Open AccessAttenuation of Endocrine‐Exocrine Pancreatic Communication in Type 2 Diabetes: Pancreatic Extracellular Matrix Ultrastructural Abnormalities
Author(s) -
Hayden Melvin R.,
Patel Kamlesh,
Habibi Javad,
Gupta Deepa,
Tekwani Seema S.,
WhaleyConnell Adam,
Sowers James R.
Publication year - 2008
Publication title -
journal of the cardiometabolic syndrome
Language(s) - English
Resource type - Journals
eISSN - 1559-4572
pISSN - 1559-4564
DOI - 10.1111/j.1559-4572.2008.00024.x
Subject(s) - pancreas , extracellular matrix , islet , endocrinology , medicine , enteroendocrine cell , endocrine system , pathology , microbiology and biotechnology , biology , diabetes mellitus , hormone
Ultrastructural observations reveal a continuous interstitial matrix connection between the endocrine and exocrine pancreas, which is lost due to fibrosis in rodent models and humans with type 2 diabetes mellitus (T2DM). Widening of the islet‐exocrine interface appears to result in loss of desmosomes and adherens junctions between islet and acinar cells and is associated with hypercellularity consisting of pericytes and inflammatory cells in T2DM pancreatic tissue. Organized fibrillar collagen was closely associated with pericytes, which are known to differentiate into myofibroblasts—pancreatic stellate cells. Of importance, some pericyte cellular processes traverse both the connecting islet‐exocrine interface and the endoacinar interstitium of the exocrine pancreas. Loss of cellular paracrine communication and extracellular matrix remodeling fibrosis in young animal models and humans may result in a dysfunctional insulino‐acinar‐ductal–incretin gut hormone axis, resulting in pancreatic insufficiency and glucagon‐like peptide deficiency, which are known to exist in prediabetes and overt T2DM in humans.