Monomethyl Branched‐Chain Fatty Acids Suppress M1 Macrophage Polarization via FABP4/PPAR‐γ Signaling Pathway
Scope Monomethyl‐branched chain fatty acids (mmBCFAs) are found in a variety of food sources and are of great interest due to their potent antiinflammatory properties. However, most of the current researches have concentrated on the relationship between mmBCFAs and intestinal inflammation, and there...
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description | Scope
Monomethyl‐branched chain fatty acids (mmBCFAs) are found in a variety of food sources and are of great interest due to their potent antiinflammatory properties. However, most of the current researches have concentrated on the relationship between mmBCFAs and intestinal inflammation, and there is a large gap in the biological mechanisms involved behind their antiinflammatory effects.
Methods and results
The present study examines the role of mmBCFAs in modulating macrophage polarization. The results demonstrate that iso‐C16:0 significantly inhibits macrophages M1 proinflammatory polarization through regulating FABP4/PPAR‐γ pathway. Proteomics and molecular biology experiments verify that metabolic reprogramming is involved in the inhibition of M1 macrophage, referring to the upregulation of fatty acid oxidation, TCA cycle, and oxidative phosphorylation, as well as downregulation of glycolytic flux.
Conclusion
In summary, this study offers a novel perspective on the antiinflammatory effects mediated by mmBCFAs.
Exogenous addition of iso‐C16:0 reprogrammed macrophage energy metabolism by upregulating the FABP4/PPAR‐γ pathway, enhancing FAO, TCA cycle, and OXPHOS, while inhibiting glycolytic pathway flux. This greatly inhibits LPS/IFN‐γ‐induced M1 proinflammatory macrophages and increases the proportion of M2 antiinflammatory macrophages. |
doi_str_mv | 10.1002/mnfr.202400310 |
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Monomethyl‐branched chain fatty acids (mmBCFAs) are found in a variety of food sources and are of great interest due to their potent antiinflammatory properties. However, most of the current researches have concentrated on the relationship between mmBCFAs and intestinal inflammation, and there is a large gap in the biological mechanisms involved behind their antiinflammatory effects.
Methods and results
The present study examines the role of mmBCFAs in modulating macrophage polarization. The results demonstrate that iso‐C16:0 significantly inhibits macrophages M1 proinflammatory polarization through regulating FABP4/PPAR‐γ pathway. Proteomics and molecular biology experiments verify that metabolic reprogramming is involved in the inhibition of M1 macrophage, referring to the upregulation of fatty acid oxidation, TCA cycle, and oxidative phosphorylation, as well as downregulation of glycolytic flux.
Conclusion
In summary, this study offers a novel perspective on the antiinflammatory effects mediated by mmBCFAs.
Exogenous addition of iso‐C16:0 reprogrammed macrophage energy metabolism by upregulating the FABP4/PPAR‐γ pathway, enhancing FAO, TCA cycle, and OXPHOS, while inhibiting glycolytic pathway flux. This greatly inhibits LPS/IFN‐γ‐induced M1 proinflammatory macrophages and increases the proportion of M2 antiinflammatory macrophages.</description><identifier>ISSN: 1613-4125</identifier><identifier>ISSN: 1613-4133</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.202400310</identifier><identifier>PMID: 39318069</identifier><language>eng</language><publisher>Germany: Wiley Subscription Services, Inc</publisher><subject>Animals ; Anti-inflammatory agents ; Anti-Inflammatory Agents - pharmacology ; beta oxidation ; Biological effects ; Biological properties ; Chain branching ; Fatty Acid-Binding Proteins - metabolism ; Fatty acids ; Fatty Acids - metabolism ; Fatty Acids - pharmacology ; Food chains ; food research ; Food sources ; Glycolysis ; inflammation ; intestines ; macrophage polarization ; Macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; metabolic reprogramming ; Mice ; Molecular biology ; monomethyl branched‐chain fatty acids ; nutrition ; Oxidation ; Oxidative phosphorylation ; Peroxisome proliferator-activated receptors ; Phosphorylation ; Polarization ; PPAR gamma - metabolism ; PPAR‐γ signaling pathway ; Proteomics ; RAW 264.7 Cells ; Signal transduction ; Signal Transduction - drug effects ; Tricarboxylic acid cycle</subject><ispartof>Molecular nutrition & food research, 2024-10, Vol.68 (20), p.e2400310-n/a</ispartof><rights>2024 Wiley‐VCH GmbH</rights><rights>2024 Wiley‐VCH GmbH.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2860-f8cf08e208f903b272fad2d5e3672a0034524e1148706a7051483eebd2a234cb3</cites><orcidid>0000-0002-8704-2937 ; 0000-0002-8259-8426</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.202400310$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmnfr.202400310$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39318069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Yuan</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Zhu, Shuang</creatorcontrib><creatorcontrib>Liu, Yuan‐fa</creatorcontrib><creatorcontrib>Liu, Sha</creatorcontrib><creatorcontrib>Xu, Yong‐jiang</creatorcontrib><title>Monomethyl Branched‐Chain Fatty Acids Suppress M1 Macrophage Polarization via FABP4/PPAR‐γ Signaling Pathway</title><title>Molecular nutrition & food research</title><addtitle>Mol Nutr Food Res</addtitle><description>Scope
Monomethyl‐branched chain fatty acids (mmBCFAs) are found in a variety of food sources and are of great interest due to their potent antiinflammatory properties. However, most of the current researches have concentrated on the relationship between mmBCFAs and intestinal inflammation, and there is a large gap in the biological mechanisms involved behind their antiinflammatory effects.
