Influence of B-Cell Impairment on Pancreatic Acini in NOD Mice and Streptozotocin-Induced Diabetic Rats.

Abstract

Exocrine pancreatic function insufficiency, even of short duration, has been reported in juvenile-onset insulin dependent diabetic patients. To evaluate the status of pancreatic acini under decreased B-cell function, tissue insulin, amylase, chymotrypsinogen and trypsinogen in the pancreas were measured in streptozotocin-induced diabetic rats and non-obese diabetic mice in various conditions.In streptozotocin diabetic rats, a dissociation of three enzyme contents was demonstrated in the condition with discontinuation of insulin injection, i. e., a marked decrease in amylase, a significant increase in chymotrypsinogen, but no significant change in trypsinogen.This dissociation was markedly improved in the insulin-treated condition.In non-obese diabetic mice, these enzyme contents were not significantly changed although severe insulitis together with the marked decrease in insulin content was observed. These data show that the cessation of B-cell function alone does not cause insufficiency of exocrine pancreas.

Decreased insulin secretion and glucose clearance in exocrine pancreas‐insufficient pigs

“…Moreover, impaired β‐cell function may result in impaired function of the exocrine pancreas (Pierzynowski & Barej, ; Yokoyama et al . ; Hardt et al . ; Ewald et al .…”

“…For instance, insulin has been shown to pass through the exocrine acinar areas of the pancreas via a local portal circulation, in concentrations higher than those in the peripheral blood (Lifson et al 1985), and in doing so affects enzyme production, which is known as the halo phenomenon (Williams & Goldfine, 1985;Schönfeld et al 1994). Moreover, impaired β-cell function may result in impaired function of the exocrine pancreas (Pierzynowski & Barej, 1984;Yokoyama et al 1988;Hardt et al 2003;Ewald et al 2007;Czakó et al 2009).…”