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Conference Paper: Exchange protein directly activated by cAMP 1 plays an important role in β3-adrenergic induction of UCP1 in WAT and thermogenesis via regulating lipolysis

TitleExchange protein directly activated by cAMP 1 plays an important role in β3-adrenergic induction of UCP1 in WAT and thermogenesis via regulating lipolysis
Authors
Issue Date2013
PublisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/
Citation
The 73rd Scientific Sessions of the American Diabetes Association (ADA), Chicago, IL., 21-25 June 2013. In Diabetes, 2013, v. 62 suppl. 1A, p. LB48, abstract no. 185-LB How to Cite?
AbstractPharmaceutical enhancement of uncoupling protein1 (UCP1) and thermogenesis has drawn great interest to counteract obesity. Previously, the exchange protein directly activated by cAMP 1 (Epac1)-deficient mice showed less induction of beige cells with a significantly less UCP1 expression in white adipose tissue (WAT) and lower circulating free fatty acid (FFA) after chronic CL316,243 (a β3-adrenergic receptor agonist, CL, 1mg/kg/day for 10 days) administration, compared to that of wild type (wt) mice. To further study the role of Epac1 in β3-adrenergic induction of UCP1 and its function, energy expenditure and thermogenesis were determined. By indirect calorimetry, the Epac1-deficient mice showed slightly lower oxygen consumption from 9-16 hours after CL (1mg/kg) administration compared to that of wt mice. By using rectal thermometer, continuously lower rectal temperature within 30 min after the ninth dose of CL administration was observed in the Epac1-deficient mice relative to that of wt mice. These results suggest that in the absence of Epac1, increase of energy expenditure and thermogenesis induced by β3-adrenergic activation are compromised, which could be due to lower FFA and UCP1 induced by CL in the Epac1-deficent mice. To test whether the reduced FFA is due to compromised lipolysis, glycerol release from WAT explants was examined ex vivo. Interestingly, Epac1-deficient WAT explants showed impaired CL-stimulated glycerol release, indicating that absence of Epac1 diminishes β3-adrenergic receptor mediated lipolysis in WAT. In addition, Western blot showed that phosphorylation of hormone sensitive lipase at Ser660 by protein kinase A (PKA) was not different in Epac1-deficient WAT explants incubated with CL (10uM) for 10 min, compared to that of wt mice. Taken together, Epac1 plays an important role in β3-adrenergic induction of UCP1 in WAT and thermogenesis via mediating lipolysis independent of PKA.
DescriptionLate Breaking Abstracts: Session - Integrated Physiology/Obesity: no. 185-LB
Open Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/184900
ISSN
2015 Impact Factor: 8.784
2015 SCImago Journal Rankings: 5.185

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_US
dc.contributor.authorTai, ACPen_US
dc.contributor.authorKai, AKLen_US
dc.contributor.authorTam, Sen_US
dc.contributor.authorLam, KSLen_US
dc.contributor.authorChung, SSMen_US
dc.contributor.authorXu, Aen_US
dc.contributor.authorChung, SKen_US
dc.date.accessioned2013-07-15T10:16:44Z-
dc.date.available2013-07-15T10:16:44Z-
dc.date.issued2013en_US
dc.identifier.citationThe 73rd Scientific Sessions of the American Diabetes Association (ADA), Chicago, IL., 21-25 June 2013. In Diabetes, 2013, v. 62 suppl. 1A, p. LB48, abstract no. 185-LBen_US
dc.identifier.issn0012-1797-
dc.identifier.urihttp://hdl.handle.net/10722/184900-
dc.descriptionLate Breaking Abstracts: Session - Integrated Physiology/Obesity: no. 185-LB-
dc.descriptionOpen Access Journal-
dc.description.abstractPharmaceutical enhancement of uncoupling protein1 (UCP1) and thermogenesis has drawn great interest to counteract obesity. Previously, the exchange protein directly activated by cAMP 1 (Epac1)-deficient mice showed less induction of beige cells with a significantly less UCP1 expression in white adipose tissue (WAT) and lower circulating free fatty acid (FFA) after chronic CL316,243 (a β3-adrenergic receptor agonist, CL, 1mg/kg/day for 10 days) administration, compared to that of wild type (wt) mice. To further study the role of Epac1 in β3-adrenergic induction of UCP1 and its function, energy expenditure and thermogenesis were determined. By indirect calorimetry, the Epac1-deficient mice showed slightly lower oxygen consumption from 9-16 hours after CL (1mg/kg) administration compared to that of wt mice. By using rectal thermometer, continuously lower rectal temperature within 30 min after the ninth dose of CL administration was observed in the Epac1-deficient mice relative to that of wt mice. These results suggest that in the absence of Epac1, increase of energy expenditure and thermogenesis induced by β3-adrenergic activation are compromised, which could be due to lower FFA and UCP1 induced by CL in the Epac1-deficent mice. To test whether the reduced FFA is due to compromised lipolysis, glycerol release from WAT explants was examined ex vivo. Interestingly, Epac1-deficient WAT explants showed impaired CL-stimulated glycerol release, indicating that absence of Epac1 diminishes β3-adrenergic receptor mediated lipolysis in WAT. In addition, Western blot showed that phosphorylation of hormone sensitive lipase at Ser660 by protein kinase A (PKA) was not different in Epac1-deficient WAT explants incubated with CL (10uM) for 10 min, compared to that of wt mice. Taken together, Epac1 plays an important role in β3-adrenergic induction of UCP1 in WAT and thermogenesis via mediating lipolysis independent of PKA.-
dc.languageengen_US
dc.publisherAmerican Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/-
dc.relation.ispartofDiabetesen_US
dc.titleExchange protein directly activated by cAMP 1 plays an important role in β3-adrenergic induction of UCP1 in WAT and thermogenesis via regulating lipolysisen_US
dc.typeConference_Paperen_US
dc.identifier.emailKai, AKL: klakai@hku.hken_US
dc.identifier.emailTam, S: stam@hkucc.hku.hk-
dc.identifier.emailLam, KSL: ksllam@hku.hk-
dc.identifier.emailXu, A: amxu@hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.authorityLam, KSL=rp00343en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros216648en_US
dc.identifier.volume62en_US
dc.identifier.issuesuppl. 1A-
dc.identifier.spageLB48-
dc.identifier.epageLB48-
dc.publisher.placeUnited States-

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