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β-cell dysfunction rather than insulin resistance is the main contributing factor for the development of postrenal transplantation diabetes mellitus

DC FieldValueLanguage
dc.contributor.author이현철-
dc.contributor.author임승길-
dc.contributor.author차봉수-
dc.contributor.author최규헌-
dc.contributor.author강신욱-
dc.contributor.author안철우-
dc.date.accessioned2016-02-19T10:59:49Z-
dc.date.available2016-02-19T10:59:49Z-
dc.date.issued2001-
dc.identifier.issn0041-1337-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/142160-
dc.description.abstractBackground. Our study was undertaken to investigate the pathogenesisand possible risk factors for postrenal transplantation diabetes mellitus(PTDM). Methods. We recruited 114 patients with normal glucose tolerance(NGT) and performed both 75-g oral glucose tolerance tests (OGTT) and shortinsulin tolerance tests 1 week before and 9–12 months aftertransplantation. Results. The subjects were classified into three groups by WorldHealth Organization criteria on the basis of OGTT after transplantation: (a)36 (31.6%) subjects with normal glucose tolerance; (b) 51 (45.7%) subjectswith impaired glucose tolerance (IGT); and (c) 27 (23.7%) subjects withpostrenal transplantation diabetes mellitus. Dosages of steroid andcyclosporine were equivalent among the three groups. Before transplantation,the fasting and 2-hr plasma glucose and proinsulin/insulin (PI/I) ratios weresignificantly higher in the IGT and PTDM groups than in the NGT group, but theinsulin sensitivity index (ISI) was not significantly different among thethree groups. In addition, the area under the curve-insulin on OGTT wassignificantly lower in the PTDM group than in the NGT group. Aftertransplantation, however, the ISI was increased in all groups. Furthermore,the ISI and PI/I ratios revealed significantly higher values in the PTDM groupthan in the NGT group aftertransplantation. Conclusions. These results revealed that fasting and 2-hr plasma glucoselevels, as well as the proinsulin/insulin ratio before transplantation, areboth possible indicators of [beta]-cell dysfunction and may be predictors forthe development of PTDM. Furthermore, [beta]-cell dysfunction, rather thaninsulin resistance, was proven to be the main factor for the pathogenesis ofPTDM.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1417~1423-
dc.relation.isPartOfTRANSPLANTATION-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHBlood Glucose/analysis-
dc.subject.MESHDiabetes Mellitus/etiology*-
dc.subject.MESHFasting/blood-
dc.subject.MESHFemale-
dc.subject.MESHGlucose Tolerance Test-
dc.subject.MESHHumans-
dc.subject.MESHInsulin/physiology-
dc.subject.MESHInsulin Resistance*-
dc.subject.MESHIslets of Langerhans/physiopathology*-
dc.subject.MESHKidney Transplantation/adverse effects*-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHProinsulin/blood-
dc.titleβ-cell dysfunction rather than insulin resistance is the main contributing factor for the development of postrenal transplantation diabetes mellitus-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJ. H. NAM-
dc.contributor.googleauthorJ. I. MUN-
dc.contributor.googleauthorS. I. KIM-
dc.contributor.googleauthorS. W. KANG-
dc.contributor.googleauthorK. H. CHOI-
dc.contributor.googleauthorK. PARK-
dc.contributor.googleauthorC. W. AHN-
dc.contributor.googleauthorB. S. CHA-
dc.contributor.googleauthorY. D. SONG-
dc.contributor.googleauthorS. K. LIM-
dc.contributor.googleauthorK. R. KIM-
dc.contributor.googleauthorH. C. LEE-
dc.contributor.googleauthorK. B. HUH-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03301-
dc.contributor.localIdA03375-
dc.contributor.localIdA03996-
dc.contributor.localIdA04043-
dc.contributor.localIdA00053-
dc.contributor.localIdA02270-
dc.relation.journalcodeJ02754-
dc.identifier.eissn1534-6080-
dc.identifier.pmid11391229-
dc.identifier.urlhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00007890-200105270-00011&LSLINK=80&D=ovft-
dc.contributor.alternativeNameLee, Hyun Chul-
dc.contributor.alternativeNameLim, Sung Kil-
dc.contributor.alternativeNameCha, Bong Soo-
dc.contributor.alternativeNameChoi, Kyu Hun-
dc.contributor.alternativeNameKang, Shin Wook-
dc.contributor.alternativeNameAhn, Chul Woo-
dc.contributor.affiliatedAuthorLee, Hyun Chul-
dc.contributor.affiliatedAuthorLim, Sung Kil-
dc.contributor.affiliatedAuthorCha, Bong Soo-
dc.contributor.affiliatedAuthorChoi, Kyu Hun-
dc.contributor.affiliatedAuthorKang, Shin Wook-
dc.contributor.affiliatedAuthorAhn, Chul Woo-
dc.rights.accessRightsnot free-
dc.citation.volume71-
dc.citation.number10-
dc.citation.startPage1417-
dc.citation.endPage1423-
dc.identifier.bibliographicCitationTRANSPLANTATION, Vol.71(10) : 1417-1423, 2001-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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