Tuberous Sclerosis Complex 1 Protein - genetics ; Tuberous Sclerosis Complex 1 Protein - metabolism ; Weight Gain ; Weight reduction</subject><ispartof>Molecular nutrition &amp; food research, 2018-09, Vol.62 (17), p.e1800283-n/a</ispartof><rights>2018 WILEY‐VCH Verlag GmbH &amp; Co. KGaA, Weinheim</rights><rights>2018 WILEY-VCH Verlag GmbH &amp; Co. KGaA, Weinheim.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3686-8e1c9dd9dd60aecb45aa6aaee6d7bf1790fee9174293940d498b16ad8e5f59623</citedby><cites>FETCH-LOGICAL-c3686-8e1c9dd9dd60aecb45aa6aaee6d7bf1790fee9174293940d498b16ad8e5f59623</cites><orcidid>0000-0001-9078-2795</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fmnfr.201800283$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmnfr.201800283$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30001482$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Paschoal, Vivian A.</creatorcontrib><creatorcontrib>Belchior, Thiago</creatorcontrib><creatorcontrib>Amano, Mariane T.</creatorcontrib><creatorcontrib>Burgos‐Silva, Marina</creatorcontrib><creatorcontrib>Peixoto, Albert S.</creatorcontrib><creatorcontrib>Magdalon, Juliana</creatorcontrib><creatorcontrib>Vieira, Thayna S.</creatorcontrib><creatorcontrib>Andrade, Maynara L.</creatorcontrib><creatorcontrib>Moreno, Mayara F.</creatorcontrib><creatorcontrib>Chimin, Patricia</creatorcontrib><creatorcontrib>Câmara, Niels O.</creatorcontrib><creatorcontrib>Festuccia, William T.</creatorcontrib><title>Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet‐Induced Obesity</title><title>Molecular nutrition &amp; food research</title><addtitle>Mol Nutr Food Res</addtitle><description>Scope To test whether myeloid cells Tsc1 deletion and therefore constitutive activation of the nutrient sensor mTORC1 protects from high‐fat diet (HFD)‐induced obesity, glucose intolerance, and adipose tissue inflammation. Methods and results Mice with Tsc1 deletion in myeloid cells (MTsc1KO) and littermate controls (MTsc1WT) were fed with HFD for 8 weeks and evaluated for body weight, glucose homeostasis, and adipose tissue inflammation. MTsc1KO mice were protected from HFD‐induced obesity and glucose intolerance. MTsc1KO, however, displayed, independently of the diet, abnormal behavior, episodes of intense movement, and muscle spasms followed by temporary paralysis. To investigate whether obesity protection was due to myeloid cells Tsc1 deletion, bone marrow was transplanted from MTsc1WT and MTsc1KO into irradiated C57BL6/J mice. Mice transplanted with MTsc1KO bone marrow displayed reduced body weight gain, adiposity, and inflammation, and enhanced energy expenditure, glucose tolerance and adipose tissue M2 macrophage content upon HFD feeding, in the absence of abnormal behavior. In vitro, Tsc1 deletion increased in a mTORC1‐dependent manner macrophage polarization to M2 profile and mRNA levels of fatty acid binding protein 4 and PPARγ. Conclusion Constitutive mTORC1 activation in myeloid cells protects mice from HFD‐induced obesity, adipose tissue inflammation, and glucose intolerance by promoting macrophage polarization to M2 pro‐resolution profile and increasing energy expenditure. Mice transplanted with Tsc1‐deficient bone marrow are protected from high‐fat‐diet‐induced obesity, adipose tissue inflammation, and glucose intolerance through a mechanism that involves macrophage polarization to the pro‐resolution M2 profile and an increase in whole‐body energy expenditure. These findings support the important role of macrophages and the nutrient sensor mTORC1 as major modulators of energy balance, metabolism, and inflammation.</description><subject>Activation</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - pathology</subject><subject>Adipose Tissue - physiology</subject><subject>adipose tissue inflammation</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Body weight</subject><subject>Body weight gain</subject><subject>Bone marrow</subject><subject>Bone marrow transplantation</subject><subject>Clonal deletion</subject><subject>Cytokines - metabolism</subject><subject>Diet</subject><subject>Diet, High-Fat - adverse effects</subject><subject>Energy expenditure</subject><subject>Fatty acid-binding protein</subject><subject>Fatty acids</subject><subject>Feeding behavior</subject><subject>Gene Expression Regulation</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>High fat diet</subject><subject>Homeostasis</subject><subject>Immunological tolerance</subject><subject>Inflammation</subject><subject>Intolerance</subject><subject>Macrophages</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Mechanistic