Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages
Aims/hypothesis Activation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs). Methods Human THP-1 macrophages w...
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| Veröffentlicht in: | Diabetologia 2015-11, Vol.58 (11), p.2627-2636 |
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| creator | Caspar-Bauguil, Sylvie Kolditz, Catherine-Ines Lefort, Corinne Vila, Isabelle Mouisel, Etienne Beuzelin, Diane Tavernier, Geneviève Marques, Marie-Adeline Zakaroff-Girard, Alexia Pecher, Christiane Houssier, Marianne Mir, Lucile Nicolas, Sarah Moro, Cédric Langin, Dominique |
| description | Aims/hypothesis
Activation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs).
Methods
Human THP-1 macrophages were treated with media from human multipotent adipose-derived stem (hMADS) adipocytes stimulated with lipolytic drugs. Macrophages were also treated with mixtures of FAs and an inhibitor of Toll-like receptor 4, since this receptor is activated by saturated FAs. Levels of mRNA and the secretion of inflammation-related molecules were measured in macrophages. FA composition was determined in adipocytes, conditioned media and macrophages. The effect of chronic inhibition or acute activation of fat cell lipolysis on ATM response was investigated in vivo in mice.
Results
Whereas palmitic acid alone activates THP-1, conditioned media from hMADS adipocyte lipolysis had no effect on IL, chemokine and cytokine gene expression, and secretion by macrophages. Mixtures of FAs representing de novo lipogenesis or habitual dietary conditions also had no effect. FAs derived from adipocyte lipolysis were taken up by macrophages and stored as triacylglycerol droplets. In vivo, chronic treatment with an antilipolytic drug did not modify gene expression and number of ATMs in mice with intact or defective
Tlr4
. Stimulation of adipocyte lipolysis increased storage of neutral lipids by macrophages without change in number and phenotype.
Conclusions/interpretation
Our data suggest that adipocyte lipolysis does not activate inflammatory pathways in ATMs, which instead may act as scavengers of FAs. |
| doi_str_mv | 10.1007/s00125-015-3719-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1727693276</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1727693276</sourcerecordid><originalsourceid>FETCH-LOGICAL-c518t-5cdc66aacff6fa2a9e1b5bdd0882eeeebdc89077095599d202849f6687eddaa03</originalsourceid><addsrcrecordid>eNqNkc-K1TAUxoM4ONfRB3AjATdu6iRpmzZLGWZUGHDjwOzCaf5cO6RNzUmFPoTvbModRQTBLBLI9zvfOYePkFecveOMdZfIGBdtxXhb1R1XFXtCDrypRcUa0T8lh12ueC_vz8lzxAfGWN028hk5F1I0bREO5McN5LxRMKNF6lOcqIdMjQuBhnGJYcMRqY10jrlAefwO2VGY6Tj7ANMEOaaNJodLnNHRYS1UchTLt7MUkOY0gtnCMWzGpRiwFFKwxbnQeURcHZ3ApLh8haPDF-TMQ0D38vG9IHc311-uPla3nz98unp_W5kyda5aY42UAMZ76UGAcnxoB2tZ3wtXzmBNr1jXMdW2SlnBRN8oL2XfOWsBWH1B3p58lxS_rQ6znkbcl4bZxRU170QnVV2u_0B56dWwXhX0zV_oQ1zTXBbZqU5JxRteKH6iytaIyXm9pHGCtGnO9B6rPsWqS6x6j1Xv875-dF6HydnfFb9yLIA4AVik-ejSH63_6foTMxewMA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1717969141</pqid></control><display><type>article</type><title>Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Caspar-Bauguil, Sylvie ; Kolditz, Catherine-Ines ; Lefort, Corinne ; Vila, Isabelle ; Mouisel, Etienne ; Beuzelin, Diane ; Tavernier, Geneviève ; Marques, Marie-Adeline ; Zakaroff-Girard, Alexia ; Pecher, Christiane ; Houssier, Marianne ; Mir, Lucile ; Nicolas, Sarah ; Moro, Cédric ; Langin, Dominique</creator><creatorcontrib>Caspar-Bauguil, Sylvie ; Kolditz, Catherine-Ines ; Lefort, Corinne ; Vila, Isabelle ; Mouisel, Etienne ; Beuzelin, Diane ; Tavernier, Geneviève ; Marques, Marie-Adeline ; Zakaroff-Girard, Alexia ; Pecher, Christiane ; Houssier, Marianne ; Mir, Lucile ; Nicolas, Sarah ; Moro, Cédric ; Langin, Dominique</creatorcontrib><description>Aims/hypothesis
Activation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs).
