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Conference Paper: Mice lacking prostaglandin E receptor subtype 4 resist diet-induced obesity despite hypertriglyceridemia

TitleMice lacking prostaglandin E receptor subtype 4 resist diet-induced obesity despite hypertriglyceridemia
Authors
KeywordsProstaglandin E receptor subtype 4
Hypertriglyceridemia
Lipoprotein lipase
Issue Date2014
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642
Citation
The 2014 Scientific Sessions of Arteriosclerosis, Thrombosis and Vascular Biology (ATVB 2014), Toronto, ON., Canada, 1-3 May 2014. In Arteriosclerosis, Thrombosis, and Vascular Biology, 2014, v. 34 suppl. 1, abstract 621 How to Cite?
AbstractOBJECTIVES: Activation of prostaglandin E receptor subtype 4 (EP4) may suppress inflammation by regulating nuclear factor kappa B (NFκB). Indeed, chronic inflammation usually is accompanied by dyslipidemia. Thus, the present study tested the hypothesis that deletion of EP4 can accelerate the occurrence of metabolic syndrome. METHODS: EP4 wild-type and knockout mice were put on a high-fat diet (HFD) for thirty weeks. Body weight and food consumption were monitored. In addition, energy expenditure and fat composition were determined by indirect calorimetry and Minispec body composition analyzer, respectively. 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. Circulating lipoprotein lipase (LPL) activity and tissue LPL activity were determined using a fluorometric assay kit and mRNA expression of lipid metabolism-related genes in adipose tissue was measured by quantitative polymerase chain reaction (Q-PCR). RESULTS: After consuming a high-fat diet for thirty weeks, EP4 knockout mice exhibited reduced body weight gain and body fat mass, not attributable to changes in food intake, fat malabsorption and energy expenditure. However, 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 circulating LPL activity, reduced LPL activity in epididymal fat and skeletal muscle, suggesting impaired hydrolysis and uptake of triglycerides in these tissues. Moreover, EP4 knockout mice had a reduced expression of CD36 in brown adipose tissue, which may indicate that the uptake of fatty acids is impaired. CONCLUSIONS: High-fat feeding of EP4 knockout mice resulted in a lean body phenotype, but caused hypertriglyceridemia resulting from impaired TG clearance, attributed to reduced LPL activity and expression of CD36. The results indicate that EP4 plays a critical role in systemic lipid homeostasis.
DescriptionPoster Abstract Presentation - Poster Session III: abstract 621
This journal suppl. published ATVB 2014 abstracts
Persistent Identifierhttp://hdl.handle.net/10722/204445
ISSN
2015 Impact Factor: 5.969
2015 SCImago Journal Rankings: 3.356

 

DC FieldValueLanguage
dc.contributor.authorCai, Yen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorTang, EHCen_US
dc.date.accessioned2014-09-19T23:52:21Z-
dc.date.available2014-09-19T23:52:21Z-
dc.date.issued2014en_US
dc.identifier.citationThe 2014 Scientific Sessions of Arteriosclerosis, Thrombosis and Vascular Biology (ATVB 2014), Toronto, ON., Canada, 1-3 May 2014. In Arteriosclerosis, Thrombosis, and Vascular Biology, 2014, v. 34 suppl. 1, abstract 621en_US
dc.identifier.issn1079-5642-
dc.identifier.urihttp://hdl.handle.net/10722/204445-
dc.descriptionPoster Abstract Presentation - Poster Session III: abstract 621-
dc.descriptionThis journal suppl. published ATVB 2014 abstracts-
dc.description.abstractOBJECTIVES: Activation of prostaglandin E receptor subtype 4 (EP4) may suppress inflammation by regulating nuclear factor kappa B (NFκB). Indeed, chronic inflammation usually is accompanied by dyslipidemia. Thus, the present study tested the hypothesis that deletion of EP4 can accelerate the occurrence of metabolic syndrome. METHODS: EP4 wild-type and knockout mice were put on a high-fat diet (HFD) for thirty weeks. Body weight and food consumption were monitored. In addition, energy expenditure and fat composition were determined by indirect calorimetry and Minispec body composition analyzer, respectively. 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. Circulating lipoprotein lipase (LPL) activity and tissue LPL activity were determined using a fluorometric assay kit and mRNA expression of lipid metabolism-related genes in adipose tissue was measured by quantitative polymerase chain reaction (Q-PCR). RESULTS: After consuming a high-fat diet for thirty weeks, EP4 knockout mice exhibited reduced body weight gain and body fat mass, not attributable to changes in food intake, fat malabsorption and energy expenditure. However, 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 circulating LPL activity, reduced LPL activity in epididymal fat and skeletal muscle, suggesting impaired hydrolysis and uptake of triglycerides in these tissues. Moreover, EP4 knockout mice had a reduced expression of CD36 in brown adipose tissue, which may indicate that the uptake of fatty acids is impaired. CONCLUSIONS: High-fat feeding of EP4 knockout mice resulted in a lean body phenotype, but caused hypertriglyceridemia resulting from impaired TG clearance, attributed to reduced LPL activity and expression of CD36. The results indicate that EP4 plays a critical role in systemic lipid homeostasis.-
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642-
dc.relation.ispartofArteriosclerosis, Thrombosis, and Vascular Biologyen_US
dc.subjectProstaglandin E receptor subtype 4-
dc.subjectHypertriglyceridemia-
dc.subjectLipoprotein lipase-
dc.titleMice lacking prostaglandin E receptor subtype 4 resist diet-induced obesity despite hypertriglyceridemiaen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_US
dc.identifier.emailTang, EHC: evatang1@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.identifier.authorityTang, EHC=rp01382en_US
dc.identifier.hkuros238794en_US
dc.identifier.volume34-
dc.identifier.issuesuppl. 1-
dc.publisher.placeUnited States-

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