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Article: Lipolytic actions of secretin in mouse adipocytes

TitleLipolytic actions of secretin in mouse adipocytes
Authors
KeywordsLipolysis
Secretin receptor
Hormone sensitive lipase
Protein kinase A
Issue Date2014
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jlr.org/
Citation
Journal of Lipid Research, 2014, v. 55 n. 2, p. 190-200 How to Cite?
AbstractSecretin (Sct), a classical gut hormone, is now known to play pleiotropic functions in the body including osmoregulation, digestion, and feeding control. As Sct has long been implicated to regulate metabolism, in this report, we have investigated a potential lipolytic action of Sct. In our preliminary studies, both Sct levels in circulation and Sct receptor (SctR) transcripts in adipose tissue were upregulated during fasting, suggesting a potential physiological relevance of Sct in regulating lipolysis. Using SctR knockout and Sct knockout mice as controls, we show that Sct is able to stimulate lipolysis in vitro in isolated adipocytes dose- and time-dependently, as well as acute lipolysis in vivo. H-89, a protein kinase A (PKA) inhibitor, was found to attenuate lipolytic effects of 1 muM Sct in vitro, while a significant increase in PKA activity upon Sct injection was observed in the adipose tissue in vivo. Sct was also found to stimulate phosphorylation at 660(ser) of hormone sensitive lipase (HSL) and to bring about the translocation of HSL from cytosol to the lipid droplet. In summary, our data demonstrate for the first time the in vivo and in vitro lipolytic effects of Sct, and that this function is mediated by PKA and HSL.
Persistent Identifierhttp://hdl.handle.net/10722/198229
ISSN
2023 Impact Factor: 5.0
2023 SCImago Journal Rankings: 2.090
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSekar, R-
dc.contributor.authorChow, BKC-
dc.date.accessioned2014-06-25T02:56:43Z-
dc.date.available2014-06-25T02:56:43Z-
dc.date.issued2014-
dc.identifier.citationJournal of Lipid Research, 2014, v. 55 n. 2, p. 190-200-
dc.identifier.issn0022-2275-
dc.identifier.urihttp://hdl.handle.net/10722/198229-
dc.description.abstractSecretin (Sct), a classical gut hormone, is now known to play pleiotropic functions in the body including osmoregulation, digestion, and feeding control. As Sct has long been implicated to regulate metabolism, in this report, we have investigated a potential lipolytic action of Sct. In our preliminary studies, both Sct levels in circulation and Sct receptor (SctR) transcripts in adipose tissue were upregulated during fasting, suggesting a potential physiological relevance of Sct in regulating lipolysis. Using SctR knockout and Sct knockout mice as controls, we show that Sct is able to stimulate lipolysis in vitro in isolated adipocytes dose- and time-dependently, as well as acute lipolysis in vivo. H-89, a protein kinase A (PKA) inhibitor, was found to attenuate lipolytic effects of 1 muM Sct in vitro, while a significant increase in PKA activity upon Sct injection was observed in the adipose tissue in vivo. Sct was also found to stimulate phosphorylation at 660(ser) of hormone sensitive lipase (HSL) and to bring about the translocation of HSL from cytosol to the lipid droplet. In summary, our data demonstrate for the first time the in vivo and in vitro lipolytic effects of Sct, and that this function is mediated by PKA and HSL.-
dc.languageeng-
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jlr.org/-
dc.relation.ispartofJournal of Lipid Research-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectLipolysis-
dc.subjectSecretin receptor-
dc.subjectHormone sensitive lipase-
dc.subjectProtein kinase A-
dc.titleLipolytic actions of secretin in mouse adipocytes-
dc.typeArticle-
dc.identifier.emailChow, BKC: bkcc@hku.hk-
dc.identifier.authorityChow, BKC=rp00681-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1194/jlr.M038042-
dc.identifier.pmid24273196-
dc.identifier.pmcidPMC3886658-
dc.identifier.scopuseid_2-s2.0-84893410553-
dc.identifier.hkuros229178-
dc.identifier.hkuros249434-
dc.identifier.volume55-
dc.identifier.issue2-
dc.identifier.spage190-
dc.identifier.epage200-
dc.identifier.isiWOS:000330535800004-
dc.publisher.placeUnited States-
dc.identifier.issnl0022-2275-

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