Heat stress promotes lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes
Heat stress (HS) results in health problems in animals. This study was conducted to investigate the effect and the underlying mechanism of HS on the proliferation and differentiation process of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were treated at 37 °C or 41.5 °C. HS up-regulated the mRNA and...
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| Veröffentlicht in: | Cell stress & chaperones 2021-05, Vol.26 (3), p.563-574 |
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| creator | Huang, Yanna Xie, Hongyue Pan, Peng Qu, Qiuhong Xia, Qin Gao, Xiaotong Zhang, Sanbao Jiang, Qinyang |
| description | Heat stress (HS) results in health problems in animals. This study was conducted to investigate the effect and the underlying mechanism of HS on the proliferation and differentiation process of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were treated at 37 °C or 41.5 °C. HS up-regulated the mRNA and protein expression level of heat shock protein 70 (HSP70). Furthermore, the proliferation of 3T3-L1 preadipocytes were significantly inhibited after HS treatment for 2 days. A large number of accumulated lipid droplets were observed under the microscope after HS treatment for 8 days. Notably, the result of oil red O staining showed that the number of lipid droplets increased significantly and the differentiation ability of the cells was enhanced after HS. Moreover, after 2 and 8 d of differentiation, HS increased the transcription levels of fat synthesis genes including peroxisome proliferators activated receptor γ (PPARγ), fatty acid binding protein 2 (AP2), fatty acid synthase (FAS) and CCAAT enhancer binding protein α (CEBPα) genes, while decreasing the transcription levels of lipid decomposition genes including ATGL and HSL genes. In addition, HS reduced the expression of AMPK and PGC-1α, as well as the dephosphorylation of AMPK. 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) can eliminate HS induced lipogenesis by activating AMPK. These results indicated that HS inhibited the proliferation of 3T3-L1 preadipocytes and promoted lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes. This work lays a theoretical foundation for improving the effect of HS on meat quality of livestock and provides a new direction for the prevention of obesity caused by HS. |
| doi_str_mv | 10.1007/s12192-021-01201-9 |
| format | Article |
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This study was conducted to investigate the effect and the underlying mechanism of HS on the proliferation and differentiation process of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were treated at 37 °C or 41.5 °C. HS up-regulated the mRNA and protein expression level of heat shock protein 70 (HSP70). Furthermore, the proliferation of 3T3-L1 preadipocytes were significantly inhibited after HS treatment for 2 days. A large number of accumulated lipid droplets were observed under the microscope after HS treatment for 8 days. Notably, the result of oil red O staining showed that the number of lipid droplets increased significantly and the differentiation ability of the cells was enhanced after HS. Moreover, after 2 and 8 d of differentiation, HS increased the transcription levels of fat synthesis genes including peroxisome proliferators activated receptor γ (PPARγ), fatty acid binding protein 2 (AP2), fatty acid synthase (FAS) and CCAAT enhancer binding protein α (CEBPα) genes, while decreasing the transcription levels of lipid decomposition genes including ATGL and HSL genes. In addition, HS reduced the expression of AMPK and PGC-1α, as well as the dephosphorylation of AMPK. 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) can eliminate HS induced lipogenesis by activating AMPK. These results indicated that HS inhibited the proliferation of 3T3-L1 preadipocytes and promoted lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes. This work lays a theoretical foundation for improving the effect of HS on meat quality of livestock and provides a new direction for the prevention of obesity caused by HS.