Tlr-4 Deficiency Selectively Protects Against Obesity Induced by Diets High in Saturated Fat
Toll‐like receptor‐4 (Tlr‐4), a key pattern recognition receptor involved in innate immune response, is activated by saturated fatty acids (SFAs). To investigate the involvement of this receptor in obesity caused by consumption of diets high in fat, we utilized male Tlr‐4‐deficient 10ScN mice and 10...
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| Veröffentlicht in: | Obesity (Silver Spring, Md.) Md.), 2008-06, Vol.16 (6), p.1248-1255 |
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| description | Toll‐like receptor‐4 (Tlr‐4), a key pattern recognition receptor involved in innate immune response, is activated by saturated fatty acids (SFAs). To investigate the involvement of this receptor in obesity caused by consumption of diets high in fat, we utilized male Tlr‐4‐deficient 10ScN mice and 10J controls. Mice were fed either low fat (low‐fat control (LFC)), high unsaturated fat (high‐fat control (HFC)), or high saturated fat + palmitate (HFP) diets ad libitum for 16 weeks. Relative to the LFC diet, the HFC diet resulted in greater epididymal fat pad weights and adipocyte hypertrophy in both Tlr‐4‐deficient and normal mice. However, the 10ScN mice were completely protected against the obesigenic effects of the HFP diet. Moreover, macrophage infiltration and monocyte chemotactic protein‐1 (MCP‐1) transcript abundance were lower in adipose tissue of 10ScN mice fed the HFP diet, and the hyperinsulinemic response was negated. Tlr‐4‐deficient mice also had markedly lower circulating concentrations of MCP‐1 and much less nuclear factor‐κB (NFκB) protein in nuclear extracts prepared from adipose tissue, irrespective of diet. In contrast, Tlr‐4 deficiency did not attenuate the induction of tumor necrosis factor‐α (TNF‐α) or interleukin‐6 (IL‐6) expression in adipose tissue. These data indicate that Tlr‐4 deficiency selectively protects against the obesigenic effects of SFA and alters obesity‐related inflammatory responses in adipose tissue. |
| doi_str_mv | 10.1038/oby.2008.210 |
| format | Article |
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To investigate the involvement of this receptor in obesity caused by consumption of diets high in fat, we utilized male Tlr‐4‐deficient 10ScN mice and 10J controls. Mice were fed either low fat (low‐fat control (LFC)), high unsaturated fat (high‐fat control (HFC)), or high saturated fat + palmitate (HFP) diets ad libitum for 16 weeks. Relative to the LFC diet, the HFC diet resulted in greater epididymal fat pad weights and adipocyte hypertrophy in both Tlr‐4‐deficient and normal mice. However, the 10ScN mice were completely protected against the obesigenic effects of the HFP diet. Moreover, macrophage infiltration and monocyte chemotactic protein‐1 (MCP‐1) transcript abundance were lower in adipose tissue of 10ScN mice fed the HFP diet, and the hyperinsulinemic response was negated. Tlr‐4‐deficient mice also had markedly lower circulating concentrations of MCP‐1 and much less nuclear factor‐κB (NFκB) protein in nuclear extracts prepared from adipose tissue, irrespective of diet. In contrast, Tlr‐4 deficiency did not attenuate the induction of tumor necrosis factor‐α (TNF‐α) or interleukin‐6 (IL‐6) expression in adipose tissue. These data indicate that Tlr‐4 deficiency selectively protects against the obesigenic effects of SFA and alters obesity‐related inflammatory responses in adipose tissue.