P-209 Poster of distinction

Incretin, glucagon and insulin levels in a patient with fasting hyperglycemia post islet cell transplant

C.R. Milner¹, D.J. Torpy², J.M. Wishart³, C.J. Drogemuller¹, D.M. Mohanasundaram¹, C. Mee¹, T. Radford¹, G.R. Russ¹, P.T. Coates^1
1 Royal Adelaide Hospital, Central Northern Adelaide Renal & Transplantation Service, Adelaide, Australia; ² Royal Adelaide Hospital, Department of Endocrinology and Metabolism, Adelaide, Australia; ³ Department of Medicine, University of Adelaide, Adelaide, Australia

Objective: Islet cell transplantation (ICT) may restore mean glycemia without exogenous insulin and eliminate hypoglycaemic episodes. Glucose regulation may not be entirely normal however, and fasting hyperglycaemia has been noted in some cases. Abnormal glucagon regulation after ICT has been reported. We sought to examine glucose regulation by frequent sampling of glucose and its regulatory hormones in a normally feeding patient exhibiting persistent fasting hyperglycemia. Methods: The islet transplant recipient had been insulin independent for 6 months. Blood tests of serial GLP-1, GIP, glucose, glucagon and insulin tests were performed over 24h, preprandial, and 1 and 2h post prandial, at bedtime and at 02:00. GLP-1, GIP and glucagon were assayed with RIA techniques, while the glucose and insulin were measured with standard biochemical assays.

Results: At each meal time the incretins rose 50-100% above their preprandial levels, while the insulin levels rose quickly 1h postprandially but quickly returned to base line levels within 2h. The glucose levels concomitantly rose 1h after the meal but reduced to preprandial levels within 2h. The glucagon levels rose slightly after each meal and remained elevated throughout the day.

Conclusions: The incretins, glucose and insulin acted in a similar manner to that of a normal individual. Glucagon levels were high-normal and did not suppress normally to food, probably contributing to the fasting hyperglycemia. A trial of metformin was unsuccessful. The results suggest a lack of normal regulation of glucagon following islet cell transplantation, consistent with measurements performed in these patients after induced hypoglycemia.

P-209 Poster of distinction

Incretin, glucagon and insulin levels in a patient with fasting hyperglycemia post islet cell transplant

C.R. Milner¹, D.J. Torpy², J.M. Wishart³, C.J. Drogemuller¹, D.M. Mohanasundaram¹, C. Mee¹, T. Radford¹, G.R. Russ¹, P.T. Coates^1
1 Royal Adelaide Hospital, Central Northern Adelaide Renal & Transplantation Service, Adelaide, Australia; ² Royal Adelaide Hospital, Department of Endocrinology and Metabolism, Adelaide, Australia; ³ Department of Medicine, University of Adelaide, Adelaide, Australia

Objective: Islet cell transplantation (ICT) may restore mean glycemia without exogenous insulin and eliminate hypoglycaemic episodes. Glucose regulation may not be entirely normal however, and fasting hyperglycaemia has been noted in some cases. Abnormal glucagon regulation after ICT has been reported. We sought to examine glucose regulation by frequent sampling of glucose and its regulatory hormones in a normally feeding patient exhibiting persistent fasting hyperglycemia. Methods: The islet transplant recipient had been insulin independent for 6 months. Blood tests of serial GLP-1, GIP, glucose, glucagon and insulin tests were performed over 24h, preprandial, and 1 and 2h post prandial, at bedtime and at 02:00. GLP-1, GIP and glucagon were assayed with RIA techniques, while the glucose and insulin were measured with standard biochemical assays.

Results: At each meal time the incretins rose 50-100% above their preprandial levels, while the insulin levels rose quickly 1h postprandially but quickly returned to base line levels within 2h. The glucose levels concomitantly rose 1h after the meal but reduced to preprandial levels within 2h. The glucagon levels rose slightly after each meal and remained elevated throughout the day.

Conclusions: The incretins, glucose and insulin acted in a similar manner to that of a normal individual. Glucagon levels were high-normal and did not suppress normally to food, probably contributing to the fasting hyperglycemia. A trial of metformin was unsuccessful. The results suggest a lack of normal regulation of glucagon following islet cell transplantation, consistent with measurements performed in these patients after induced hypoglycemia.