PANCREATIC ENDOCRINE FUNCTION IN RECIPIENTS OF SEGMENTAL AND WHOLE PANCREAS TRANSPLANTATION

Citation
E. Christiansen et al., PANCREATIC ENDOCRINE FUNCTION IN RECIPIENTS OF SEGMENTAL AND WHOLE PANCREAS TRANSPLANTATION, The Journal of clinical endocrinology and metabolism, 81(11), 1996, pp. 3972-3979
Citations number
44
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
81
Issue
11
Year of publication
1996
Pages
3972 - 3979
Database
ISI
SICI code
0021-972X(1996)81:11<3972:PEFIRO>2.0.ZU;2-W
Abstract
To determine potential abnormalities in beta-cell function after pancr eas transplantation, the secretory capacity of the pancreatic grafts w as assessed by measuring the glucose-potentiating effect on arginine-i nduced insulin secretion in recipients of cadaveric segmental (SPx; n = 8) and whole organ pancreas grafts (WPx; n = 6) and compared to that in nondiabetic kidney transplant recipients (Kx; n = 6) and normal co ntrols (Ns; n = 7). alpha-Cell adaptation to increasing hyperglycemia and the glucagon response to arginine stimulation were also studied. T he secretory capacity of the beta-cell to arginine-induced (5 g L-argi nine) insulin secretion was measured at fasting plasma glucose and 15 and 30 mmol/L glucose. Insulin secretion was evaluated by the calculat ion of insulin secretion rates. Insulin sensitivity was markedly reduc ed in all three transplanted groups compared to that in normal subject s (P < 0.05). The prestimulation insulin secretion rate and maximal in sulin secretion rate in response to hyperglycemia and arginine were si gnificantly lower in SPx than in WPx, Kx, or Ns (P < 0.05). The increm ental amount of insulin secreted in response to arginine was reduced b y 40-70% in SPx depending on glycemia compared to that in all other gr oups (P < 0.05), among which there were no statistical differences. Bo th SPx and WPx demonstrated suppression of glucagon release in respons e to graded hyper glycemia, but failure to adequately suppress arginin e-induced glucagon release. In conclusion, recipients of cadaveric seg mental pancreas grafts display a markedly reduced maximal insulin secr etory reserve capacity. This impairment was primarily due to an insuff icient beta-cell mass. Taking the concomitant insulin resistance into account, recipients of a cadaver whole organ pancreas graft had an imp aired insulin secretory reserve capacity as well.