The impact of impaired insulin release and insulin resistance on glucose intolerance after renal transplantation

被引:58
作者
Hjelmesæth, J [1 ]
Hagen, M [1 ]
Hartmann, A [1 ]
Midtvedt, K [1 ]
Egeland, T [1 ]
Jenssen, T [1 ]
机构
[1] Univ Oslo, Rikshosp, Dept Med, Nephrol Sect, N-0027 Oslo, Norway
关键词
glucose intolerance; insulin resistance; insulin secretion; post-transplant diabetes mellitus; prednisolone; renal transplantation;
D O I
10.1034/j.1399-0012.2002.02059.x
中图分类号
R61 [外科手术学];
学科分类号
摘要
The current knowledge of the pathogenesis of post-transplant glucose intolerance is sparse. This study was undertaken to assess the relative importance of insulin secretion (ISec) and insulin sensitivity ( IS) in the pathogenesis of post-transplant diabetes mellitus (PTDM), impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) after renal transplantation. An oral glucose tolerance test (OGTT) was performed in 167 non-diabetic recipients 10 wk after renal transplantation. Fasting, 1-h and 2-h insulin and glucose levels were used to estimate the insulin secretory response and IS. One year after transplantation 89 patients were re-examined with an OGTT including measurements of fasting and 2 h glucose. Ten weeks after transplantation the PTDM-patients had significantly lower ISec and IS than patients with IGT/IFG, who again had lower ISec and IS than those with normal glucose tolerance (NGT). One year later, a similar difference in baseline ISec was observed between the three groups, whereas baseline IS did not differ significantly. Patients who improved their glucose tolerance during the first year, were mainly characterized by a significantly greater baseline ISec, and they received a significantly higher median prednisolone dose at baseline with a subsequent larger dose reduction during the first year, than the patients who had their glucose tolerance unchanged or worsened. In conclusion, both impaired ISec and IS characterize patients with PTDM and IGT/IFG in the early course after renal transplantation. The presence of defects in insulin release, rather than insulin action, indicates a poor prognosis regarding later normalization of glucose tolerance.
引用
收藏
页码:389 / 396
页数:8
相关论文
共 29 条
[1]  
Andrews RC, 1999, CLIN SCI, V96, P513, DOI 10.1042/cs0960513
[2]   Restoration of early rise in plasma insulin levels improves the glucose tolerance of type 2 diabetic patients [J].
Bruttomesso, D ;
Pianta, A ;
Mari, A ;
Valerio, A ;
Marescotti, MC ;
Avogaro, A ;
Tiengo, A ;
Del Prato, S .
DIABETES, 1999, 48 (01) :99-105
[3]   INSULIN RESISTANCE AND INSULIN DEFICIENCY IN THE PATHOGENESIS OF POSTTRANSPLANTATION DIABETES IN MAN [J].
EKSTRAND, AV ;
ERIKSSON, JG ;
GRONHAGENRISKA, C ;
AHONEN, PJ ;
GROOP, LC .
TRANSPLANTATION, 1992, 53 (03) :563-568
[4]  
Gavin JR, 2000, DIABETES CARE, V23, pS4
[5]   The genetic basis of type 2 diabetes mellitus: Impaired insulin secretion versus impaired insulin sensitivity [J].
Gerich, JE .
ENDOCRINE REVIEWS, 1998, 19 (04) :491-503
[6]   Family history of diabetes in middle-aged Swedish men is a gender unrelated factor which associates with insulinopenia in newly diagnosed diabetic subjects [J].
Grill, V ;
Persson, G ;
Carlsson, S ;
Norman, A ;
Alvarsson, M ;
Östensson, CG ;
Svanström, L ;
Efendic, S .
DIABETOLOGIA, 1999, 42 (01) :15-23
[7]   IMPAIRED GLUCOSE-TOLERANCE IN THE UNITED-STATES POPULATION [J].
HARRIS, MI .
DIABETES CARE, 1989, 12 (07) :464-474
[8]  
Henriksen JE, 1997, DIABETOLOGIA, V40, P1439
[9]   Glucose intolerance after renal transplantation depends upon prednisolone dose and recipient age [J].
Hjelmesaeth, J ;
Hartmann, A ;
Kofstad, J ;
Stenstrom, J ;
Leivestad, T ;
Egeland, T ;
Fauchald, P .
TRANSPLANTATION, 1997, 64 (07) :979-983
[10]   Tapering off prednisolone and cyclosporin the first year after renal transplantation:: the effect on glucose tolerance [J].
Hjelmesæth, J ;
Hartmann, A ;
Kofstad, J ;
Egeland, T ;
Stenstrom, J ;
Fauchald, P .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2001, 16 (04) :829-835