Artigo Acesso aberto Revisado por pares

β-Cell Function Following Human Islet Transplantation for Type 1 Diabetes

2005; American Diabetes Association; Volume: 54; Issue: 1 Linguagem: Inglês

10.2337/diabetes.54.1.100

ISSN

1939-327X

Autores

Michael R. Rickels, Mark H. Schutta, James F. Markmann, Clyde F. Barker, Ali Naji, Karen L. Teff,

Tópico(s)

Diabetes Management and Research

Resumo

Islet transplantation can provide metabolic stability for patients with type 1 diabetes; however, more than one donor pancreas is usually required to achieve insulin independence. To evaluate possible mechanistic defects underlying impaired graft function, we studied five subjects at 3 months and four subjects at 12 months following intraportal islet transplantation who had received comparable islet equivalents per kilogram (12,601 ± 1,732 vs. 14,384 ± 2,379, respectively). C-peptide responses, as measures of β-cell function, were significantly impaired in both transplant groups when compared with healthy control subjects (P < 0.05) after intravenous glucose (0.3 g/kg), an orally consumed meal (600 kcal), and intravenous arginine (5 g), with the greatest impairment to intravenous glucose and a greater impairment seen in the 12-month compared with the 3-month transplant group. A glucose-potentiated arginine test, performed only in insulin-independent transplant subjects (n = 5), demonstrated significant impairments in the glucose-potentiation slope (P < 0.05) and the maximal response to arginine (ARmax; P < 0.05), a measure of β-cell secretory capacity. Because ARmax provides an estimate of the functional β-cell mass, these results suggest that a low engrafted β-cell mass may account for the functional defects observed after islet transplantation.

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