Insulin inhibits lipolysis in adipocytes via the evolutionarily conserved mTORC1-Egr1-ATGL-mediated pathway.
Identifieur interne : 000F88 ( Main/Corpus ); précédent : 000F87; suivant : 000F89Insulin inhibits lipolysis in adipocytes via the evolutionarily conserved mTORC1-Egr1-ATGL-mediated pathway.
Auteurs : Partha Chakrabarti ; Ju Youn Kim ; Maneet Singh ; Yu-Kyong Shin ; Jessica Kim ; Joerg Kumbrink ; Yuanyuan Wu ; Mi-Jeong Lee ; Kathrin H. Kirsch ; Susan K. Fried ; Konstantin V. KandrorSource :
- Molecular and cellular biology [ 1098-5549 ] ; 2013.
English descriptors
- KwdEn :
- 3T3-L1 Cells (MeSH), Adipocytes (metabolism), Animals (MeSH), Cells, Cultured (MeSH), DNA-Binding Proteins (genetics), DNA-Binding Proteins (metabolism), Early Growth Response Protein 1 (genetics), Early Growth Response Protein 1 (metabolism), Evolution, Molecular (MeSH), HEK293 Cells (MeSH), Humans (MeSH), Insulin (metabolism), Lipase (genetics), Lipase (metabolism), Lipolysis (MeSH), Male (MeSH), Mechanistic Target of Rapamycin Complex 1 (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Multiprotein Complexes (genetics), Multiprotein Complexes (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Transcription Factors (genetics), Transcription Factors (metabolism).
- MESH :
- chemical , genetics : DNA-Binding Proteins, Early Growth Response Protein 1, Lipase, Multiprotein Complexes, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- genetics : Saccharomyces cerevisiae.
- metabolism : Adipocytes, DNA-Binding Proteins, Early Growth Response Protein 1, Insulin, Lipase, Multiprotein Complexes, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- 3T3-L1 Cells, Animals, Cells, Cultured, Evolution, Molecular, HEK293 Cells, Humans, Lipolysis, Male, Mechanistic Target of Rapamycin Complex 1, Mice, Mice, Inbred C57BL, Signal Transduction.
Abstract
One of the basic functions of insulin in the body is to inhibit lipolysis in adipocytes. Recently, we have found that insulin inhibits lipolysis and promotes triglyceride storage by decreasing transcription of adipose triglyceride lipase via the mTORC1-mediated pathway (P. Chakrabarti et al., Diabetes 59:775-781, 2010), although the mechanism of this effect remained unknown. Here, we used a genetic screen in Saccharomyces cerevisiae in order to identify a transcription factor that mediates the effect of Tor1 on the expression of the ATGL ortholog in yeast. This factor, Msn4p, has homologues in mammalian cells that form a family of early growth response transcription factors. One member of the family, Egr1, is induced by insulin and nutrients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in cultured adipocytes. Feeding animals a high-fat diet increases the activity of mTORC1 and the expression of Egr1 while decreasing ATGL levels in epididymal fat. We suggest that the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important component of the antilipolytic effect of insulin in the mammalian organism.
DOI: 10.1128/MCB.01584-12
PubMed: 23858058
PubMed Central: PMC3753874
Links to Exploration step
pubmed:23858058Le document en format XML
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<term>Animals (MeSH)</term>
<term>Cells, Cultured (MeSH)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>DNA-Binding Proteins (metabolism)</term>
<term>Early Growth Response Protein 1 (genetics)</term>
<term>Early Growth Response Protein 1 (metabolism)</term>
<term>Evolution, Molecular (MeSH)</term>
<term>HEK293 Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Insulin (metabolism)</term>
<term>Lipase (genetics)</term>
<term>Lipase (metabolism)</term>
<term>Lipolysis (MeSH)</term>
<term>Male (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Multiprotein Complexes (genetics)</term>
<term>Multiprotein Complexes (metabolism)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>TOR Serine-Threonine Kinases (metabolism)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
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<term>Early Growth Response Protein 1</term>
<term>Lipase</term>
<term>Multiprotein Complexes</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transcription Factors</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adipocytes</term>
<term>DNA-Binding Proteins</term>
<term>Early Growth Response Protein 1</term>
<term>Insulin</term>
<term>Lipase</term>
<term>Multiprotein Complexes</term>
<term>Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>3T3-L1 Cells</term>
<term>Animals</term>
<term>Cells, Cultured</term>
<term>Evolution, Molecular</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Lipolysis</term>
<term>Male</term>
<term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
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<front><div type="abstract" xml:lang="en">One of the basic functions of insulin in the body is to inhibit lipolysis in adipocytes. Recently, we have found that insulin inhibits lipolysis and promotes triglyceride storage by decreasing transcription of adipose triglyceride lipase via the mTORC1-mediated pathway (P. Chakrabarti et al., Diabetes 59:775-781, 2010), although the mechanism of this effect remained unknown. Here, we used a genetic screen in Saccharomyces cerevisiae in order to identify a transcription factor that mediates the effect of Tor1 on the expression of the ATGL ortholog in yeast. This factor, Msn4p, has homologues in mammalian cells that form a family of early growth response transcription factors. One member of the family, Egr1, is induced by insulin and nutrients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in cultured adipocytes. Feeding animals a high-fat diet increases the activity of mTORC1 and the expression of Egr1 while decreasing ATGL levels in epididymal fat. We suggest that the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important component of the antilipolytic effect of insulin in the mammalian organism. </div>
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<Abstract><AbstractText>One of the basic functions of insulin in the body is to inhibit lipolysis in adipocytes. Recently, we have found that insulin inhibits lipolysis and promotes triglyceride storage by decreasing transcription of adipose triglyceride lipase via the mTORC1-mediated pathway (P. Chakrabarti et al., Diabetes 59:775-781, 2010), although the mechanism of this effect remained unknown. Here, we used a genetic screen in Saccharomyces cerevisiae in order to identify a transcription factor that mediates the effect of Tor1 on the expression of the ATGL ortholog in yeast. This factor, Msn4p, has homologues in mammalian cells that form a family of early growth response transcription factors. One member of the family, Egr1, is induced by insulin and nutrients and directly inhibits activity of the ATGL promoter in vitro and expression of ATGL in cultured adipocytes. Feeding animals a high-fat diet increases the activity of mTORC1 and the expression of Egr1 while decreasing ATGL levels in epididymal fat. We suggest that the evolutionarily conserved mTORC1-Egr1-ATGL regulatory pathway represents an important component of the antilipolytic effect of insulin in the mammalian organism. </AbstractText>
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