Methods and results
The present study examines the role of mmBCFAs in modulating macrophage polarization. The results demonstrate that iso‐C16:0 significantly inhibits macrophages M1 proinflammatory polarization through regulating FABP4/PPAR‐γ pathway. Proteomics and molecular biology experiments verify that metabolic reprogramming is involved in the inhibition of M1 macrophage, referring to the upregulation of fatty acid oxidation, TCA cycle, and oxidative phosphorylation, as well as downregulation of glycolytic flux.
Conclusion
In summary, this study offers a novel perspective on the antiinflammatory effects mediated by mmBCFAs.
Exogenous addition of iso‐C16:0 reprogrammed macrophage energy metabolism by upregulating the FABP4/PPAR‐γ pathway, enhancing FAO, TCA cycle, and OXPHOS, while inhibiting glycolytic pathway flux. This greatly inhibits LPS/IFN‐γ‐induced M1 proinflammatory macrophages and increases the proportion of M2 antiinflammatory macrophages.</description><subject>Animals</subject><subject>Anti-inflammatory agents</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>beta oxidation</subject><subject>Biological effects</subject><subject>Biological properties</subject><subject>Chain branching</subject><subject>Fatty Acid-Binding Proteins - metabolism</subject><subject>Fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Acids - pharmacology</subject><subject>Food chains</subject><subject>food research</subject><subject>Food sources</subject><subject>Glycolysis</subject><subject>inflammation</subject><subject>intestines</subject><subject>macrophage polarization</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>metabolic reprogramming</subject><subject>Mice</subject><subject>Molecular biology</subject><subject>monomethyl branched‐chain fatty acids</subject><subject>nutrition</subject><subject>Oxidation</subject><subject>Oxidative phosphorylation</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phosphorylation</subject><subject>Polarization</subject><subject>PPAR gamma - metabolism</subject><subject>PPAR‐γ signaling pathway</subject><subject>Proteomics</subject><subject>RAW 264.7 Cells</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Tricarboxylic acid cycle</subject><issn>1613-4125</issn><issn>1613-4133</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0btu2zAUBmAiSJGkadaOBYEsXewcXiRRo2PEbYA4FZJ2Fo4lymKgW0iphjr1EfoufY8-RJ6kNJx4yNJOPMN3fuDwJ-Q9gykD4Bd1U9gpBy4BBIMDcsJCJiaSCXG4n3lwTN4697AlXIojcixiwRSE8Ql5XLZNW-u-HCt6abHJSp0__fw1L9E0dIF9P9JZZnJH74eus9o5umR0iZltuxLXmiZthdb8wN60Df1ukC5ml4m8SJLZnY_585vem3WDlWnWNMG-3OD4jrwpsHL67Pk9Jd8WV1_nnyc3Xz5dz2c3k4yrECaFygpQmoMqYhArHvECc54HWoQRR3-KDLjUjEkVQYgRBH4SWq9yjlzIbCVOycddbmfbx0G7Pq2Ny3RVYaPbwaWCBULJWMXxf1CIJedee3r-ij60g_UXbhWHSEAUh15Nd8r_k3NWF2lnTY12TBmk297SbW_pvje_8OE5dljVOt_zl6I8kDuwMZUe_xGXLm8Xd1IpEH8BdmCjlQ</recordid><startdate>202410</startdate><enddate>202410</enddate><creator>He, Yuan</creator><creator>Zhang, Yu</creator><creator>Zhu, Shuang</creator><creator>Liu, Yuan‐fa</creator><creator>Liu, Sha</creator><creator>Xu, Yong‐jiang</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><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0002-8704-2937</orcidid><orcidid>https://orcid.org/0000-0002-8259-8426</orcidid></search><sort><creationdate>202410</creationdate><title>Monomethyl Branched‐Chain Fatty Acids Suppress M1 Macrophage Polarization via FABP4/PPAR‐γ Signaling Pathway</title><author>He, Yuan ; Zhang, Yu ; Zhu, Shuang ; Liu, Yuan‐fa ; Liu, Sha ; Xu, Yong‐jiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2860-f8cf08e208f903b272fad2d5e3672a0034524e1148706a7051483eebd2a234cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Anti-inflammatory agents</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>beta oxidation</topic><topic>Biological effects</topic><topic>Biological properties</topic><topic>Chain branching</topic><topic>Fatty Acid-Binding Proteins - metabolism</topic><topic>Fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Acids - pharmacology</topic><topic>Food chains</topic><topic>food research</topic><topic>Food sources</topic><topic>Glycolysis</topic><topic>inflammation</topic><topic>intestines</topic><topic>macrophage polarization</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>metabolic