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KCI 후보 SCIE SCOPUS
신이식후 당뇨병의 발병원인에 있어서 인슐린 분비능과 저항성의 역할
The Role of β-cell Dysfunction and Insulin Resistance in the Development of Post - renal Transplantation Diabetes Mellitus
남재현(Jae Hyun Nam),이현철(Hyun Chul Lee),안철우(Churl Woo Ahn),문장일(Jang Il Mun),김순일(Soon Il Kim),박기일(Ki Il Park),송영득(Young Duk Song),임승길(Sung Kil Lim),김경래(Kyung Rae Kim),허갑범(Kap Bum Huh)
UCI I410-ECN-0102-2009-510-004775063
* 발행 기관의 요청으로 구매가 불가능한 자료입니다.

Background: Our study was undertaken to investigate the pathogenesis and possible risk factors for post-renal transplantation diabetes mellitus(PTDM). Methods: we recruited 114 patients with normal glucose tolerance, and performed the 75g oral glucose tolerance tests(OGTT) and the short insulin tolerance tests 1 week before and 9∼12 months after transplantation, respectively. Results: The subjects were classified into three groups on the basis of OGTT after transplantation by WHO criteria: 1) 36(31.6%) subjects with normal glucose tolerance; 2) 51(45.7%) subjects with impaired glucose tolerance; and 3) 27(23.7%) subjects with post-renal transplantation diabetes mellitus. Dosages of steroid and cyclosporin-A(CsA) were equivalent among the 3 groups. Before transplantation, the fasting and 2-h plasma glucose, and proinsulin/insulin(PI/I) ratios were significantly higher in the IGT and PTDM groups than in the NGT group, but insulin sensitivity index(ISI) was not different among 3 groups. In addition, the area under the curve(AUC)-insulin on OGTT was significantly lower in the PTDM group than in the NGT group. After transplantation, however, ISI was increased in all groups. Furthermore, the ISI and PI/I ratios revealed significantly higher values in the PTDM group than in the NGT group after transplantation. Conclusion: These results revealed that fasting and 2-h plasma glucose levels, as well as proinsulin/insulin ratio before transplantation, which may all be indicators of β-cell dysfunction, could be the predictors for the development of PTDM and β-cell dysfunction rather than insulin resistance was proved to be the main factor for the pathogenesis of PTDM(J Kor Diabetes Asso 485∼496, 2000).

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