Target of Rapamycin Complex 1 - genetics</subject><subject>Mechanistic Target of Rapamycin Complex 1 - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>mRNA</subject><subject>mTORC1</subject><subject>Muscles</subject><subject>Myeloid cells</subject><subject>Myeloid Cells - metabolism</subject><subject>Nutrients</subject><subject>Obesity</subject><subject>Obesity - etiology</subject><subject>Obesity - genetics</subject><subject>Panniculitis - metabolism</subject><subject>Panniculitis - pathology</subject><subject>Paralysis</subject><subject>Polarization</subject><subject>Proteins</subject><subject>Spasms</subject><subject>Tsc1 deletion</subject><subject>Tuberous Sclerosis Complex 1</subject><subject>Tuberous Sclerosis Complex 1 Protein - genetics</subject><subject>Tuberous Sclerosis Complex 1 Protein - metabolism</subject><subject>Weight Gain</subject><subject>Weight reduction</subject><issn>1613-4125</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0EoqVw5YgsceGyi__FsY9VSqFSt4vKco4cZyJcJXaxHVBuXLnxGfkkuGy7By5II70Z6TdPM3oIvaRkTQlhbyc_xDUjVJVB8UfomErKV4Jy_vjQs-oIPUvphhBOmeBP0REnhFCh2DH62QSfsstzdt8An9oiJrvgcRhw_gL4as7Rgc_4E_gUIp522-uGYufxZoExuB43MI4JX_h-ttDjbsG7ZCk-gxH--nyMIYPNCW-cBTzEMOEzB_n3j18PK9sOksvLc_RkMGOCF_d6gj6fv9s1H1aX2_cXzenlynKp5EoBtbrvS0liwHaiMkYaAyD7uhtorckAoGktmOZakF5o1VFpegXVUGnJ-Al6s_e9jeHrDCm3k0u2PGE8hDm1jNSECVbVsqCv_0Fvwhx9ua5QWmlecyUKtd5TNoaUIgztbXSTiUtLSXsXUnsXUnsIqSy8ureduwn6A_6QSgHEHvjuRlj-Y9durs6vOSeS_wG7cJ7O</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Paschoal, Vivian A.</creator><creator>Belchior, Thiago</creator><creator>Amano, Mariane T.</creator><creator>Burgos‐Silva, Marina</creator><creator>Peixoto, Albert S.</creator><creator>Magdalon, Juliana</creator><creator>Vieira, Thayna S.</creator><creator>Andrade, Maynara L.</creator><creator>Moreno, Mayara F.</creator><creator>Chimin, Patricia</creator><creator>Câmara, Niels O.</creator><creator>Festuccia, William T.</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9078-2795</orcidid></search><sort><creationdate>201809</creationdate><title>Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet‐Induced Obesity</title><author>Paschoal, Vivian A. ; Belchior, Thiago ; Amano, Mariane T. ; Burgos‐Silva, Marina ; Peixoto, Albert S. ; Magdalon, Juliana ; Vieira, Thayna S. ; Andrade, Maynara L. ; Moreno, Mayara F. ; Chimin, Patricia ; Câmara, Niels O. ; Festuccia, William T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3686-8e1c9dd9dd60aecb45aa6aaee6d7bf1790fee9174293940d498b16ad8e5f59623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activation</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - pathology</topic><topic>Adipose Tissue - physiology</topic><topic>adipose tissue inflammation</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Body weight</topic><topic>Body weight gain</topic><topic>Bone marrow</topic><topic>Bone marrow transplantation</topic><topic>Clonal deletion</topic><topic>Cytokines - metabolism</topic><topic>Diet</topic><topic>Diet, High-Fat - adverse effects</topic><topic>Energy expenditure</topic><topic>Fatty acid-binding protein</topic><topic>Fatty acids</topic><topic>Feeding behavior</topic><topic>Gene Expression Regulation</topic><topic>Glucose</topic><topic>Glucose tolerance</topic><topic>High fat diet</topic><topic>Homeostasis</topic><topic>Immunological tolerance</topic><topic>Inflammation</topic><topic>Intolerance</topic><topic>Macrophages</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Mechanistic Target of Rapamycin Complex 1 - genetics</topic><topic>Mechanistic Target of Rapamycin Complex 1 - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>mRNA</topic><topic>mTORC1</topic><topic>Muscles</topic><topic>Myeloid cells</topic><topic>Myeloid Cells - metabolism</topic><topic>Nutrients</topic><topic>Obesity</topic><topic>Obesity - etiology</topic><topic>Obesity - genetics</topic><topic>Panniculitis - metabolism</topic><topic>Panniculitis - pathology</topic><topic>Paralysis</topic><topic>Polarization</topic><topic>Proteins</topic><topic>Spasms</topic><topic>Tsc1 deletion</topic><topic>Tuberous Sclerosis Complex 1</topic><topic>Tuberous Sclerosis Complex 1 Protein - genetics</topic><topic>Tuberous Sclerosis Complex 1 Protein - metabolism</topic><topic>Weight Gain</topic><topic>Weight reduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Paschoal, Vivian A.</creatorcontrib><creatorcontrib>Belchior, Thiago</creatorcontrib><creatorcontrib>Amano, Mariane T.</creatorcontrib><creatorcontrib>Burgos‐Silva, Marina</creatorcontrib><creatorcontrib>Peixoto, Albert S.