Methods
Human THP-1 macrophages were treated with media from human multipotent adipose-derived stem (hMADS) adipocytes stimulated with lipolytic drugs. Macrophages were also treated with mixtures of FAs and an inhibitor of Toll-like receptor 4, since this receptor is activated by saturated FAs. Levels of mRNA and the secretion of inflammation-related molecules were measured in macrophages. FA composition was determined in adipocytes, conditioned media and macrophages. The effect of chronic inhibition or acute activation of fat cell lipolysis on ATM response was investigated in vivo in mice.
Results
Whereas palmitic acid alone activates THP-1, conditioned media from hMADS adipocyte lipolysis had no effect on IL, chemokine and cytokine gene expression, and secretion by macrophages. Mixtures of FAs representing de novo lipogenesis or habitual dietary conditions also had no effect. FAs derived from adipocyte lipolysis were taken up by macrophages and stored as triacylglycerol droplets. In vivo, chronic treatment with an antilipolytic drug did not modify gene expression and number of ATMs in mice with intact or defective
Tlr4
. Stimulation of adipocyte lipolysis increased storage of neutral lipids by macrophages without change in number and phenotype.
Conclusions/interpretation
Our data suggest that adipocyte lipolysis does not activate inflammatory pathways in ATMs, which instead may act as scavengers of FAs.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-015-3719-0</identifier><identifier>PMID: 26245186</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adipocytes ; Adipocytes - cytology ; Adipocytes - metabolism ; Adipose Tissue - cytology ; Adipose Tissue - metabolism ; Adrenergic beta-3 Receptor Agonists - pharmacology ; Animals ; Body fat ; Cell Line ; Dioxoles - pharmacology ; Fatty acids ; Fatty Acids - metabolism ; Fatty Acids - pharmacology ; Gene expression ; Glycerol ; Human Physiology ; Humans ; Hypotheses ; Inflammation ; Inflammation - metabolism ; Insulin resistance ; Internal Medicine ; Lipolysis - physiology ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Mice ; Mice, Knockout ; Obesity ; Palmitic Acid - pharmacology ; Proteins ; Stem Cells - cytology ; Stem Cells - metabolism ; Toll-Like Receptor 4 - antagonists & inhibitors ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism ; Triglycerides - metabolism</subject><ispartof>Diabetologia, 2015-11, Vol.58 (11), p.2627-2636</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-5cdc66aacff6fa2a9e1b5bdd0882eeeebdc89077095599d202849f6687eddaa03</citedby><cites>FETCH-LOGICAL-c518t-5cdc66aacff6fa2a9e1b5bdd0882eeeebdc89077095599d202849f6687eddaa03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-015-3719-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-015-3719-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27926,27927,41490,42559,51321</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26245186$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Caspar-Bauguil, Sylvie</creatorcontrib><creatorcontrib>Kolditz, Catherine-Ines</creatorcontrib><creatorcontrib>Lefort, Corinne</creatorcontrib><creatorcontrib>Vila, Isabelle</creatorcontrib><creatorcontrib>Mouisel, Etienne</creatorcontrib><creatorcontrib>Beuzelin, Diane</creatorcontrib><creatorcontrib>Tavernier, Geneviève</creatorcontrib><creatorcontrib>Marques, Marie-Adeline</creatorcontrib><creatorcontrib>Zakaroff-Girard, Alexia</creatorcontrib><creatorcontrib>Pecher, Christiane</creatorcontrib><creatorcontrib>Houssier, Marianne</creatorcontrib><creatorcontrib>Mir, Lucile</creatorcontrib><creatorcontrib>Nicolas, Sarah</creatorcontrib><creatorcontrib>Moro, Cédric</creatorcontrib><creatorcontrib>Langin, Dominique</creatorcontrib><title>Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
Activation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs).
Methods
Human THP-1 macrophages were treated with media from human multipotent adipose-derived stem (hMADS) adipocytes stimulated with lipolytic drugs. Macrophages were also treated with mixtures of FAs and an inhibitor of Toll-like receptor 4, since this receptor is activated by saturated FAs. Levels of mRNA and the secretion of inflammation-related molecules were measured in macrophages. FA composition was determined in adipocytes, conditioned media and macrophages. The effect of chronic inhibition or acute activation of fat cell lipolysis on ATM response was investigated in vivo in mice.
