Role of GPR81 in lactate-mediated reduction of adipose lipolysis
Heavy exercise or oxygen deficit often links with higher levels of arterial lactate and lower levels of plasma free fatty acids (FFA). Treatment with lactate reduces circulating levels of FFA in vivo and lipolysis in adipose tissues in vitro. However, the underlying mechanism has remained unclear. H...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2008-12, Vol.377 (3), p.987-991 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Cai, Tian-Quan Ren, Ning Jin, Lan Cheng, Kang Kash, Shera Chen, Ruoping Wright, Samuel D. Taggart, Andrew K.P. Waters, M. Gerard |
| description | Heavy exercise or oxygen deficit often links with higher levels of arterial lactate and lower levels of plasma free fatty acids (FFA). Treatment with lactate reduces circulating levels of FFA
in vivo and lipolysis in adipose tissues
in vitro. However, the underlying mechanism has remained unclear. Here we employ pharmacological and genetic approaches to show that GPR81, an orphan G-protein-coupled receptor with relatively restricted expression in the adipose tissues, functions as a receptor for lactate and can mediate an anti-lipolytic effect of lactate. GPR81 may thus function as a sensor of lactate that can modulate the FFA pool under exercise or conditions of oxygen deficit. |
| doi_str_mv | 10.1016/j.bbrc.2008.10.088 |
| format | Article |
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in vivo and lipolysis in adipose tissues
in vitro. However, the underlying mechanism has remained unclear. Here we employ pharmacological and genetic approaches to show that GPR81, an orphan G-protein-coupled receptor with relatively restricted expression in the adipose tissues, functions as a receptor for lactate and can mediate an anti-lipolytic effect of lactate. GPR81 may thus function as a sensor of lactate that can modulate the FFA pool under exercise or conditions of oxygen deficit.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2008.10.088</identifier><identifier>PMID: 18952058</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adipose Tissue - drug effects ; Adipose Tissue - metabolism ; Animals ; CHO Cells ; Cricetinae ; Cricetulus ; Exercise ; Fatty Acids, Nonesterified - metabolism ; Free fatty acids ; Humans ; Lactic acid ; Lactic Acid - metabolism ; Lactic Acid - pharmacology ; Ligands ; Lipolysis - drug effects ; Lipolysis - genetics ; Mice ; Orphan GPCR ; Oxygen deficit ; Receptors, G-Protein-Coupled - agonists ; Receptors, G-Protein-Coupled - genetics ; Receptors, G-Protein-Coupled - physiology ; Receptors, Nicotinic - genetics ; Receptors, Nicotinic - physiology ; Transfection</subject><ispartof>Biochemical and biophysical research communications, 2008-12, Vol.377 (3), p.987-991</ispartof><rights>2008 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-c52a0f05f802d1a0ed2aa66e770aae9a340c047e99109893125bebf4002114273</citedby><cites>FETCH-LOGICAL-c451t-c52a0f05f802d1a0ed2aa66e770aae9a340c047e99109893125bebf4002114273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X08020901$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18952058$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cai, Tian-Quan</creatorcontrib><creatorcontrib>Ren, Ning</creatorcontrib><creatorcontrib>Jin, Lan</creatorcontrib><creatorcontrib>Cheng, Kang</creatorcontrib><creatorcontrib>Kash, Shera</creatorcontrib><creatorcontrib>Chen, Ruoping</creatorcontrib><creatorcontrib>Wright, Samuel D.</creatorcontrib><creatorcontrib>Taggart, Andrew K.P.</creatorcontrib><creatorcontrib>Waters, M. Gerard</creatorcontrib><title>Role of GPR81 in lactate-mediated reduction of adipose lipolysis</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Heavy exercise or oxygen deficit often links with higher levels of arterial lactate and lower levels of plasma free fatty acids (FFA). Treatment with lactate reduces circulating levels of FFA