reprogramming</topic><topic>Mice</topic><topic>Molecular biology</topic><topic>monomethyl branched‐chain fatty acids</topic><topic>nutrition</topic><topic>Oxidation</topic><topic>Oxidative phosphorylation</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phosphorylation</topic><topic>Polarization</topic><topic>PPAR gamma - metabolism</topic><topic>PPAR‐γ signaling pathway</topic><topic>Proteomics</topic><topic>RAW 264.7 Cells</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Tricarboxylic acid cycle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Yuan</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Zhu, Shuang</creatorcontrib><creatorcontrib>Liu, Yuan‐fa</creatorcontrib><creatorcontrib>Liu, Sha</creatorcontrib><creatorcontrib>Xu, Yong‐jiang</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 & 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><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular nutrition & food research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Yuan</au><au>Zhang, Yu</au><au>Zhu, Shuang</au><au>Liu, Yuan‐fa</au><au>Liu, Sha</au><au>Xu, Yong‐jiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monomethyl Branched‐Chain Fatty Acids Suppress M1 Macrophage Polarization via FABP4/PPAR‐γ Signaling Pathway</atitle><jtitle>Molecular nutrition & food research</jtitle><addtitle>Mol Nutr Food Res</addtitle><date>2024-10</date><risdate>2024</risdate><volume>68</volume><issue>20</issue><spage>e2400310</spage><epage>n/a</epage><pages>e2400310-n/a</pages><issn>1613-4125</issn><issn>1613-4133</issn><eissn>1613-4133</eissn><abstract>Scope
Monomethyl‐branched chain fatty acids (mmBCFAs) are found in a variety of food sources and are of great interest due to their potent antiinflammatory properties. However, most of the current researches have concentrated on the relationship between mmBCFAs and intestinal inflammation, and there is a large gap in the biological mechanisms involved behind their antiinflammatory effects.
Methods and results
The present study examines the role of mmBCFAs in modulating macrophage polarization. The results demonstrate that iso‐C16:0 significantly inhibits macrophages M1 proinflammatory polarization through regulating FABP4/PPAR‐γ pathway. Proteomics and molecular biology experiments verify that metabolic reprogramming is involved in the inhibition of M1 macrophage, referring to the upregulation of fatty acid oxidation, TCA cycle, and oxidative phosphorylation, as well as downregulation of glycolytic flux.
Conclusion
In summary, this study offers a novel perspective on the antiinflammatory effects mediated by mmBCFAs.
Exogenous addition of iso‐C16:0 reprogrammed macrophage energy metabolism by upregulating the FABP4/PPAR‐γ pathway, enhancing FAO, TCA cycle, and OXPHOS, while inhibiting glycolytic pathway flux. This greatly inhibits LPS/IFN‐γ‐induced M1 proinflammatory macrophages and increases the proportion of M2 antiinflammatory macrophages.</abstract><cop>Germany</cop><pub>Wiley Subscription Services, Inc</pub><pmid>39318069</pmid><doi>10.1002/mnfr.202400310</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-8704-2937</orcidid><orcidid>https://orcid.org/0000-0002-8259-8426</orcidid></addata></record> |
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subjects | Animals Anti-inflammatory agents Anti-Inflammatory Agents - pharmacology beta oxidation Biological effects Biological properties Chain branching Fatty Acid-Binding Proteins - metabolism Fatty acids Fatty Acids - metabolism Fatty Acids - pharmacology Food chains food research Food sources Glycolysis inflammation intestines macrophage polarization Macrophages Macrophages - drug effects Macrophages - metabolism metabolic reprogramming Mice Molecular biology monomethyl branched‐chain fatty acids nutrition Oxidation Oxidative phosphorylation Peroxisome proliferator-activated receptors Phosphorylation Polarization PPAR gamma - metabolism PPAR‐γ signaling pathway Proteomics RAW 264.7 Cells Signal transduction Signal Transduction - drug effects Tricarboxylic acid cycle |
title | Monomethyl Branched‐Chain Fatty Acids Suppress M1 Macrophage Polarization via FABP4/PPAR‐γ Signaling Pathway |
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