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The PPARδ Agonist GW501516 Improves Lipolytic/Lipogenic Balance through CPT1 and PEPCK during the Development of Pre-Implantation Bovine Embryos
The PPARs (peroxisome proliferator-activated receptors) play critical roles in the regulation of lipid and glucose metabolism. PPARδ, a member of the PPARs family, is associated with decreased susceptibility to ectopic lipid deposition and is implicated in the regulation of mitochondrial processes....
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Published in: | International journal of molecular sciences 2019-12, Vol.20 (23), p.6066 |
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creator | Idrees, Muhammad Xu, Lianguang El Sheikh, Marwa Sidrat, Tabinda Song, Seok-Hwan Joo, Myeong-Don Lee, Kyeong-Lim Kong, Il-Keun |
description | The PPARs (peroxisome proliferator-activated receptors) play critical roles in the regulation of lipid and glucose metabolism. PPARδ, a member of the PPARs family, is associated with decreased susceptibility to ectopic lipid deposition and is implicated in the regulation of mitochondrial processes. The current study aimed to determine the role of PPARδ in fatty acid β-oxidation and its influence on PEPCK for the lipogenic/lipolytic balance during in vitro bovine oocyte maturation and embryo development. Activation of PPARδ by GW501516, but not 2-BP, was indicated by intact embryonic PEPCK (cytosolic) and CPT1 expression and the balance between free fatty acids and mitochondrial β-oxidation that reduced ROS and inhibited p-NF-κB nuclear localization. Genes involved in lipolysis, fatty acid oxidation, and apoptosis showed significant differences after the GW501516 treatment relative to the control- and 2-BP-treated embryos. GSK3787 reversed the PPARδ-induced effects by reducing PEPCK and CPT1 expression and the mitochondrial membrane potential, revealing the importance of PPARδ/PEPCK and PPARδ/CPT1 for controlling lipolysis during embryo development. In conclusion, GW501516-activated PPARδ maintained the correlation between lipolysis and lipogenesis by enhancing PEPCK and CPT1 to improve bovine embryo quality. |
doi_str_mv | 10.3390/ijms20236066 |
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PPARδ, a member of the PPARs family, is associated with decreased susceptibility to ectopic lipid deposition and is implicated in the regulation of mitochondrial processes. The current study aimed to determine the role of PPARδ in fatty acid β-oxidation and its influence on PEPCK for the lipogenic/lipolytic balance during in vitro bovine oocyte maturation and embryo development. Activation of PPARδ by GW501516, but not 2-BP, was indicated by intact embryonic PEPCK (cytosolic) and CPT1 expression and the balance between free fatty acids and mitochondrial β-oxidation that reduced ROS and inhibited p-NF-κB nuclear localization. Genes involved in lipolysis, fatty acid oxidation, and apoptosis showed significant differences after the GW501516 treatment relative to the control- and 2-BP-treated embryos. GSK3787 reversed the PPARδ-induced effects by reducing PEPCK and CPT1 expression and the mitochondrial membrane potential, revealing the importance of PPARδ/PEPCK and PPARδ/CPT1 for controlling lipolysis during embryo development. In conclusion, GW501516-activated PPARδ maintained the correlation between lipolysis and lipogenesis by enhancing PEPCK and CPT1 to improve bovine embryo quality.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms20236066</identifier><identifier>PMID: 31810173</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Animals ; Apoptosis ; Carnitine O-Palmitoyltransferase - genetics ; Cattle ; Cell growth ; Embryonic Development - genetics ; Embryos ; Fatty acids ; Fatty Acids, Nonesterified - metabolism ; Gametocytes ; Glucose metabolism ; Homeostasis ; In vitro fertilization ; Lipid metabolism ; Lipid Metabolism - genetics ; Lipids ; Lipogenesis ; Lipogenesis - drug effects ; Lipolysis ; Lipolysis - drug effects ; Localization ; Medical research ; Membrane potential ; Metabolism ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - genetics ; Muscle, Skeletal - growth & development ; Muscle, Skeletal - metabolism ; NF-κB protein ; Oxidation ; Oxidation-Reduction ; Peroxisome proliferator-activated receptors ; Phosphoenolpyruvate Carboxylase - genetics ; PPAR delta - genetics ; Proteins ; Roles ; Thiazoles - pharmacology ; Triglycerides</subject><ispartof>International journal of molecular sciences, 2019-12, Vol.20 (23), p.6066</ispartof><rights>2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). 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PPARδ, a member of the PPARs family, is associated with decreased susceptibility to ectopic lipid deposition and is implicated in the regulation of mitochondrial processes. The current study aimed to determine the role of PPARδ in fatty acid β-oxidation and its influence on PEPCK for the lipogenic/lipolytic balance during in vitro bovine oocyte maturation and embryo development. Activation of PPARδ by GW501516, but not 2-BP, was indicated by intact embryonic PEPCK (cytosolic) and CPT1 expression and the balance between free fatty acids and mitochondrial β-oxidation that reduced ROS and inhibited p-NF-κB nuclear localization. Genes involved in lipolysis, fatty acid oxidation, and apoptosis showed significant differences after the GW501516 treatment relative to the control- and 2-BP-treated embryos. GSK3787 reversed the PPARδ-induced effects by reducing PEPCK and CPT1 expression and the mitochondrial membrane potential, revealing the importance of PPARδ/PEPCK and PPARδ/CPT1 for controlling lipolysis during embryo development. In conclusion, GW501516-activated PPARδ maintained the correlation between lipolysis and lipogenesis by enhancing PEPCK and CPT1 to improve bovine embryo quality.