Galectin-3 Activates PPARγ and Supports White Adipose Tissue Formation and High-Fat Diet-Induced Obesity
Galectin-3, a β-galactoside-binding lectin, is elevated in obesity and type 2 diabetes mellitus, and metformin treatment reduces these galectin-3 levels. However, the role of galectin-3 in adipogenesis remains controversial. We found that 17-month-old galectin-3-deficient (lgals3−/−) mice had decrea...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2015-01, Vol.156 (1), p.147-156 |
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| creator | Baek, Jung-Hwan Kim, Seok-Jun Kang, Hyeok Gu Lee, Hyun-Woo Kim, Jung-Hoon Hwang, Kyung-A Song, Jaewhan Chun, Kyung-Hee |
| description | Galectin-3, a β-galactoside-binding lectin, is elevated in obesity and type 2 diabetes mellitus, and metformin treatment reduces these galectin-3 levels. However, the role of galectin-3 in adipogenesis remains controversial. We found that 17-month-old galectin-3-deficient (lgals3−/−) mice had decreased body size and epididymal white adipose tissue (eWAT) without related inflammatory diseases when fed normal chow. Galectin-3 knockdown significantly reduced adipocyte differentiation in 3T3-L1 cells and also decreased the expression of peroxisome proliferator-activated receptor (PPAR)-γ, ccaat-enhancer-binding protein α, and ccaat-enhancer-binding protein β. Endogenous galectin-3 directly interacted with PPARγ, and galectin-3 ablation reduced the nuclear accumulation and transcriptional activation of PPARγ. After a 12-week high-fat diet (60% fat), lgals3−/− mice had lower body weight and eWAT mass than lgals3+/+ mice. Moreover, the expression of PPARγ and other lipogenic genes was drastically decreased in the eWAT and liver of lgals3−/− mice. We suggest that galectin-3 directly activates PPARγ and leads to adipocyte differentiation in vitro and in vivo. Furthermore, galectin-3 might be a potential therapeutic target in metabolic syndromes as a PPARγ regulator. |
| doi_str_mv | 10.1210/en.2014-1374 |
| format | Article |
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However, the role of galectin-3 in adipogenesis remains controversial. We found that 17-month-old galectin-3-deficient (lgals3−/−) mice had decreased body size and epididymal white adipose tissue (eWAT) without related inflammatory diseases when fed normal chow. Galectin-3 knockdown significantly reduced adipocyte differentiation in 3T3-L1 cells and also decreased the expression of peroxisome proliferator-activated receptor (PPAR)-γ, ccaat-enhancer-binding protein α, and ccaat-enhancer-binding protein β. Endogenous galectin-3 directly interacted with PPARγ, and galectin-3 ablation reduced the nuclear accumulation and transcriptional activation of PPARγ. After a 12-week high-fat diet (60% fat), lgals3−/− mice had lower body weight and eWAT mass than lgals3+/+ mice. Moreover, the expression of PPARγ and other lipogenic genes was drastically decreased in the eWAT and liver of lgals3−/− mice. We suggest that galectin-3 directly activates PPARγ and leads to adipocyte differentiation in vitro and in vivo. Furthermore, galectin-3 might be a potential therapeutic target in metabolic syndromes as a PPARγ regulator.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2014-1374</identifier><identifier>PMID: 25343273</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>3T3-L1 Cells ; Ablation ; Adipocytes ; Adipocytes - cytology ; Adipocytes - metabolism ; Adipogenesis ; Adipose tissue ; Adipose Tissue, White - physiology ; Adiposity ; Animals ; Body fat ; Body size ; Body weight ; CCAAT/enhancer-binding protein ; Cell Differentiation ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diet ; Dietary Fats - administration & dosage ; Dietary Fats - adverse effects ; Differentiation ; Dose-Response Relationship, Drug ; Female ; Galactosides ; Galectin 3 - genetics ; Galectin 3 - metabolism ; Galectin-3 ; Gene Expression Regulation - physiology ; HEK293 Cells ; High fat diet ; Humans ; Inflammatory diseases ; Male ; Metabolic disorders ; Metabolic syndrome ; Metformin ; Mice ; Mice, Knockout ; Obesity ; Obesity - chemically induced ; Obesity - metabolism ; Peroxisome proliferator-activated receptors ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Proteins ; Therapeutic targets ; Transcription activation</subject><ispartof>Endocrinology (Philadelphia), 2015-01, Vol.156 (1), p.147-156</ispartof><rights>Copyright © 2015 by the Endocrine Society</rights><rights>Copyright © 2015 by the Endocrine Society 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-7231c669206c542eb13afca57913ed33aaec341f5dfa676a4f24c993ae144bd63</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25343273$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baek, Jung-Hwan</creatorcontrib><creatorcontrib>Kim, Seok-Jun</creatorcontrib><creatorcontrib>Kang, Hyeok