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Conference Paper: Role of Prostaglandin E Receptor Subtype 4 (EP4) in the Regulation of Triglyceride Metabolism

TitleRole of Prostaglandin E Receptor Subtype 4 (EP4) in the Regulation of Triglyceride Metabolism
Authors
Issue Date2013
PublisherMedcom Limited. The Journal's web site is located at http://www.hkcchk.com/journals.php
Citation
The 17th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), The University of Hong Kong, Hong Kong, China, 23 November 2013. In Journal of the Hong Kong College of Cardiology, 2013, v. 21 n. 2, p. 65, abstract no. OP4 How to Cite?
AbstractObjectives: Hypertriglyceridemia is strongly associated with future risk of insulin resistance, diabetes and cardiovascular disease. Interestingly, it has been recently demonstrated that mice lacking cyclic AMP-responsive element-binding protein H (CREB-H) showed higher plasma triglyceride concentrations compared to wild-type mice. As an upstream stimulating factor of CREB-H, prostaglandin E receptor subtype 4 (EP4) may participate in the regulation of triglyceride metabolism. Thus, we tested whether or not deletion of EP4 influences triglyceride metabolism, and if so, to explore the underlying mechanisms. Methods: EP4 wild-type and knockout mice were put on a high-fat diet (HFD) for thirty weeks and changes in plasma triglycerides were monitored. The impact of EP4 deletion on the ability to synthesize hepatic very low density lipoprotein (VLDL)-triglyceride (TG) and intestinal chylomicron (CM)-TG, as well as the ability to clear TG during HFD was examined. Lipoprotein lipase (LPL) activity and mRNA expression of LPL and CD36 in brown adipose tissue (BAT) were determined by fluorometric assay kit and quantitative polymerase chain reaction (Q-PCR), respectively. Results: After thirty weeks of high-fat diet, EP4 knockout mice had a higher plasma TG level than wild-type mice. The deletion of EP4 did not influence hepatic VLDL-TG production or intestinal CM-TG synthesis but impaired TG clearance rate. EP4 knockout mice had a decreased mRNA expression and activity of LPL in their BAT, suggesting impaired hydrolysis and uptake of triglycerides in this tissue. Moreover, EP4 knockout mice had a reduced expression of CD36 in BAT, which may indicate that the uptake of fatty acids is impaired. Conclusions: Deletion of EP4 in high-fat fed mice resulted in hypertriglyceridemia. The hypertriglyceridemia that accompanies EP4 deficiency is the result of impaired TG clearance, attributed to reduced mRNA expression of LPL and CD36, and impaired LPL activity in BAT. The results indicate that EP4 plays a critical role in systemic lipid homeostasis.
DescriptionConference Theme: Translating Advances in Science into Improvements in Cardiovascular Health
Oral Presentation
Persistent Identifierhttp://hdl.handle.net/10722/204446
ISSN
2015 SCImago Journal Rankings: 0.102

 

DC FieldValueLanguage
dc.contributor.authorCai, Yen_US
dc.contributor.authorVanhoutte, PMGRen_US
dc.contributor.authorTang, EHCen_US
dc.date.accessioned2014-09-19T23:52:21Z-
dc.date.available2014-09-19T23:52:21Z-
dc.date.issued2013en_US
dc.identifier.citationThe 17th Annual Scientific Meeting of the Institute of Cardiovascular Science and Medicine (ICSM), The University of Hong Kong, Hong Kong, China, 23 November 2013. In Journal of the Hong Kong College of Cardiology, 2013, v. 21 n. 2, p. 65, abstract no. OP4en_US
dc.identifier.issn1027-7811-
dc.identifier.urihttp://hdl.handle.net/10722/204446-
dc.descriptionConference Theme: Translating Advances in Science into Improvements in Cardiovascular Health-
dc.descriptionOral Presentation-
dc.description.abstractObjectives: Hypertriglyceridemia is strongly associated with future risk of insulin resistance, diabetes and cardiovascular disease. Interestingly, it has been recently demonstrated that mice lacking cyclic AMP-responsive element-binding protein H (CREB-H) showed higher plasma triglyceride concentrations compared to wild-type mice. As an upstream stimulating factor of CREB-H, prostaglandin E receptor subtype 4 (EP4) may participate in the regulation of triglyceride metabolism. Thus, we tested whether or not deletion of EP4 influences triglyceride metabolism, and if so, to explore the underlying mechanisms. Methods: EP4 wild-type and knockout mice were put on a high-fat diet (HFD) for thirty weeks and changes in plasma triglycerides were monitored. The impact of EP4 deletion on the ability to synthesize hepatic very low density lipoprotein (VLDL)-triglyceride (TG) and intestinal chylomicron (CM)-TG, as well as the ability to clear TG during HFD was examined. Lipoprotein lipase (LPL) activity and mRNA expression of LPL and CD36 in brown adipose tissue (BAT) were determined by fluorometric assay kit and quantitative polymerase chain reaction (Q-PCR), respectively. Results: After thirty weeks of high-fat diet, EP4 knockout mice had a higher plasma TG level than wild-type mice. The deletion of EP4 did not influence hepatic VLDL-TG production or intestinal CM-TG synthesis but impaired TG clearance rate. EP4 knockout mice had a decreased mRNA expression and activity of LPL in their BAT, suggesting impaired hydrolysis and uptake of triglycerides in this tissue. Moreover, EP4 knockout mice had a reduced expression of CD36 in BAT, which may indicate that the uptake of fatty acids is impaired. Conclusions: Deletion of EP4 in high-fat fed mice resulted in hypertriglyceridemia. The hypertriglyceridemia that accompanies EP4 deficiency is the result of impaired TG clearance, attributed to reduced mRNA expression of LPL and CD36, and impaired LPL activity in BAT. The results indicate that EP4 plays a critical role in systemic lipid homeostasis.-
dc.languageengen_US
dc.publisherMedcom Limited. The Journal's web site is located at http://www.hkcchk.com/journals.php-
dc.relation.ispartofJournal of the Hong Kong College of Cardiologyen_US
dc.titleRole of Prostaglandin E Receptor Subtype 4 (EP4) in the Regulation of Triglyceride Metabolismen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hken_US
dc.identifier.emailTang, EHC: evatang1@hku.hken_US
dc.identifier.authorityVanhoutte, PMGR=rp00238en_US
dc.identifier.authorityTang, EHC=rp01382en_US
dc.identifier.hkuros238801en_US
dc.identifier.volume21-
dc.identifier.issue2-
dc.identifier.spage65, abstract no. OP4-
dc.identifier.epage65, abstract no. OP4-
dc.publisher.placeHong Kong-

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