Endocrine Abstracts

Glucagon-like peptide-1 (GLP-1) is known to stimulate insulin and somatostatin secretion in pancreatic islet cells. The exogenous somatostatin inhibits insulin secretion, but GLP-1 increases insulin secretion in spite of stimulating somatostatin secretion from δ-cell. So, we investigated whether there exists a time difference of insulin and somatostatin secretion inside the islets after GLP-1 stimulation or insulin secretion depends on secreted GLP-1 or somatostatin concentration inside the islets. We isolated pancreatic islets from five 8-week-old Sprague–Dawley rats by collagenase digestion. The islets were incubated in RPMI-1640 medium before experiments. In vitro, insulin and somatostatin measured at 5, 10, and 30 min depending on glucose (2.7, 5.5, and 16.7 mM as hypo-, normo-, and hyperglycaemic condition respectively) and GLP-1 concentrations (0, 0.1, and 10 ng/ml) from culture media using ELISA kit. Each well contained 30 islets/well. Insulin secretion showed continuously increased by time and GLP-1 concentration at any glucose concentration. Somatostatin secretion was increased significantly 10 min later after GLP-1 administration at hypo- and normoglycaemia. However, in hyperglycaemia, insulin secretion showed the same pattern compared with the other glycaemic conditions, but somatostatin was maximally stimulated until 10 min and decreased after that without GLP-1 administration. Adding the GLP-1, somatostatin was increased continuously until 30 min. This suggested hyperglycaemic condition itself might need more insulin secretion in the β-cell than somatostatin secretion in δ-cell. Therefore, we observed time lag of intraislet somatostatin secretion was existed with GLP-1 stimulation. We observed GLP-1 induced insulin secretion is noted earlier in β-cell than somatostatin secretion in δ-cell of rat islets. Hyperglycaemic condition might primarily secrete insulin even though and inhibit somatostatin secretion inside the islets.