Impaired islet function and normal exocrine enzyme secretion occur with low inter-regional variation in type 1 diabetes

Cell Rep. 2024 Jun 25;43(6):114346. doi: 10.1016/j.celrep.2024.114346. Epub 2024 Jun 7.

Abstract

Histopathological heterogeneity in the human pancreas is well documented; however, functional evidence at the tissue level is scarce. Herein, we investigate in situ glucose-stimulated islet and carbachol-stimulated acinar cell secretion across the pancreas head (PH), body (PB), and tail (PT) regions in donors without diabetes (ND; n = 15), positive for one islet autoantibody (1AAb+; n = 7), and with type 1 diabetes (T1D; <14 months duration, n = 5). Insulin, glucagon, pancreatic amylase, lipase, and trypsinogen secretion along with 3D tissue morphometrical features are comparable across regions in ND. In T1D, insulin secretion and beta-cell volume are significantly reduced within all regions, while glucagon and enzymes are unaltered. Beta-cell volume is lower despite normal insulin secretion in 1AAb+, resulting in increased volume-adjusted insulin secretion versus ND. Islet and acinar cell secretion in 1AAb+ are consistent across the PH, PB, and PT. This study supports low inter-regional variation in pancreas slice function and, potentially, increased metabolic demand in 1AAb+.

Keywords: 3D morphometry; CP: Immunology; CP: Metabolism; exocrine pancreas enzymes; function; glucagon; human; insulin; pancreas regions; pancreas tissue slices; secretion; type 1 diabetes.

MeSH terms

  • Acinar Cells / metabolism
  • Acinar Cells / pathology
  • Adult
  • Amylases / metabolism
  • Autoantibodies / immunology
  • Diabetes Mellitus, Type 1* / metabolism
  • Diabetes Mellitus, Type 1* / pathology
  • Female
  • Glucagon / metabolism
  • Glucose / metabolism
  • Humans
  • Insulin Secretion / drug effects
  • Insulin* / metabolism
  • Insulin-Secreting Cells / metabolism
  • Insulin-Secreting Cells / pathology
  • Islets of Langerhans* / metabolism
  • Islets of Langerhans* / pathology
  • Male
  • Middle Aged

Substances

  • Insulin
  • Glucagon
  • Glucose
  • Autoantibodies
  • Amylases