Gu</creatorcontrib><creatorcontrib>Lee, Hyun-Woo</creatorcontrib><creatorcontrib>Kim, Jung-Hoon</creatorcontrib><creatorcontrib>Hwang, Kyung-A</creatorcontrib><creatorcontrib>Song, Jaewhan</creatorcontrib><creatorcontrib>Chun, Kyung-Hee</creatorcontrib><title>Galectin-3 Activates PPARγ and Supports White Adipose Tissue Formation and High-Fat Diet-Induced Obesity</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Galectin-3, a β-galactoside-binding lectin, is elevated in obesity and type 2 diabetes mellitus, and metformin treatment reduces these galectin-3 levels. However, the role of galectin-3 in adipogenesis remains controversial. We found that 17-month-old galectin-3-deficient (lgals3−/−) mice had decreased body size and epididymal white adipose tissue (eWAT) without related inflammatory diseases when fed normal chow. Galectin-3 knockdown significantly reduced adipocyte differentiation in 3T3-L1 cells and also decreased the expression of peroxisome proliferator-activated receptor (PPAR)-γ, ccaat-enhancer-binding protein α, and ccaat-enhancer-binding protein β. Endogenous galectin-3 directly interacted with PPARγ, and galectin-3 ablation reduced the nuclear accumulation and transcriptional activation of PPARγ. After a 12-week high-fat diet (60% fat), lgals3−/− mice had lower body weight and eWAT mass than lgals3+/+ mice. Moreover, the expression of PPARγ and other lipogenic genes was drastically decreased in the eWAT and liver of lgals3−/− mice. We suggest that galectin-3 directly activates PPARγ and leads to adipocyte differentiation in vitro and in vivo. Furthermore, galectin-3 might be a potential therapeutic target in metabolic syndromes as a PPARγ regulator.</description><subject>3T3-L1 Cells</subject><subject>Ablation</subject><subject>Adipocytes</subject><subject>Adipocytes - cytology</subject><subject>Adipocytes - metabolism</subject><subject>Adipogenesis</subject><subject>Adipose tissue</subject><subject>Adipose Tissue, White - physiology</subject><subject>Adiposity</subject><subject>Animals</subject><subject>Body fat</subject><subject>Body size</subject><subject>Body weight</subject><subject>CCAAT/enhancer-binding protein</subject><subject>Cell Differentiation</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diet</subject><subject>Dietary Fats - administration & dosage</subject><subject>Dietary Fats - adverse effects</subject><subject>Differentiation</subject><subject>Dose-Response Relationship, Drug</subject><subject>Female</subject><subject>Galactosides</subject><subject>Galectin 3 - genetics</subject><subject>Galectin 3 - metabolism</subject><subject>Galectin-3</subject><subject>Gene Expression Regulation - physiology</subject><subject>HEK293 Cells</subject><subject>High fat diet</subject><subject>Humans</subject><subject>Inflammatory diseases</subject><subject>Male</subject><subject>Metabolic disorders</subject><subject>Metabolic syndrome</subject><subject>Metformin</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Obesity</subject><subject>Obesity - chemically induced</subject><subject>Obesity - metabolism</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Proteins</subject><subject>Therapeutic targets</subject><subject>Transcription activation</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10UFrFDEUB_Agil2rN88S8GAPpiZ5mQlzXFq3LRRatOIxZDNvbMpuMiYZoZ_L79HPZNbdVpD29Hjw488_eYS8FfxQSME_YTiUXCgmQKtnZCY61TAtNH9OZpwLYFpKvUde5XxTV6UUvCR7sgEFUsOM-BO7Qld8YEDndf6yBTO9vJx_uftNbejp12kcYyqZfr_2Bem892PMSK98zhPSRUxrW3wMf-2p_3HNFrbQY4-FnYV-ctjTiyVmX25fkxeDXWV8s5v75Nvi89XRKTu_ODk7mp8zpwBKrQvCtW0neesaJXEpwA7ONroTgD2AtehAiaHpB9vq1qpBKtd1YLE-btm3sE8Otrljij8nzMWsfXa4WtmAccpGtNCpTkstKn3_H72JUwq1nQEBvAVQXFb1catcijknHMyY_NqmWyO42ZzAYDCbE5jNCSp_twudlmvsH_D9n1fwYQviND4VxXZRsJUY-uiSDzgmzPlfy0cL_AGQjZ1l</recordid><startdate>201501</startdate><enddate>201501</enddate><creator>Baek, Jung-Hwan</creator><creator>Kim, Seok-Jun</creator><creator>Kang, Hyeok Gu</creator><creator>Lee, Hyun-Woo</creator><creator>Kim, Jung-Hoon</creator><creator>Hwang, Kyung-A</creator><creator>Song, Jaewhan</creator><creator>Chun, Kyung-Hee</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201501</creationdate><title>Galectin-3 Activates PPARγ and Supports White Adipose Tissue Formation and High-Fat Diet-Induced Obesity</title><author>Baek, Jung-Hwan ; Kim, Seok-Jun ; Kang, Hyeok Gu ; Lee, Hyun-Woo ; Kim, Jung-Hoon ; Hwang, Kyung-A ; Song, Jaewhan ; Chun, Kyung-Hee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-7231c669206c542eb13afca57913ed33aaec341f5dfa676a4f24c993ae144bd63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>3T3-L1 Cells</topic><topic>Ablation</topic><topic>Adipocytes</topic><topic>Adipocytes - cytology</topic><topic>Adipocytes - metabolism</topic><topic>Adipogenesis</topic><topic>Adipose tissue</topic><topic>Adipose Tissue, White - physiology</topic><topic>Adiposity</topic><topic>Animals</topic><topic>Body fat</topic><topic>Body size</topic><topic>Body weight</topic><topic>CCAAT/enhancer-binding protein</topic><topic>Cell Differentiation</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diet</topic><topic>Dietary Fats - administration & dosage</topic><topic>Dietary Fats - adverse effects</topic><topic>Differentiation</topic><topic>Dose-Response Relationship, Drug</topic><topic>Female</topic><topic>Galactosides</topic><topic>Galectin 3 - genetics</topic><topic>Galectin 3 - metabolism</topic><topic>Galectin-3</topic><topic>Gene Expression Regulation - physiology</topic><topic>HEK293 Cells</topic><topic>High fat diet</topic><topic>Humans</topic><topic>Inflammatory diseases</topic><topic>Male</topic><topic>Metabolic disorders</topic><topic>Metabolic syndrome</topic><topic>Metformin</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Obesity</topic><topic>Obesity - chemically induced</topic><topic>Obesity - metabolism</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>PPAR gamma - genetics</topic><topic>PPAR gamma - metabolism</topic><topic>Proteins</topic><topic>Therapeutic targets</topic><topic>Transcription activation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baek, Jung-Hwan</creatorcontrib><creatorcontrib>Kim, Seok-Jun</creatorcontrib><creatorcontrib>Kang, Hyeok Gu</creatorcontrib><creatorcontrib>Lee, Hyun-Woo</creatorcontrib><creatorcontrib>Kim, Jung-Hoon</creatorcontrib><creatorcontrib>Hwang, Kyung-A</creatorcontrib><creatorcontrib>Song, Jaewhan</creatorcontrib><creatorcontrib>Chun, Kyung-Hee</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baek, Jung-Hwan</au><au>Kim, Seok-Jun</au><au>Kang, Hyeok Gu</au><au>Lee, Hyun-Woo</au><au>Kim, Jung-Hoon</au><au>Hwang, Kyung-A</au><au>Song, Jaewhan</au><au>Chun, Kyung-Hee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Galectin-3 Activates PPARγ and Supports White Adipose Tissue Formation and High-Fat Diet-Induced Obesity</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2015-01</date><risdate>2015</risdate><volume>156</volume><issue>1</issue><spage>147</spage><epage>156</epage><pages>147-156</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>Galectin-3, a β-galactoside-binding lectin, is elevated in obesity and type 2 diabetes mellitus, and metformin treatment reduces these galectin-3 levels. However, the role of galectin-3 in adipogenesis remains controversial. We found that 17-month-old galectin-3-deficient (lgals3−/−) mice had decreased body size and epididymal white adipose tissue (eWAT) without related inflammatory diseases when fed normal chow. Galectin-3 knockdown significantly reduced adipocyte differentiation in 3T3-L1 cells and also decreased the expression of peroxisome proliferator-activated receptor (PPAR)-γ, ccaat-enhancer-binding protein α, and ccaat-enhancer-binding protein β. Endogenous galectin-3 directly interacted with PPARγ, and galectin-3 ablation reduced the nuclear accumulation and transcriptional activation of PPARγ. After a 12-week high-fat diet (60% fat), lgals3−/− mice had lower body weight and eWAT mass than lgals3+/+ mice. Moreover, the expression of PPARγ and other lipogenic genes was drastically decreased in the eWAT and liver of lgals3−/− mice. We suggest that galectin-3 directly activates PPARγ and leads to adipocyte differentiation in vitro and in vivo. Furthermore, galectin-3 might be a potential therapeutic target in metabolic syndromes as a PPARγ regulator.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>25343273</pmid><doi>10.1210/en.2014-1374</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3T3-L1 Cells Ablation Adipocytes Adipocytes - cytology Adipocytes - metabolism Adipogenesis Adipose tissue Adipose Tissue, White - physiology Adiposity Animals Body fat Body size Body weight CCAAT/enhancer-binding protein Cell Differentiation Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diet Dietary Fats - administration & dosage Dietary Fats - adverse effects Differentiation Dose-Response Relationship, Drug Female Galactosides Galectin 3 - genetics Galectin 3 - metabolism Galectin-3 Gene Expression Regulation - physiology HEK293 Cells High fat diet Humans Inflammatory diseases Male Metabolic disorders Metabolic syndrome Metformin Mice Mice, Knockout Obesity Obesity - chemically induced Obesity - metabolism Peroxisome proliferator-activated receptors PPAR gamma - genetics PPAR gamma - metabolism Proteins Therapeutic targets Transcription activation |
| title | Galectin-3 Activates PPARγ and Supports White Adipose Tissue Formation and High-Fat Diet-Induced Obesity |
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