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Peripheral effect of alpha-melanocyte-stimulating hormone on fatty acid oxidation in skeletal muscle

DC FieldValueLanguage
dc.contributor.author김세화-
dc.contributor.author이유미-
dc.contributor.author임승길-
dc.contributor.author차봉수-
dc.contributor.author김똘미-
dc.date.accessioned2014-12-21T16:43:22Z-
dc.date.available2014-12-21T16:43:22Z-
dc.date.issued2007-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/96228-
dc.description.abstractTo study the peripheral effects of melanocortin on fuel homeostasis in skeletal muscle, we assessed palmitate oxidation and AMP kinase activity in alpha-melanocyte-stimulating hormone (alpha-MSH)-treated muscle cells. After alpha-MSH treatment, carnitine palmitoyltransferase-1 and fatty acid oxidation (FAO) increased in a dose-dependent manner. A strong melanocortin agonist, NDP-MSH, also stimulated FAO in primary culture muscle cells and C2C12 cells. However, [Glu6]alpha-MSH-ND, which has ample MC4R and MC3R agonistic activity, stimulated FAO only at high concentrations (10(-5) M). JKC-363, a selective MC4R antagonist, did not suppress alpha-MSH-induced FAO. Meanwhile, SHU9119, which has both antagonistic activity on MC3R and MC4R and agonistic activity on both MC1R and MC5R, increased the effect of alpha-MSH on FAO in both C2C12 and primary muscle cells. Small interference RNA against MC5R suppressed the alpha-MSH-induced FAO effectively. cAMP analogues mimicked the effect of alpha-MSH on FAO, and the effects of both alpha-MSH and cAMP analogue-mediated FAO were antagonized by a protein kinase A inhibitor (H89) and a cAMP antagonist ((Rp)-cAMP). Acetyl-CoA carboxylase activity was suppressed by alpha-MSH and cAMP analogues by phosphorylation through AMP-activated protein kinase activation in C2C12 cells. Taken together, these results suggest that alpha-MSH increases FAO in skeletal muscle, in which MC5R may play a major role. Furthermore, these results suggest that alpha-MSH-induced FAO involves cAMP-protein kinase A-mediated AMP-activated protein kinase activation.-
dc.description.statementOfResponsibilityopen-
dc.format.extent2862~2870-
dc.relation.isPartOfJOURNAL OF BIOLOGICAL CHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCells, Cultured-
dc.subject.MESHDNA Primers-
dc.subject.MESHFatty Acids/metabolism*-
dc.subject.MESHHindlimb-
dc.subject.MESHKinetics-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMitochondria, Muscle/physiology-
dc.subject.MESHMuscle, Skeletal/drug effects-
dc.subject.MESHMuscle, Skeletal/embryology-
dc.subject.MESHMuscle, Skeletal/metabolism*-
dc.subject.MESHMyoblasts/drug effects-
dc.subject.MESHMyoblasts/metabolism-
dc.subject.MESHOxidation-Reduction-
dc.subject.MESHReceptor, Melanocortin, Type 1/genetics-
dc.subject.MESHReceptor, Melanocortin, Type 1/physiology*-
dc.subject.MESHRecombinant Proteins/metabolism-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHalpha-MSH/pharmacology*-
dc.titlePeripheral effect of alpha-melanocyte-stimulating hormone on fatty acid oxidation in skeletal muscle-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJuan Ji An-
dc.contributor.googleauthorYumie Rhee-
dc.contributor.googleauthorSung-Kil Lim-
dc.contributor.googleauthorWon Tae Lee-
dc.contributor.googleauthorJa-Hyun Baik-
dc.contributor.googleauthorBong Soo Cha-
dc.contributor.googleauthorYoung-Jun Jin-
dc.contributor.googleauthorJung Hee Hwang-
dc.contributor.googleauthorDong-He Han-
dc.contributor.googleauthorDol Mi Kim-
dc.contributor.googleauthorSe Hwa Kim-
dc.identifier.doi10.1074/jbc.M603454200-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03012-
dc.contributor.localIdA03375-
dc.contributor.localIdA03996-
dc.contributor.localIdA00418-
dc.contributor.localIdA00609-
dc.relation.journalcodeJ01258-
dc.identifier.eissn1083-351X-
dc.identifier.pmid17127674-
dc.contributor.alternativeNameKim, Se Hwa-
dc.contributor.alternativeNameRhee, Yumie-
dc.contributor.alternativeNameLim, Sung Kil-
dc.contributor.alternativeNameCha, Bong Soo-
dc.contributor.alternativeNameKim, Dol Mi-
dc.contributor.affiliatedAuthorRhee, Yumie-
dc.contributor.affiliatedAuthorLim, Sung Kil-
dc.contributor.affiliatedAuthorCha, Bong Soo-
dc.contributor.affiliatedAuthorKim, Dol Mi-
dc.contributor.affiliatedAuthorKim, Se Hwa-
dc.rights.accessRightsfree-
dc.citation.volume282-
dc.citation.number5-
dc.citation.startPage2862-
dc.citation.endPage2870-
dc.identifier.bibliographicCitationJOURNAL OF BIOLOGICAL CHEMISTRY, Vol.282(5) : 2862-2870, 2007-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Institute of Endocrinology (내분비연구소) > 1. Journal Papers

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