</description><identifier>ISSN: 1930-7381</identifier><identifier>EISSN: 1930-739X</identifier><identifier>DOI: 10.1038/oby.2008.210</identifier><identifier>PMID: 18421279</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adipocytes ; adipose tissue ; Adipose Tissue - cytology ; Adipose Tissue - metabolism ; Adiposity - drug effects ; Adiposity - physiology ; animal disease models ; Animals ; Blood Glucose - metabolism ; Body fat ; Chemokine CCL2 - metabolism ; Cytokines ; deficiency diseases ; Diet ; diet-related diseases ; Dietary Fats - adverse effects ; Dietary Fats - pharmacology ; Energy Intake - physiology ; epididymis ; Fatty acids ; Fatty Acids - pharmacology ; Gene expression ; high fat diet ; hypertrophy ; immune response ; inflammation ; Insulin - blood ; Insulin Resistance - physiology ; Interleukin-6 - metabolism ; macrophage activation ; Macrophages - cytology ; Male ; metabolic syndrome ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; NF-kappa B - metabolism ; Nutrition ; nutrition-genotype interaction ; Obesity ; Obesity - chemically induced ; Obesity - metabolism ; Obesity - prevention & control ; overweight ; Physiology ; Proteins ; Random Allocation ; receptors ; risk reduction ; saturated fatty acids ; Toll-Like Receptor 4 - deficiency ; Toll-Like Receptor 4 - genetics ; Toll-like receptor-4 (Tlr-4) ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF</subject><ispartof>Obesity (Silver Spring, Md.), 2008-06, Vol.16 (6), p.1248-1255</ispartof><rights>2008 North American Association for the Study of Obesity (NAASO)</rights><rights>Copyright Nature Publishing Group Jun 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4864-f2510ba35040b3d93eb3bb97de135bf66061bdb150f4e8a79d9c2af5c8357e643</citedby><cites>FETCH-LOGICAL-c4864-f2510ba35040b3d93eb3bb97de135bf66061bdb150f4e8a79d9c2af5c8357e643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1038%2Foby.2008.210$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1038%2Foby.2008.210$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18421279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Davis, Jeremy E</creatorcontrib><creatorcontrib>Gabler, Nicholas K</creatorcontrib><creatorcontrib>Walker-Daniels, Jennifer</creatorcontrib><creatorcontrib>Spurlock, Michael E</creatorcontrib><title>Tlr-4 Deficiency Selectively Protects Against Obesity Induced by Diets High in Saturated Fat</title><title>Obesity (Silver Spring, Md.)</title><addtitle>Obesity (Silver Spring)</addtitle><description>Toll‐like receptor‐4 (Tlr‐4), a key pattern recognition receptor involved in innate immune response, is activated by saturated fatty acids (SFAs). To investigate the involvement of this receptor in obesity caused by consumption of diets high in fat, we utilized male Tlr‐4‐deficient 10ScN mice and 10J controls. Mice were fed either low fat (low‐fat control (LFC)), high unsaturated fat (high‐fat control (HFC)), or high saturated fat + palmitate (HFP) diets ad libitum for 16 weeks. Relative to the LFC diet, the HFC diet resulted in greater epididymal fat pad weights and adipocyte hypertrophy in both Tlr‐4‐deficient and normal mice. However, the 10ScN mice were completely protected against the obesigenic effects of the HFP diet. Moreover, macrophage infiltration and monocyte chemotactic protein‐1 (MCP‐1) transcript abundance were lower in adipose tissue of 10ScN mice fed the HFP diet, and the hyperinsulinemic response was negated. Tlr‐4‐deficient mice also had markedly lower circulating concentrations of MCP‐1 and much less nuclear factor‐κB (NFκB) protein in nuclear extracts prepared from adipose tissue, irrespective of diet. In contrast, Tlr‐4 deficiency did not attenuate the induction of tumor necrosis factor‐α (TNF‐α) or interleukin‐6 (IL‐6) expression in adipose tissue. These data indicate that Tlr‐4 deficiency selectively protects against the obesigenic effects of SFA and alters obesity‐related inflammatory responses in adipose tissue.