</description><identifier>ISSN: 1355-8145</identifier><identifier>EISSN: 1466-1268</identifier><identifier>DOI: 10.1007/s12192-021-01201-9</identifier><identifier>PMID: 33743152</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>3T3-L1 Cells ; Accumulation ; Adipocytes - drug effects ; Adipocytes - metabolism ; Adipogenesis - drug effects ; Adipogenesis - genetics ; Adipogenesis - physiology ; AMP-Activated Protein Kinases - metabolism ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; CCAAT/enhancer-binding protein ; Cell Biology ; Cell differentiation ; Dephosphorylation ; Differentiation ; Droplets ; Fatty acid-binding protein ; Fatty acids ; Fatty-acid synthase ; Gene expression ; Genes ; Health problems ; Heat shock proteins ; Heat stress ; Heat tolerance ; Hot Temperature ; Hsp70 protein ; Immunology ; Lipids ; Lipogenesis ; Livestock ; Meat ; Mice ; Neurosciences ; Original Paper ; PPAR gamma - genetics ; PPAR gamma - metabolism ; Preadipocytes ; Proteins ; Signal transduction ; Signal Transduction - physiology ; Signaling ; Transcription</subject><ispartof>Cell stress & chaperones, 2021-05, Vol.26 (3), p.563-574</ispartof><rights>Cell Stress Society International 2021</rights><rights>Cell Stress Society International 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-104acfb54af9b91d5749ecb9830ae2245ef7f7584cc251cb86dde609d2c08c4b3</citedby><cites>FETCH-LOGICAL-c474t-104acfb54af9b91d5749ecb9830ae2245ef7f7584cc251cb86dde609d2c08c4b3</cites><orcidid>0000-0002-0835-9347</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8065074/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8065074/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,41488,42557,51319,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33743152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Yanna</creatorcontrib><creatorcontrib>Xie, Hongyue</creatorcontrib><creatorcontrib>Pan, Peng</creatorcontrib><creatorcontrib>Qu, Qiuhong</creatorcontrib><creatorcontrib>Xia, Qin</creatorcontrib><creatorcontrib>Gao, Xiaotong</creatorcontrib><creatorcontrib>Zhang, Sanbao</creatorcontrib><creatorcontrib>Jiang, Qinyang</creatorcontrib><title>Heat stress promotes lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes</title><title>Cell stress & chaperones</title><addtitle>Cell Stress and Chaperones</addtitle><addtitle>Cell Stress Chaperones</addtitle><description>Heat stress (HS) results in health problems in animals. This study was conducted to investigate the effect and the underlying mechanism of HS on the proliferation and differentiation process of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were treated at 37 °C or 41.5 °C. HS up-regulated the mRNA and protein expression level of heat shock protein 70 (HSP70). Furthermore, the proliferation of 3T3-L1 preadipocytes were significantly inhibited after HS treatment for 2 days. A large number of accumulated lipid droplets were observed under the microscope after HS treatment for 8 days. Notably, the result of oil red O staining showed that the number of lipid droplets increased significantly and the differentiation ability of the cells was enhanced after HS. Moreover, after 2 and 8 d of differentiation, HS increased the transcription levels of fat synthesis genes including peroxisome proliferators activated receptor γ (PPARγ), fatty acid binding protein 2 (AP2), fatty acid synthase (FAS) and CCAAT enhancer binding protein α (CEBPα) genes, while decreasing the transcription levels of lipid decomposition genes including ATGL and HSL genes. In addition, HS reduced the expression of AMPK and PGC-1α, as well as the dephosphorylation of AMPK. 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) can eliminate HS induced lipogenesis by activating AMPK. These results indicated that HS inhibited the proliferation of 3T3-L1 preadipocytes and promoted lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes. This work lays a theoretical foundation for improving the effect of HS on meat quality of livestock and provides a new direction for the prevention of obesity caused by HS.</description><subject>3T3-L1 Cells</subject><subject>Accumulation</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - metabolism</subject><subject>Adipogenesis - drug effects</subject><subject>Adipogenesis - genetics</subject><subject>Adipogenesis - physiology</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>CCAAT/enhancer-binding protein</subject><subject>Cell Biology</subject><subject>Cell differentiation</subject><subject>Dephosphorylation</subject><subject>Differentiation</subject><subject>Droplets</subject><subject>Fatty acid-binding protein</subject><subject>Fatty acids</subject><subject>Fatty-acid synthase</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Health problems</subject><subject>Heat shock proteins</subject><subject>Heat stress</subject><subject>Heat tolerance</subject><subject>Hot Temperature</subject><subject>Hsp70 