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Diabetes in the rat is associated with a reversible postreceptor defect in cholecystokinin action

Journal Article · · Gastroenterology; (United States)
OSTI ID:6310287

Diabetes in the rat is associated with a selective decrease in the sensitivity of pancreatic acini to the secretagogue cholecystokinin. In these animals the concentration of cholecystokinin-33 that maximally stimulates amylase release from isolated pancreatic acini shifts from 300 pM in normal animals to 1 nM in animals made diabetic with streptozotocin. To evaluate the role of the cholecystokinin receptor in this loss of sensitivity, specific 125I-cholecystokinin-33 binding to its receptors on acini was measured. When compared with controls, acini from diabetic rats bound more cholecystokinin at all hormone concentrations. In diabetes, the total cholecystokinin binding capacity of acini increased from 157 fmol/mg to 362 fmol/mg acinar protein. Moreover, the amount of cholecystokinin bound at a maximally stimulating cholecystokinin concentration increased fourfold from 11 to 44 fmol/mg acinar protein. When diabetes was reversed by treatment with insulin, both the altered secretory responses and the increased binding of 125I-cholecystokinin returned to normal. These data indicate, therefore, that the decreased sensitivity of pancreatic acini from diabetic rats is due to an impaired ability of receptor bound cholecystokinin to initiate its cellular response.

Research Organization:
Cell Biology Research Laboratory, Harold Brunn Institute, Mount Zion Hospital and Medical Center, San Francisco, California
OSTI ID:
6310287
Journal Information:
Gastroenterology; (United States), Journal Name: Gastroenterology; (United States) Vol. 87:4; ISSN GASTA
Country of Publication:
United States
Language:
English