DC Field | Value | Language |
---|---|---|
dc.contributor.advisor | Kim, Hail | - |
dc.contributor.advisor | 김하일 | - |
dc.contributor.author | Moon, Joon Ho | - |
dc.date.accessioned | 2023-06-23T19:33:19Z | - |
dc.date.available | 2023-06-23T19:33:19Z | - |
dc.date.issued | 2020 | - |
dc.identifier.uri | http://library.kaist.ac.kr/search/detail/view.do?bibCtrlNo=1006541&flag=dissertation | en_US |
dc.identifier.uri | http://hdl.handle.net/10203/309033 | - |
dc.description | 학위논문(박사) - 한국과학기술원 : 의과학대학원, 2020.2,[vi, 103 p. :] | - |
dc.description.abstract | 1) during lactation and 2) perinatal period. During lactation, circulating prolactin activates PRLR-STAT5-TPH1 cascade to produce 5-HT in β cells. 5-HT stimulates β cell proliferation through HTR2B in an autocrine/paracrine manner, while intracellular 5-HT acts as an antioxidant to mitigate the intracellular oxidative stress in β cells. Taken together, 5-HT mediates the long-term beneficial effects of lactation on female metabolic health by increasing β cell proliferation and reducing oxidative stress in β cells. During perinatal period, newly developed β cells produce 5-HT shortly after a surge of growth hormone (GH), and 5-HT function in an autocrine/paracrine manner to drive β cell proliferation. In β cell-specific Tph1 KO mice, β cell proliferation was reduced to one-fourth during perinatal period. Furthermore, adult Tph1 βKO mice exhibited impaired glucose tolerance with decreased β cell mass and impaired insulin secretion. Disruption of Htr2b in β cells resulted in decreased β cell proliferation and mass indicating that HTR2B is the downstream of 5-HT in β cell proliferation. GH induced β cell 5-HT production during perinatal period comprising the GHR-STAT5-TPH1-5-HT-HTR2B axis in the perinatal β cell proliferation. Taken together, 5-HT plays a critical role in the glucose homeostasis and determination of β cell mass and by regulating β cell proliferation during lactation and perinatal period and exerting antioxidant activity by scavenging oxidative stress. | - |
dc.description.abstract | Impaired pancreatic β cell function is a predisposing factor in the development of type 2 diabetes. Various causes for β cell failure include ER stress glucolipotoxicity, mitochondrial dysfunction, etc. Recent advances in genetics discovered a number of genetic alterations that increases the risk of type 2 diabetes. However, ways to prevent β cells from failure are yet to be discovered. Serotonin (5-hydroxytryptamine, 5-HT), previously known as a neurotransmitter, is produced in different peripheral tissues to exert various functions. In this thesis, I focused on two physiological periods that pancreatic β cells produce 5-HT | - |
dc.language | eng | - |
dc.publisher | 한국과학기술원 | - |
dc.subject | Serotonin▼aPancreatic beta cell▼aLactation▼aPerinatal period▼aProliferation▼aOxidative stress | - |
dc.subject | 세로토닌▼a베타세포▼a수유▼a출생 전후▼a증식▼a산화스트레스 | - |
dc.title | Serotonin regulates maternal-perinatal pancreatic beta cell mass and function | - |
dc.title.alternative | 세로토닌이 모체-태아의 췌장 베타세포 양과 기능에 미치는 영향 | - |
dc.type | Thesis(Ph.D) | - |
dc.identifier.CNRN | 325007 | - |
dc.description.department | 한국과학기술원 :의과학대학원, | - |
dc.contributor.alternativeauthor | 문준호 | - |
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