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in vitro. However, the underlying mechanism has remained unclear. Here we employ pharmacological and genetic approaches to show that GPR81, an orphan G-protein-coupled receptor with relatively restricted expression in the adipose tissues, functions as a receptor for lactate and can mediate an anti-lipolytic effect of lactate. GPR81 may thus function as a sensor of lactate that can modulate the FFA pool under exercise or conditions of oxygen deficit.</description><subject>Adipose Tissue - drug effects</subject><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Cricetulus</subject><subject>Exercise</subject><subject>Fatty Acids, Nonesterified - metabolism</subject><subject>Free fatty acids</subject><subject>Humans</subject><subject>Lactic acid</subject><subject>Lactic Acid - metabolism</subject><subject>Lactic Acid - pharmacology</subject><subject>Ligands</subject><subject>Lipolysis - drug effects</subject><subject>Lipolysis - genetics</subject><subject>Mice</subject><subject>Orphan GPCR</subject><subject>Oxygen deficit</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Receptors, G-Protein-Coupled - genetics</subject><subject>Receptors, G-Protein-Coupled - physiology</subject><subject>Receptors, Nicotinic - genetics</subject><subject>Receptors, Nicotinic - physiology</subject><subject>Transfection</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFKw0AQhhdRtFZfwIPk5C11ZpNsdsGDUrQKBaUoeFs2mwlsSZu6mwp9eze04E1PPwzf_Mx8jF0hTBBQ3C4nVeXthAPIOJiAlEdshKAg5Qj5MRsBgEi5ws8zdh7CEgAxF-qUnaFUBYdCjtj9omsp6Zpk9raQmLh10hrbm57SFdUuZp14qre2d916wEztNl2gpI3R7oILF-ykMW2gy0OO2cfT4_v0OZ2_zl6mD_PU5gX2qS24gQaKRgKv0QDV3BghqCzBGFImy8FCXpJS8QGpMuRFRVWTA_B4NC-zMbvZ925897Wl0OuVC5ba1qyp2wYtlETBVfYviKoQiCKPIN-D1ncheGr0xruV8TuNoAfBeqkHwXoQPMyi4Lh0fWjfVtHQ78rBaATu9gBFGd-OvA7W0dpGm55sr-vO_dX_A935ih0</recordid><startdate>20081219</startdate><enddate>20081219</enddate><creator>Cai, Tian-Quan</creator><creator>Ren, Ning</creator><creator>Jin, Lan</creator><creator>Cheng, Kang</creator><creator>Kash, Shera</creator><creator>Chen, Ruoping</creator><creator>Wright, Samuel D.</creator><creator>Taggart, Andrew K.P.</creator><creator>Waters, M. 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in vitro. However, the underlying mechanism has remained unclear. Here we employ pharmacological and genetic approaches to show that GPR81, an orphan G-protein-coupled receptor with relatively restricted expression in the adipose tissues, functions as a receptor for lactate and can mediate an anti-lipolytic effect of lactate. GPR81 may thus function as a sensor of lactate that can modulate the FFA pool under exercise or conditions of oxygen deficit.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>18952058</pmid><doi>10.1016/j.bbrc.2008.10.088</doi><tpages>5</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adipose Tissue - drug effects Adipose Tissue - metabolism Animals CHO Cells Cricetinae Cricetulus Exercise Fatty Acids, Nonesterified - metabolism Free fatty acids Humans Lactic acid Lactic Acid - metabolism Lactic Acid - pharmacology Ligands Lipolysis - drug effects Lipolysis - genetics Mice Orphan GPCR Oxygen deficit Receptors, G-Protein-Coupled - agonists Receptors, G-Protein-Coupled - genetics Receptors, G-Protein-Coupled - physiology Receptors, Nicotinic - genetics Receptors, Nicotinic - physiology Transfection |
| title | Role of GPR81 in lactate-mediated reduction of adipose lipolysis |
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