SEQUENTIAL METABOLIC STUDIES OF PANCREAS ALLOGRAFT FUNCTION IN TYPE-1 DIABETIC RECIPIENTS

被引:11
作者
COTTRELL, DA [1 ]
HENRY, ML [1 ]
ODORISIO, TM [1 ]
TESI, RJ [1 ]
FERGUSON, RM [1 ]
OSEI, K [1 ]
机构
[1] OHIO STATE UNIV HOSP,DEPT MED,COLUMBUS,OH 43210
关键词
PANCREAS TRANSPLANTATION; ALLOGRAFT REJECTION; PHASES OF INSULIN SECRETION; BETA-CELL FUNCTION; HYPERINSULINEMIA;
D O I
10.1111/j.1464-5491.1992.tb01814.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We have previously shown that the loss of acute first phase insulin secretion precedes pancreas allograft rejection and development of glucose intolerance in Type 1 diabetic patients. In order to examine whether there is a progressive loss of phases of insulin secretion and beta-cell function in technically successful pancreas transplants during the first year, we measured glucose, insulin, and C-peptide responses to physiological (mixed meal) and pharmacological (IV glucose and IV glucagon) stimulation in 27 glucose-tolerant, insulin-independent allograft recipients af 3, 6, and 12 months. Mean +/- SE fasting serum glucose levels were normalized throughout the study period. Postprandial serum glucose profiles tended to increase by 12 months compared to 3 and 6 months, although peak glucose levels were not statistically different. Following pancreas transplantation, basal serum insulin levels were high at 3 months (163 +/- 17 pM), 6 months (165 +/- 22 pM), and 12 months (248 +/- 54 pM, p = NS) in the Type 1 diabetic pancreas allograft recipients when compared to normal (25 +/- 3 pM). We observed slight elevations in postprandial insulin and C-peptide profiles at 12 months compared to 3 and 6 months. Following IV glucose and glucagon stimulation, serum insulin and C-peptide levels as well as phases of insulin release did not differ over the 12-month study period. Similarly, the glucose decay constant (K(G)) was nearly identical at 3, 6, and 12 months. In summary, 1 year following successful whole cadaveric, heterotopic pancreas transplantation in Type 1 diabetic recipients, fasting serum glucose remains normalized, while postprandial glucose tends to rise. This alteration in post-mixed meal glucose tolerance is achieved at the expense of elevated basal and post-stimulation insulin and C-peptide levels, suggesting worsening of the insulin-resistant state in such patients. The upward trend in glucose levels was observed only after mixed meal but not intravenous glucose stimulation. In addition, the acute first and second phase insulin release to both glucose and non-glucose stimuli, which are more sensitive markers for beta-cell dysfunction, were preserved 12 months following pancreas transplantation in Type 1 diabetic recipients.
引用
收藏
页码:438 / 443
页数:6
相关论文
共 17 条
[1]  
Sutherland DER, Moudry KC, Dunn DL, Goetz FC, Najarian JS., Pancreas‐transplant outcome in relation to presence or absence of end‐stage renal disease, timing of transplant, surgical technique, and donor source, Diabetes, 38, pp. 10-12, (1989)
[2]  
Sutherland DER, Moudry KC, Fryd DS., Results of pancreastransplant registry, Diabetes, 38, pp. 46-54, (1989)
[3]  
Henry ML, Osei K., O'Dorisio TM, Tesi RJ, Ferguson RM., Concomitant reduction in urinary amylase and acute first phase insulin release predict pancreatic allograft transplant rejection in type 1 diabetic recipients, Clinical Transplantation, 5, pp. 112-120, (1991)
[4]  
Sollinger HW, Strata RJ, Kalayogu M., Pirsch JD, Belzer FO., Pancreas transplantation with pancreatico‐cystostomy and quadruple immunosuppression, Surgery, 102, pp. 674-679, (1987)
[5]  
Kuzuya H., Beix PM, Horwitz DL, Steiner DF, Rubenstein AH., Determination of free and total insulin and C‐peptide in insulin‐treated diabetes, Diabetes, 26, pp. 22-29, (1971)
[6]  
Osei K., Henry ML, O'Dorisio TM, Tesi RJ, Sommer BG, Ferguson RM., Physiological and pharmacological stimulation of pancreatic islet hormone secretion in type 1 diabetic pancreas allograft recipients, Diabetes, 39, pp. 1235-1242, (1990)
[7]  
Ostman J., Bolinder J., Gunnarsson R., Brattstrom C., Tyden G., Wahren J., Et al., Effects of pancreas transplantation on metabolic and hormonal profiles in IDDM patients, Diabetes, 38, pp. 88-93, (1989)
[8]  
Robertson RP, Abid M., Sutherland D., Diem P., Glucose homeostasis and insulin secretion in human recipients of pancreas transplantation, Diabetes, 38, pp. 97-98, (1989)
[9]  
Diem P., Abid M., Redmon B., Sutherland D., Robertson RP., Systemic venous drainage of pancreas allograft as independent cause of hyperinsulinemia in type 1 diabetic recipients, Diabetes, 39, pp. 534-540, (1990)
[10]  
Rizza R., Mandarino L., Genest J., Baker B., Gerich J., Production of insulin resistance by hyperinsulinemia in man, Diabetologia, 28, pp. 70-75, (1985)