protein</subject><subject>Immunology</subject><subject>Lipids</subject><subject>Lipogenesis</subject><subject>Livestock</subject><subject>Meat</subject><subject>Mice</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>PPAR gamma - genetics</subject><subject>PPAR gamma - metabolism</subject><subject>Preadipocytes</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Signaling</subject><subject>Transcription</subject><issn>1355-8145</issn><issn>1466-1268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhS0EomXgBVggS2y6Mfj6Jz8bpGpUWsRUdFHWluM4M66SONgOaB6LF-kz1WFK-Vl0ZUvnO8fX9yD0Gug7oLR8H4FBzQhlQCgwCqR-go5BFAUBVlRP851LSSoQ8gi9iPGGZlNZwnN0xHkpOEh2jKYLqxOOKdgY8RT84JONuHeTa7E2Zh7mXifnR9zssRt3rnHJjVucdhafXl59JlfnawK3P3F021H3izTptPuhFxrza042kGOtbt3kzT5nv0TPOt1H--r-XKGvH8-u1xdk8-X80_p0Q4woRSJAhTZdI4Xu6qaGVpaitqapK061ZUxI25VdKSthDJNgmqpoW1vQumWGVkY0fIU-HHKnuRlsa-yYgu7VFNygw1557dS_yuh2auu_q4oWkub1rNDJfUDw32YbkxpcNLbv9Wj9HBWTlAsuhCwy-vY_9MbPIe9joaAULA9fZ4odKBN8jMF2D8MAVUuh6lCoyoWqX4WqxfTm7288WH43mAF-AGKWxq0Nf95-JPYOQXWtHg</recordid><startdate>20210501</startdate><enddate>20210501</enddate><creator>Huang, Yanna</creator><creator>Xie, Hongyue</creator><creator>Pan, Peng</creator><creator>Qu, Qiuhong</creator><creator>Xia, Qin</creator><creator>Gao, Xiaotong</creator><creator>Zhang, Sanbao</creator><creator>Jiang, Qinyang</creator><general>Springer Netherlands</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>7QL</scope><scope>7QP</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0835-9347</orcidid></search><sort><creationdate>20210501</creationdate><title>Heat stress promotes lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes</title><author>Huang, Yanna ; 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This study was conducted to investigate the effect and the underlying mechanism of HS on the proliferation and differentiation process of 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were treated at 37 °C or 41.5 °C. HS up-regulated the mRNA and protein expression level of heat shock protein 70 (HSP70). Furthermore, the proliferation of 3T3-L1 preadipocytes were significantly inhibited after HS treatment for 2 days. A large number of accumulated lipid droplets were observed under the microscope after HS treatment for 8 days. Notably, the result of oil red O staining showed that the number of lipid droplets increased significantly and the differentiation ability of the cells was enhanced after HS. Moreover, after 2 and 8 d of differentiation, HS increased the transcription levels of fat synthesis genes including peroxisome proliferators activated receptor γ (PPARγ), fatty acid binding protein 2 (AP2), fatty acid synthase (FAS) and CCAAT enhancer binding protein α (CEBPα) genes, while decreasing the transcription levels of lipid decomposition genes including ATGL and HSL genes. In addition, HS reduced the expression of AMPK and PGC-1α, as well as the dephosphorylation of AMPK. 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) can eliminate HS induced lipogenesis by activating AMPK. These results indicated that HS inhibited the proliferation of 3T3-L1 preadipocytes and promoted lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes. This work lays a theoretical foundation for improving the effect of HS on meat quality of livestock and provides a new direction for the prevention of obesity caused by HS.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>33743152</pmid><doi>10.1007/s12192-021-01201-9</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0835-9347</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 3T3-L1 Cells Accumulation Adipocytes - drug effects Adipocytes - metabolism Adipogenesis - drug effects Adipogenesis - genetics Adipogenesis - physiology AMP-Activated Protein Kinases - metabolism Animals Biochemistry Biomedical and Life Sciences Biomedicine Cancer Research CCAAT/enhancer-binding protein Cell Biology Cell differentiation Dephosphorylation Differentiation Droplets Fatty acid-binding protein Fatty acids Fatty-acid synthase Gene expression Genes Health problems Heat shock proteins Heat stress Heat tolerance Hot Temperature Hsp70 protein Immunology Lipids Lipogenesis Livestock Meat Mice Neurosciences Original Paper PPAR gamma - genetics PPAR gamma - metabolism Preadipocytes Proteins Signal transduction Signal Transduction - physiology Signaling Transcription |
| title | Heat stress promotes lipid accumulation by inhibiting the AMPK-PGC-1α signaling pathway in 3T3-L1 preadipocytes |
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