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Carnitine O-Palmitoyltransferase - genetics</subject><subject>Cattle</subject><subject>Cell growth</subject><subject>Embryonic Development - genetics</subject><subject>Embryos</subject><subject>Fatty acids</subject><subject>Fatty Acids, Nonesterified - metabolism</subject><subject>Gametocytes</subject><subject>Glucose metabolism</subject><subject>Homeostasis</subject><subject>In vitro fertilization</subject><subject>Lipid metabolism</subject><subject>Lipid Metabolism - genetics</subject><subject>Lipids</subject><subject>Lipogenesis</subject><subject>Lipogenesis - drug effects</subject><subject>Lipolysis</subject><subject>Lipolysis - drug effects</subject><subject>Localization</subject><subject>Medical research</subject><subject>Membrane potential</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - 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genetics</topic><topic>Cattle</topic><topic>Cell growth</topic><topic>Embryonic Development - genetics</topic><topic>Embryos</topic><topic>Fatty acids</topic><topic>Fatty Acids, Nonesterified - metabolism</topic><topic>Gametocytes</topic><topic>Glucose metabolism</topic><topic>Homeostasis</topic><topic>In vitro fertilization</topic><topic>Lipid metabolism</topic><topic>Lipid Metabolism - genetics</topic><topic>Lipids</topic><topic>Lipogenesis</topic><topic>Lipogenesis - drug effects</topic><topic>Lipolysis</topic><topic>Lipolysis - drug effects</topic><topic>Localization</topic><topic>Medical research</topic><topic>Membrane potential</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - genetics</topic><topic>Muscle, Skeletal - growth & development</topic><topic>Muscle, Skeletal - metabolism</topic><topic>NF-κB protein</topic><topic>Oxidation</topic><topic>Oxidation-Reduction</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phosphoenolpyruvate Carboxylase - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Idrees, Muhammad</au><au>Xu, Lianguang</au><au>El Sheikh, Marwa</au><au>Sidrat, Tabinda</au><au>Song, Seok-Hwan</au><au>Joo, Myeong-Don</au><au>Lee, Kyeong-Lim</au><au>Kong, Il-Keun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The PPARδ Agonist GW501516 Improves Lipolytic/Lipogenic Balance through CPT1 and PEPCK during the Development of Pre-Implantation Bovine Embryos</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2019-12-02</date><risdate>2019</risdate><volume>20</volume><issue>23</issue><spage>6066</spage><pages>6066-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The PPARs (peroxisome proliferator-activated receptors) play critical roles in the regulation of lipid and glucose metabolism. PPARδ, a member of the PPARs family, is associated with decreased susceptibility to ectopic lipid deposition and is implicated in the regulation of mitochondrial processes. The current study aimed to determine the role of PPARδ in fatty acid β-oxidation and its influence on PEPCK for the lipogenic/lipolytic balance during in vitro bovine oocyte maturation and embryo development. Activation of PPARδ by GW501516, but not 2-BP, was indicated by intact embryonic PEPCK (cytosolic) and CPT1 expression and the balance between free fatty acids and mitochondrial β-oxidation that reduced ROS and inhibited p-NF-κB nuclear localization. Genes involved in lipolysis, fatty acid oxidation, and apoptosis showed significant differences after the GW501516 treatment relative to the control- and 2-BP-treated embryos. GSK3787 reversed the PPARδ-induced effects by reducing PEPCK and CPT1 expression and the mitochondrial membrane potential, revealing the importance of PPARδ/PEPCK and PPARδ/CPT1 for controlling lipolysis during embryo development. In conclusion, GW501516-activated PPARδ maintained the correlation between lipolysis and lipogenesis by enhancing PEPCK and CPT1 to improve bovine embryo quality.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>31810173</pmid><doi>10.3390/ijms20236066</doi><orcidid>https://orcid.org/0000-0001-5567-1088</orcidid><orcidid>https://orcid.org/0000-0001-6707-2736</orcidid><orcidid>https://orcid.org/0000-0002-9715-0691</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Apoptosis Carnitine O-Palmitoyltransferase - genetics Cattle Cell growth Embryonic Development - genetics Embryos Fatty acids Fatty Acids, Nonesterified - metabolism Gametocytes Glucose metabolism Homeostasis In vitro fertilization Lipid metabolism Lipid Metabolism - genetics Lipids Lipogenesis Lipogenesis - drug effects Lipolysis Lipolysis - drug effects Localization Medical research Membrane potential Metabolism Mitochondria Mitochondria - drug effects Mitochondria - genetics Muscle, Skeletal - growth & development Muscle, Skeletal - metabolism NF-κB protein Oxidation Oxidation-Reduction Peroxisome proliferator-activated receptors Phosphoenolpyruvate Carboxylase - genetics PPAR delta - genetics Proteins Roles Thiazoles - pharmacology Triglycerides |
title | The PPARδ Agonist GW501516 Improves Lipolytic/Lipogenic Balance through CPT1 and PEPCK during the Development of Pre-Implantation Bovine Embryos |
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