</creatorcontrib><creatorcontrib>Magdalon, Juliana</creatorcontrib><creatorcontrib>Vieira, Thayna S.</creatorcontrib><creatorcontrib>Andrade, Maynara L.</creatorcontrib><creatorcontrib>Moreno, Mayara F.</creatorcontrib><creatorcontrib>Chimin, Patricia</creatorcontrib><creatorcontrib>Câmara, Niels O.</creatorcontrib><creatorcontrib>Festuccia, William T.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular nutrition &amp; food research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Paschoal, Vivian A.</au><au>Belchior, Thiago</au><au>Amano, Mariane T.</au><au>Burgos‐Silva, Marina</au><au>Peixoto, Albert S.</au><au>Magdalon, Juliana</au><au>Vieira, Thayna S.</au><au>Andrade, Maynara L.</au><au>Moreno, Mayara F.</au><au>Chimin, Patricia</au><au>Câmara, Niels O.</au><au>Festuccia, William T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet‐Induced Obesity</atitle><jtitle>Molecular nutrition &amp; food research</jtitle><addtitle>Mol Nutr Food Res</addtitle><date>2018-09</date><risdate>2018</risdate><volume>62</volume><issue>17</issue><spage>e1800283</spage><epage>n/a</epage><pages>e1800283-n/a</pages><issn>1613-4125</issn><eissn>1613-4133</eissn><abstract>Scope To test whether myeloid cells Tsc1 deletion and therefore constitutive activation of the nutrient sensor mTORC1 protects from high‐fat diet (HFD)‐induced obesity, glucose intolerance, and adipose tissue inflammation. Methods and results Mice with Tsc1 deletion in myeloid cells (MTsc1KO) and littermate controls (MTsc1WT) were fed with HFD for 8 weeks and evaluated for body weight, glucose homeostasis, and adipose tissue inflammation. MTsc1KO mice were protected from HFD‐induced obesity and glucose intolerance. MTsc1KO, however, displayed, independently of the diet, abnormal behavior, episodes of intense movement, and muscle spasms followed by temporary paralysis. To investigate whether obesity protection was due to myeloid cells Tsc1 deletion, bone marrow was transplanted from MTsc1WT and MTsc1KO into irradiated C57BL6/J mice. Mice transplanted with MTsc1KO bone marrow displayed reduced body weight gain, adiposity, and inflammation, and enhanced energy expenditure, glucose tolerance and adipose tissue M2 macrophage content upon HFD feeding, in the absence of abnormal behavior. In vitro, Tsc1 deletion increased in a mTORC1‐dependent manner macrophage polarization to M2 profile and mRNA levels of fatty acid binding protein 4 and PPARγ. Conclusion Constitutive mTORC1 activation in myeloid cells protects mice from HFD‐induced obesity, adipose tissue inflammation, and glucose intolerance by promoting macrophage polarization to M2 pro‐resolution profile and increasing energy expenditure. Mice transplanted with Tsc1‐deficient bone marrow are protected from high‐fat‐diet‐induced obesity, adipose tissue inflammation, and glucose intolerance through a mechanism that involves macrophage polarization to the pro‐resolution M2 profile and an increase in whole‐body energy expenditure. These findings support the important role of macrophages and the nutrient sensor mTORC1 as major modulators of energy balance, metabolism, and inflammation.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30001482</pmid><doi>10.1002/mnfr.201800283</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0001-9078-2795</orcidid></addata></record>
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subjects Activation
Adipose tissue
Adipose Tissue - pathology
Adipose Tissue - physiology
adipose tissue inflammation
Animal tissues
Animals
Body weight
Body weight gain
Bone marrow
Bone marrow transplantation
Clonal deletion
Cytokines - metabolism
Diet
Diet, High-Fat - adverse effects
Energy expenditure
Fatty acid-binding protein
Fatty acids
Feeding behavior
Gene Expression Regulation
Glucose
Glucose tolerance
High fat diet
Homeostasis
Immunological tolerance
Inflammation
Intolerance
Macrophages
Macrophages - pathology
Male
Mechanistic Target of Rapamycin Complex 1 - genetics
Mechanistic Target of Rapamycin Complex 1 - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
mRNA
mTORC1
Muscles
Myeloid cells
Myeloid Cells - metabolism
Nutrients
Obesity
Obesity - etiology
Obesity - genetics
Panniculitis - metabolism
Panniculitis - pathology
Paralysis
Polarization
Proteins
Spasms
Tsc1 deletion
Tuberous Sclerosis Complex 1
Tuberous Sclerosis Complex 1 Protein - genetics
Tuberous Sclerosis Complex 1 Protein - metabolism
Weight Gain
Weight reduction
title Constitutive Activation of the Nutrient Sensor mTORC1 in Myeloid Cells Induced by Tsc1 Deletion Protects Mice from Diet‐Induced Obesity
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