EYES2023 ESE Young Endocrinologists and Scientists (EYES) 2023 Oral communication 7: Diabetes, Obesity and Metabolism (7 abstracts)
Effects of chronic pancreatitis in beta-cell function and incretin secretion
Gea Ciccarelli 1 , Gianfranco Di Giuseppe 2 , Laura Soldovieri 2 , Michela Brunetti 2 , Umberto Capece 2 , Simona Moffa 2 , Francesca Cinti 2 , Andrea Giaccari 2 & Teresa Mezza 2
1Fondazione Policlinico Universitario A. Gemelli, Endocrinologia e Diabetologia, Rome, Italy; 2Fondazione Policlinico Universitario A. Gemelli, Rome, Italy.
Background: Chronic pancreatitis (CP) is the most frequent cause of diabetes of the exocrine pancreas (DEP). Although the specific alterations of DEP are not completely understood, individuals with DEP are considered affected by pancreatic endocrine insufficiency and treated with insulin. To investigate the functional alterations of DEP, we evaluated differences in glucose metabolism in patients with and without CP, classified according to their glucose tolerance (NGT, IGT, DM).
Methods: We recruited 50 patients with CP and 96 individuals without CP (NCP). All participants underwent OGTT, hyperglycemic clamp (HC), hyperinsulinemic euglycemic clamp and mixed meal test (MMT) with measurement of GLP-1 and glucagon. Basal insulin secretion rate (ISR), total ISR, rate secretion and β-cell glucose sensitivity (RS and GS) were estimated by mathematical models from OGTT, MMT and HC.
Results: Comparing individuals classified into NGT, IGT or DM based on OGTT-derived glucose tolerance, we found no differences in beta-cell function derived by OGTT and MMT. GLP-1 and glucagon secretion during MMT was not significantly different in the two groups. Of note, we found that insulin secretion after arginine stimulus in HC, an indirect measure of beta-cell mass, is reduced only in diabetic patients with CP compared to diabetic patients without CP (P=0.023). No difference was found in insulin sensitivity evaluated as glucose uptake at hyperinsulinemic euglycemic clamp.
Conclusion: At equivalent levels of glucose tolerance, patients with CP had similar beta-cell function and GLP-1 and glucagon secretion to individuals without CP. People with DEP have a lower beta-cell response to a maximus stimulus than patients with DM without CP, but analogous residual beta-cell function, so they could benefit from other therapies apart from insulin. Future studies are warranted to investigate differences in beta-cell function decline between type 2 diabetes mellitus and DEP.
Volume 93
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Endocrine Abstracts
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