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dc.contributor.authorJaechan Leem-
dc.contributor.authorHae-min Shim-
dc.contributor.authorHochan Cho-
dc.contributor.authorJae-Hyung Park-
dc.date.accessioned2019-09-17T16:30:54Z-
dc.date.available2019-09-17T16:30:54Z-
dc.date.issued2018-
dc.identifier.citationBiochemical and Biophysical Research Communications, Vol.503(1) : 278-284, 2018-
dc.identifier.issn1090-2104-
dc.identifier.otheroak-2018-1582-
dc.identifier.urihttp://kumel.medlib.dsmc.or.kr/handle/2015.oak/41722-
dc.description.abstractOlfactory receptors (ORs) are G protein-coupled receptors that mediate olfactory chemosensation, leading to the perception of smell. ORs are expressed in many tissues, but their functions are largely unknown. Here, we show that the olfactory receptor Olfr15 is highly and selectively expressed in both mouse pancreatic b-cells and MIN6 cells. In addition, octanoic acid (OA), a medium-chain fatty acid, potentiates glucose-stimulated insulin secretion (GSIS). The OA-induced enhancement of GSIS was inhibited by Olfr15 knockdown. Treatment with a PLC inhibitor or an Ins(1,4,5)P3 receptor (IP3R) antagonist also blocked the OA-induced enhancement of GSIS. These results suggest that OA potentiates GSIS via Olfr15 though the PLC-IP3 pathway. Furthermore, long-term treatment with OA increased cellular glucose uptake in MIN6 cells by up-regulating the expression of glucokinase (GK). Moreover, this process was blocked by an IP3R antagonist and a Ca2þ/calmodulin-dependent protein kinase kinase (CaMKK) inhibitor. Similarly, OA stimulated GK promoter activity, while either Olfr15 or CaMKIV knockdown blocked the stimulatory effect of OA on GK promoter activity. These results suggest that longterm treatment of OA induces GK promoter activity via Olfr15 through the IP3-CaMKK/CaMKIV pathway. In islets from type 2 diabetic mice, the expression level of Olfr15 and the OA-induced enhancement of GSIS were strongly reduced. Collectively, our results highlight the crucial role of the olfactory receptor Olfr15 in potentiating GSIS in pancreatic b-cells, suggesting that Olfr15 may be an important therapeutic target in type 2 diabetes.-
dc.description.statementofresponsibilityprohibition-
dc.publisherSchool of Medicine (의과대학)-
dc.rightsBY_NC_ND-
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.0/kr-
dc.subjectOlfactory receptor-
dc.subjectOctanoic acid-
dc.subjectInsulin secretion-
dc.subjectGlucokinase-
dc.subjectPancreatic b-cell-
dc.subjectType 2 diabetes-
dc.titleOctanoic acid potentiates glucose-stimulated insulin secretion and expression of glucokinase through the olfactory receptor in pancreatic b-cells-
dc.typeArticle-
dc.contributor.localauthor조호찬-
dc.contributor.localauthor박재형-
dc.contributor.alternativelocalauthorCho, Ho Chan-
dc.contributor.alternativelocalauthorPark, Jae Hyung-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.departmentDept. of Physiology (생리학)-
dc.citation.volume503-
dc.citation.number1-
dc.citation.startpage278-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.citation.endpage284-
dc.identifier.doi10.1016/j.bbrc.2018.06.015-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0006291X18313275?via%3Dihub-


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