Results
Whereas palmitic acid alone activates THP-1, conditioned media from hMADS adipocyte lipolysis had no effect on IL, chemokine and cytokine gene expression, and secretion by macrophages. Mixtures of FAs representing de novo lipogenesis or habitual dietary conditions also had no effect. FAs derived from adipocyte lipolysis were taken up by macrophages and stored as triacylglycerol droplets. In vivo, chronic treatment with an antilipolytic drug did not modify gene expression and number of ATMs in mice with intact or defective
Tlr4
. Stimulation of adipocyte lipolysis increased storage of neutral lipids by macrophages without change in number and phenotype.
Conclusions/interpretation
Our data suggest that adipocyte lipolysis does not activate inflammatory pathways in ATMs, which instead may act as scavengers of FAs.</description><subject>Adipocytes</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - metabolism</subject><subject>Adipose Tissue - cytology</subject><subject>Adipose Tissue - metabolism</subject><subject>Adrenergic beta-3 Receptor Agonists - pharmacology</subject><subject>Animals</subject><subject>Body fat</subject><subject>Cell Line</subject><subject>Dioxoles - pharmacology</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Acids - pharmacology</subject><subject>Gene expression</subject><subject>Glycerol</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Insulin resistance</subject><subject>Internal Medicine</subject><subject>Lipolysis - physiology</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Obesity</subject><subject>Palmitic Acid - pharmacology</subject><subject>Proteins</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>Toll-Like Receptor 4 - antagonists & inhibitors</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><subject>Triglycerides - metabolism</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNkc-K1TAUxoM4ONfRB3AjATdu6iRpmzZLGWZUGHDjwOzCaf5cO6RNzUmFPoTvbModRQTBLBLI9zvfOYePkFecveOMdZfIGBdtxXhb1R1XFXtCDrypRcUa0T8lh12ueC_vz8lzxAfGWN028hk5F1I0bREO5McN5LxRMKNF6lOcqIdMjQuBhnGJYcMRqY10jrlAefwO2VGY6Tj7ANMEOaaNJodLnNHRYS1UchTLt7MUkOY0gtnCMWzGpRiwFFKwxbnQeURcHZ3ApLh8haPDF-TMQ0D38vG9IHc311-uPla3nz98unp_W5kyda5aY42UAMZ76UGAcnxoB2tZ3wtXzmBNr1jXMdW2SlnBRN8oL2XfOWsBWH1B3p58lxS_rQ6znkbcl4bZxRU170QnVV2u_0B56dWwXhX0zV_oQ1zTXBbZqU5JxRteKH6iytaIyXm9pHGCtGnO9B6rPsWqS6x6j1Xv875-dF6HydnfFb9yLIA4AVik-ejSH63_6foTMxewMA</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>Caspar-Bauguil, Sylvie</creator><creator>Kolditz, Catherine-Ines</creator><creator>Lefort, Corinne</creator><creator>Vila, Isabelle</creator><creator>Mouisel, Etienne</creator><creator>Beuzelin, Diane</creator><creator>Tavernier, Geneviève</creator><creator>Marques, Marie-Adeline</creator><creator>Zakaroff-Girard, Alexia</creator><creator>Pecher, Christiane</creator><creator>Houssier, Marianne</creator><creator>Mir, Lucile</creator><creator>Nicolas, Sarah</creator><creator>Moro, Cédric</creator><creator>Langin, Dominique</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20151101</creationdate><title>Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages</title><author>Caspar-Bauguil, Sylvie ; Kolditz, Catherine-Ines ; Lefort, Corinne ; Vila, Isabelle ; Mouisel, Etienne ; Beuzelin, Diane ; Tavernier, Geneviève ; Marques, Marie-Adeline ; Zakaroff-Girard, Alexia ; Pecher, Christiane ; Houssier, Marianne ; Mir, Lucile ; Nicolas, Sarah ; Moro, Cédric ; Langin, Dominique</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c518t-5cdc66aacff6fa2a9e1b5bdd0882eeeebdc89077095599d202849f6687eddaa03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adipocytes</topic><topic>Adipocytes - cytology</topic><topic>Adipocytes - metabolism</topic><topic>Adipose Tissue - cytology</topic><topic>Adipose Tissue - metabolism</topic><topic>Adrenergic beta-3 Receptor Agonists - pharmacology</topic><topic>Animals</topic><topic>Body fat</topic><topic>Cell Line</topic><topic>Dioxoles - pharmacology</topic><topic>Fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Acids - pharmacology</topic><topic>Gene expression</topic><topic>Glycerol</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Insulin resistance</topic><topic>Internal Medicine</topic><topic>Lipolysis - physiology</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Obesity</topic><topic>Palmitic Acid - pharmacology</topic><topic>Proteins</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - metabolism</topic><topic>Toll-Like Receptor 4 - antagonists & inhibitors</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><topic>Triglycerides - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Caspar-Bauguil, Sylvie</creatorcontrib><creatorcontrib>Kolditz, Catherine-Ines</creatorcontrib><creatorcontrib>Lefort, Corinne</creatorcontrib><creatorcontrib>Vila, Isabelle</creatorcontrib><creatorcontrib>Mouisel, Etienne</creatorcontrib><creatorcontrib>Beuzelin, Diane</creatorcontrib><creatorcontrib>Tavernier, Geneviève</creatorcontrib><creatorcontrib>Marques, Marie-Adeline</creatorcontrib><creatorcontrib>Zakaroff-Girard, Alexia</creatorcontrib><creatorcontrib>Pecher, Christiane</creatorcontrib><creatorcontrib>Houssier, Marianne</creatorcontrib><creatorcontrib>Mir, Lucile</creatorcontrib><creatorcontrib>Nicolas, Sarah</creatorcontrib><creatorcontrib>Moro, Cédric</creatorcontrib><creatorcontrib>Langin, Dominique</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database (Proquest)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Caspar-Bauguil, Sylvie</au><au>Kolditz, Catherine-Ines</au><au>Lefort, Corinne</au><au>Vila, Isabelle</au><au>Mouisel, Etienne</au><au>Beuzelin, Diane</au><au>Tavernier, Geneviève</au><au>Marques, Marie-Adeline</au><au>Zakaroff-Girard, Alexia</au><au>Pecher, Christiane</au><au>Houssier, Marianne</au><au>Mir, Lucile</au><au>Nicolas, Sarah</au><au>Moro, Cédric</au><au>Langin, Dominique</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>58</volume><issue>11</issue><spage>2627</spage><epage>2636</epage><pages>2627-2636</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
Activation of macrophages by fatty acids (FAs) is a potential mechanism linking obesity to adipose tissue (AT) inflammation and insulin resistance. Here, we investigated the effects of FAs released during adipocyte lipolysis on AT macrophages (ATMs).
Methods
Human THP-1 macrophages were treated with media from human multipotent adipose-derived stem (hMADS) adipocytes stimulated with lipolytic drugs. Macrophages were also treated with mixtures of FAs and an inhibitor of Toll-like receptor 4, since this receptor is activated by saturated FAs. Levels of mRNA and the secretion of inflammation-related molecules were measured in macrophages. FA composition was determined in adipocytes, conditioned media and macrophages. The effect of chronic inhibition or acute activation of fat cell lipolysis on ATM response was investigated in vivo in mice.
Results
Whereas palmitic acid alone activates THP-1, conditioned media from hMADS adipocyte lipolysis had no effect on IL, chemokine and cytokine gene expression, and secretion by macrophages. Mixtures of FAs representing de novo lipogenesis or habitual dietary conditions also had no effect. FAs derived from adipocyte lipolysis were taken up by macrophages and stored as triacylglycerol droplets. In vivo, chronic treatment with an antilipolytic drug did not modify gene expression and number of ATMs in mice with intact or defective
Tlr4
. Stimulation of adipocyte lipolysis increased storage of neutral lipids by macrophages without change in number and phenotype.
Conclusions/interpretation
Our data suggest that adipocyte lipolysis does not activate inflammatory pathways in ATMs, which instead may act as scavengers of FAs.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26245186</pmid><doi>10.1007/s00125-015-3719-0</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetologia, 2015-11, Vol.58 (11), p.2627-2636 |
| issn | 0012-186X 1432-0428 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Adipocytes Adipocytes - cytology Adipocytes - metabolism Adipose Tissue - cytology Adipose Tissue - metabolism Adrenergic beta-3 Receptor Agonists - pharmacology Animals Body fat Cell Line Dioxoles - pharmacology Fatty acids Fatty Acids - metabolism Fatty Acids - pharmacology Gene expression Glycerol Human Physiology Humans Hypotheses Inflammation Inflammation - metabolism Insulin resistance Internal Medicine Lipolysis - physiology Macrophages - cytology Macrophages - drug effects Macrophages - metabolism Male Medicine Medicine & Public Health Metabolic Diseases Metabolism Mice Mice, Knockout Obesity Palmitic Acid - pharmacology Proteins Stem Cells - cytology Stem Cells - metabolism Toll-Like Receptor 4 - antagonists & inhibitors Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism Triglycerides - metabolism |
| title | Fatty acids from fat cell lipolysis do not activate an inflammatory response but are stored as triacylglycerols in adipose tissue macrophages |
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