Pancreatic islet reserve in type 1 diabetes

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by pancreatic islet beta cell loss and dysfunction resulting in insulin deficiency and hyperglycemia. During a presymptomatic phase of established beta cell autoimmunity, beta cell loss may first be evident through assessment of beta cell secretory capacity, a measure of functional beta cell mass. Reduction in pancreatic islet beta cell reserve eventually manifests as impaired first-phase insulin response to glucose and abnormal glucose tolerance, which progresses until the functional capacity for beta cell secretion can no longer meet the demand for insulin to control glycemia. A functional beta cell mass of similar to 25% of normal may be required to avoid symptomatic T1D but is already associated with dysregulated glucagon secretion. With symptomatic T1D, stimulated C-peptide levels >0.60 ng/mL (0.200 pmol/mL) indicate the presence of clinically meaningful residual beta cell function for contributing to glycemic control, although even higher residual C-peptide appears necessary for evidencing glucose-dependent islet beta and alpha cell function that may contribute to maintaining (near)normal glycemia. beta cell replacement by islet transplantation can restore a physiologic reserve capacity for insulin secretion, confirming thresholds for functional beta cell mass required for independence from insulin therapy.

Automated summary

Type 1 diabetes is characterized by loss and dysfunction of pancreatic islet beta cells, leading to insulin deficiency and hyperglycemia. Assessment of beta cell secretory capacity can detect the loss of beta cells during a presymptomatic phase of autoimmune attack. Islet transplantation can restore physiologic reserve capacity for insulin secretion.