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Cited 2 time in webofscience Cited 3 time in scopus
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Pancreatic Beta-cell Dysfunction in Type 2 Diabetes

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dc.contributor.authorKhin, Phyu Phyu-
dc.contributor.authorLee, Jong Han-
dc.contributor.authorJun, Hee-Sook-
dc.date.accessioned2023-09-19T01:40:09Z-
dc.date.available2023-09-19T01:40:09Z-
dc.date.created2023-03-26-
dc.date.issued2023-01-
dc.identifier.issn1721-727X-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89112-
dc.description.abstractPancreatic β-cells produce and secrete insulin to maintain blood glucose levels within a narrow range. Defects in the function and mass of β-cells play a significant role in the development and progression of diabetes. Increased β-cell deficiency and β-cell apoptosis are observed in the pancreatic islets of patients with type 2 diabetes. At an early stage, β-cells adapt to insulin resistance, and their insulin secretion increases, but they eventually become exhausted, and the β-cell mass decreases. Various causal factors, such as high glucose, free fatty acids, inflammatory cytokines, and islet amyloid polypeptides, contribute to the impairment of β-cell function. Therefore, the maintenance of β-cell function is a logical approach for the treatment and prevention of diabetes. In this review, we provide an overview of the role of these risk factors in pancreatic β-cell loss and the associated mechanisms. A better understanding of the molecular mechanisms underlying pancreatic β-cell loss will provide an opportunity to identify novel therapeutic targets for type 2 diabetes. © The Author(s) 2023.-
dc.language영어-
dc.language.isoen-
dc.publisherSAGE Publications Inc.-
dc.relation.isPartOfEuropean Journal of Inflammation-
dc.titlePancreatic Beta-cell Dysfunction in Type 2 Diabetes-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid001061140200001-
dc.identifier.doi10.1177/1721727X231154152-
dc.identifier.bibliographicCitationEuropean Journal of Inflammation, v.21-
dc.description.isOpenAccessY-
dc.identifier.scopusid2-s2.0-85147226899-
dc.citation.titleEuropean Journal of Inflammation-
dc.citation.volume21-
dc.contributor.affiliatedAuthorKhin, Phyu Phyu-
dc.contributor.affiliatedAuthorJun, Hee-Sook-
dc.type.docTypeReview-
dc.subject.keywordAuthorglucotoxicity-
dc.subject.keywordAuthorlipotoxicity-
dc.subject.keywordAuthormechanisms-
dc.subject.keywordAuthorβ-cell death-
dc.subject.keywordAuthorβ-cell loss-
dc.subject.keywordPlusSTIMULATED INSULIN-SECRETION-
dc.subject.keywordPlusUNFOLDED PROTEIN RESPONSE-
dc.subject.keywordPlusFATTY-ACID PALMITATE-
dc.subject.keywordPlusELECTRICAL-ACTIVITY-
dc.subject.keywordPlusEUROPEAN SUBJECTS-
dc.subject.keywordPlusER STRESS-
dc.subject.keywordPlusAUTOPHAGY-
dc.subject.keywordPlusGLUCOSE-
dc.subject.keywordPlusMASS-
dc.subject.keywordPlusAPOPTOSIS-
dc.relation.journalResearchAreaImmunology-
dc.relation.journalWebOfScienceCategoryImmunology-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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