Involvement of Cellular Calcium in Exocrine Pancreatic Insufficiency during Streptozotocin-Induced Diabetes Mellitus

• Published in: Archives of physiology and biochemistry Vol. 109; no. 3; pp. 252 - 259
• Main Authors: Singh, J., Yago, M. D., Adeghate, E.
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01-07-2001; Taylor & Francis
• Subjects: Amylases - analysis; Amylases - secretion; Animals; Calcium - metabolism; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - metabolism; Electric Stimulation; Exocrine Pancreatic Insufficiency - etiology; Exocrine Pancreatic Insufficiency - metabolism; Female; Fluorescent Dyes; Fura-2; Glucagon - pharmacology; Insulin - pharmacology; Islets of Langerhans - metabolism; Islets of Langerhans - secretion; Rats; Rats, Sprague-Dawley; Sincalide - pharmacology; Somatostatin - pharmacology
• ISSN: 1381-3455; 1744-4160
• DOI: 10.1076/apab.109.3.252.11585

This study investigates the effects of the islet hormones insulin (Ins), glucagon (Glu), and somatostatin (Som) with nerve stimulation (EFS) acetylcholine (ACh) and cholecytokinin-octapeptide (CCK-8) on amylase secretion and intracellular free calcium concentration [Ca2+]i in the pancreas of age-matched control and diabetic rats. Either Ins, Glu or Som elicited small increases in amylase secretion from the pancreas of age-matched control animals compared to a much larger increase in amylase secretion with either EFS, ACh or CCK-8. Combining the islet hormones with either EFS, ACh or CCK-8 resulted in marked potentiation of amylase output. In the diabetic pancreas, the islet hormones had no effect on amylase secretion compared to diabetic control. Moreover, either EFS, ACh or CCK-8 evoked a much smaller increase in amylase output compared to age-matched control. In addition, the islet hormones failed to potentiate the secretory effects of either EFS, ACh or CCK-8. In fura-2 loaded acinar cells from age-matched control pancreas either Ins or Glu elicited a small increase in [Ca2+]i whereas Som had no effect. Both ACh and CCK-8 evoked large increases in [Ca2+]i compared to control. Combining either Ins, Glu or Som with either ACh or CCK-8 resulted in a marked elevation in [Ca2+]i compared to the responses obtained with either the islet hormones, ACh or CCK-8 alone. In diabetic fura-2 loaded pancreatic acinar cells, the islet hormones had no effect on [Ca2+]i compared to control and moreover, the responses were much smaller than those obtained in acinar cells from age-matched control. Both ACh and CCK-8 induced large increases in [Ca2+]i in diabetic acinar cells. However, combining the islet hormones with either ACh or CCK-8 failed to enhance [Ca2+]i compared to the reponses obtained in acinar cells from age-matched control. The results suggests that [Ca2+]i homeostasis is deranged during diabetes mellitus and this in turn is probably associated with reduced pancreatic amylase secretion.