[Frontiers in Bioscience 2, d271-282, June 1, 1997]
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THE ROLE OF LANGERHANS ISLETS IN PANCREATIC DUCTAL ADENOCARCINOMA
Parviz M. Pour

The UNMC/Eppley Cancer Center, University of Nebraska Medical Center, Omaha, NE

Received 5/6/97 Accepted 6/2/97

4.INTERACTION OF ENDOCRINE AND EXOCRINE PANCREAS

Bensley's observation (24) was confirmed in recent years in Syrian golden hamsters treated with N-nitrosobis(2-oxopropyl)amine (BOP), a potent pancreatic carcinogen in this species (29) and in guinea pigs treated with alloxan (30). In hamsters, the histologically invisible ductules surrounding some islets (periinsular ductules) and within the islets (intrainsular ductules) could be revealed in a few islets by the retrograde injection of India ink into the main pancreatic duct (31; Fig. 1). These rare intrainsular ductular structures were found by a stroke of luck at the ultrastructural level. These findings may explain how the pancreatic hormones find their way into the pancreatic ducts (28). Despite embryological recognition of the origin of islet and acinar cells from the primitive tubules (ductules), controversies have remained on the origin of new islet cells in the mature organ. Some hold the viewpoint that their origin was from the existing islets, and others claimed the ductular cells as the progenitor cells. The latter notion was recently supported by showing that ductules contain both islet b-cells and non b-precursor cells (32).


Fig. 1. Traces of india ink (black) in periinsular and intrainsular (arrow) ductules. H&E, X210.

There is also data implying that islets control the physiological function of the exocrine pancreas. It is generally accepted that islet hormones, including insulin, glucagon, and somatostatin, functionally affect the exocrine pancreas, possibly by both paracrine and endocrine pathways (26). In several disease states both endocrine and exocrine pancreas are affected. Infantile hyperinsulinemic hypoglycemia is a good example. In this disease, the characteristic focal or diffuse proliferation of islet cells (33) is often associated with proliferation of centroacinar cells and alteration of acinar cells. This response of all three cell components of the pancreas to certain pathological insults may be due to their functional dependency or reflect damage to pancreatic multipotent (stem) cells from which all pancreatic parenchymal cells arise.