PubMed · 5668796
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R O Wolf, L L Taylor. 1968. Isozyme demonstration technic.. https://pubmed.ncbi.nlm.nih.gov/5668796/
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BACKGROUND: Acinar cell inhibitors (eg, atropine) fail to ameliorate clinical and experimental acute pancreatitis. We hypothesized that amelioration of pancreatic acinar cell hyperstimulation after bile and pancreatic duct ligation is better with gut replacement of bile and pancreatic juice than with cholinergic- and cholecystokinin (CCK)-receptor blockade. METHODS: Using acinar cell amylase activity as an index of hyperstimulation, we studied 63 rats in two sets of experiments. Bile-pancreatic juice exclusion from gut--without (set one) and with (set two) bile and pancreatic duct obstruction--was treated with atropine and CCK-receptor antagonist L-364,718, or with enteral replacement of bile-pancreatic juice. RESULTS: In the set one experiment, acinar cell hyperstimulation after bile-pancreatic juice exclusion was reversed by combined L-364,718 and atropine pretreatment. In set two, acinar cell hyperstimulation after bile and pancreatic duct ligation was reversed by enteral bile and pancreatic juice replacement, but not by combined L-364,718 and atropine pretreatment. CONCLUSIONS: According to this experimental corollary of early gallstone impaction, prevention of acinar cell hyperstimulation after duct occlusion should be aimed at the source of the response to bile-pancreatic juice exclusion, namely, the gut, rather than at the target of the response, the pancreatic acinar cell.
We have generated transgenic mice overexpressing TGF-beta 1 in pancreatic beta cells. This resulted in massive fibrosis of the pancreas; in adult mice, most of the acini were replaced by fibrotic and adipose tissues. A conspicuous disorganization of the islets of Langerhans was also observed; however, the number of beta cells was not decreased and the mice were normoglycemic. Backcrossing to transgenic mice overexpressing TNF-alpha in their islet beta cells (which also remain normoglycemic, (1)) yielded double transgenics, most of which became diabetic by the age of 4 months; histological analysis revealed a dramatic decrease in insulin-containing beta cells.
Sorting between the regulated and the constitutive secretory pathway in exocrine cells is thought to involve aggregation of regulated secretory proteins. This study demonstrates that, unlike endocrine secretory proteins, exocrine secretory proteins, including amylase, do not undergo homotypic aggregation under the conditions found in the sorting organelles. Also, unlike other exocrine proteins, amylase does not aggregate with chondroitin sulfate. Since amylase exhibits heterotypic aggregation, the role of protein concentration in amylase sorting was tested in AR42J cells. Secretion was stimulated with substance P and cholecystokinin from both untreated and dexamethasone-treated cells, with more efficient stimulation from dexamethasone-treated cells. These results indicate that amylase sorting is enhanced when its expression is stimulated by dexamethasone treatment.