</description><subject>Adipocytes</subject><subject>adipose tissue</subject><subject>Adipose Tissue - cytology</subject><subject>Adipose Tissue - metabolism</subject><subject>Adiposity - drug effects</subject><subject>Adiposity - physiology</subject><subject>animal disease models</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>Body fat</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Cytokines</subject><subject>deficiency diseases</subject><subject>Diet</subject><subject>diet-related diseases</subject><subject>Dietary Fats - adverse effects</subject><subject>Dietary Fats - pharmacology</subject><subject>Energy Intake - physiology</subject><subject>epididymis</subject><subject>Fatty acids</subject><subject>Fatty Acids - pharmacology</subject><subject>Gene expression</subject><subject>high fat diet</subject><subject>hypertrophy</subject><subject>immune response</subject><subject>inflammation</subject><subject>Insulin - blood</subject><subject>Insulin Resistance - physiology</subject><subject>Interleukin-6 - metabolism</subject><subject>macrophage activation</subject><subject>Macrophages - cytology</subject><subject>Male</subject><subject>metabolic syndrome</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Mutant Strains</subject><subject>NF-kappa B - metabolism</subject><subject>Nutrition</subject><subject>nutrition-genotype interaction</subject><subject>Obesity</subject><subject>Obesity - chemically induced</subject><subject>Obesity - metabolism</subject><subject>Obesity - prevention & control</subject><subject>overweight</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Random Allocation</subject><subject>receptors</subject><subject>risk reduction</subject><subject>saturated fatty acids</subject><subject>Toll-Like Receptor 4 - deficiency</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-like receptor-4 (Tlr-4)</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><issn>1930-7381</issn><issn>1930-739X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kctLxDAQh4MoPlZvnjXg1a6TJn3k6FtBWGFXUBBC0k7XSG3XpFX635tlF715yoR8-U3mCyGHDMYMeH7WmmEcA-TjmMEG2WWSQ5Rx-bz5W-dsh-x5_w4gUkjYNtlhuYhZnMld8jqrXSToFVa2sNgUA51ijUVnv7Ae6KNru7Dx9HyubeM7OjHobTfQ-6bsCyypGeiVxQDc2fkbtQ2d6q53ugtHN7rbJ1uVrj0erNcRebq5nl3eRQ-T2_vL84eoEHkqoipOGBjNExBgeCk5Gm6MzEpkPDFVmkLKTGlYApXAXGeylEWsq6TIeZJhKviInKxyF6797NF36r3tXRNaqqAIwqxMsECdrqjCtd47rNTC2Q_thgAtuVwFlWqpUgWVAT9ah_bmA8s_eO0uALACvm2Nw79hanLxIuXyocerK5VulZ4769XTNAbGgSVZLMN__QCcvIZL</recordid><startdate>200806</startdate><enddate>200806</enddate><creator>Davis, Jeremy E</creator><creator>Gabler, Nicholas K</creator><creator>Walker-Daniels, Jennifer</creator><creator>Spurlock, Michael E</creator><general>Blackwell Publishing Ltd</general><scope>FBQ</scope><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>K9.</scope></search><sort><creationdate>200806</creationdate><title>Tlr-4 Deficiency Selectively Protects Against Obesity Induced by Diets High in Saturated Fat</title><author>Davis, Jeremy E ; Gabler, Nicholas K ; Walker-Daniels, Jennifer ; Spurlock, Michael E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4864-f2510ba35040b3d93eb3bb97de135bf66061bdb150f4e8a79d9c2af5c8357e643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adipocytes</topic><topic>adipose tissue</topic><topic>Adipose Tissue - cytology</topic><topic>Adipose Tissue - metabolism</topic><topic>Adiposity - drug effects</topic><topic>Adiposity - physiology</topic><topic>animal disease models</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>Body fat</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Cytokines</topic><topic>deficiency diseases</topic><topic>Diet</topic><topic>diet-related diseases</topic><topic>Dietary Fats - adverse effects</topic><topic>Dietary Fats - pharmacology</topic><topic>Energy Intake - physiology</topic><topic>epididymis</topic><topic>Fatty acids</topic><topic>Fatty Acids - pharmacology</topic><topic>Gene expression</topic><topic>high fat diet</topic><topic>hypertrophy</topic><topic>immune response</topic><topic>inflammation</topic><topic>Insulin - blood</topic><topic>Insulin Resistance - physiology</topic><topic>Interleukin-6 - metabolism</topic><topic>macrophage activation</topic><topic>Macrophages - cytology</topic><topic>Male</topic><topic>metabolic syndrome</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Mutant Strains</topic><topic>NF-kappa B - metabolism</topic><topic>Nutrition</topic><topic>nutrition-genotype interaction</topic><topic>Obesity</topic><topic>Obesity - chemically induced</topic><topic>Obesity - metabolism</topic><topic>Obesity - prevention & control</topic><topic>overweight</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Random Allocation</topic><topic>receptors</topic><topic>risk reduction</topic><topic>saturated fatty acids</topic><topic>Toll-Like Receptor 4 - deficiency</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-like receptor-4 (Tlr-4)</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Davis, Jeremy E</creatorcontrib><creatorcontrib>Gabler, Nicholas K</creatorcontrib><creatorcontrib>Walker-Daniels, Jennifer</creatorcontrib><creatorcontrib>Spurlock, Michael E</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Obesity (Silver Spring, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Davis, Jeremy E</au><au>Gabler, Nicholas K</au><au>Walker-Daniels, Jennifer</au><au>Spurlock, Michael E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tlr-4 Deficiency Selectively Protects Against Obesity Induced by Diets High in Saturated Fat</atitle><jtitle>Obesity (Silver Spring, Md.)</jtitle><addtitle>Obesity (Silver Spring)</addtitle><date>2008-06</date><risdate>2008</risdate><volume>16</volume><issue>6</issue><spage>1248</spage><epage>1255</epage><pages>1248-1255</pages><issn>1930-7381</issn><eissn>1930-739X</eissn><abstract>Toll‐like receptor‐4 (Tlr‐4), a key pattern recognition receptor involved in innate immune response, is activated by saturated fatty acids (SFAs). To investigate the involvement of this receptor in obesity caused by consumption of diets high in fat, we utilized male Tlr‐4‐deficient 10ScN mice and 10J controls. Mice were fed either low fat (low‐fat control (LFC)), high unsaturated fat (high‐fat control (HFC)), or high saturated fat + palmitate (HFP) diets ad libitum for 16 weeks. Relative to the LFC diet, the HFC diet resulted in greater epididymal fat pad weights and adipocyte hypertrophy in both Tlr‐4‐deficient and normal mice. However, the 10ScN mice were completely protected against the obesigenic effects of the HFP diet. Moreover, macrophage infiltration and monocyte chemotactic protein‐1 (MCP‐1) transcript abundance were lower in adipose tissue of 10ScN mice fed the HFP diet, and the hyperinsulinemic response was negated. Tlr‐4‐deficient mice also had markedly lower circulating concentrations of MCP‐1 and much less nuclear factor‐κB (NFκB) protein in nuclear extracts prepared from adipose tissue, irrespective of diet. In contrast, Tlr‐4 deficiency did not attenuate the induction of tumor necrosis factor‐α (TNF‐α) or interleukin‐6 (IL‐6) expression in adipose tissue. These data indicate that Tlr‐4 deficiency selectively protects against the obesigenic effects of SFA and alters obesity‐related inflammatory responses in adipose tissue.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18421279</pmid><doi>10.1038/oby.2008.210</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adipocytes adipose tissue Adipose Tissue - cytology Adipose Tissue - metabolism Adiposity - drug effects Adiposity - physiology animal disease models Animals Blood Glucose - metabolism Body fat Chemokine CCL2 - metabolism Cytokines deficiency diseases Diet diet-related diseases Dietary Fats - adverse effects Dietary Fats - pharmacology Energy Intake - physiology epididymis Fatty acids Fatty Acids - pharmacology Gene expression high fat diet hypertrophy immune response inflammation Insulin - blood Insulin Resistance - physiology Interleukin-6 - metabolism macrophage activation Macrophages - cytology Male metabolic syndrome Mice Mice, Inbred C57BL Mice, Knockout Mice, Mutant Strains NF-kappa B - metabolism Nutrition nutrition-genotype interaction Obesity Obesity - chemically induced Obesity - metabolism Obesity - prevention & control overweight Physiology Proteins Random Allocation receptors risk reduction saturated fatty acids Toll-Like Receptor 4 - deficiency Toll-Like Receptor 4 - genetics Toll-like receptor-4 (Tlr-4) Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF |
| title | Tlr-4 Deficiency Selectively Protects Against Obesity Induced by Diets High in Saturated Fat |
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