Augmentation of secretagogue-induced amylase secretion in pancreatic acini of heat-exposed rats.
1. The effects of prolonged heat exposure on pancreatic exocrine secretion were investigated to evaluate the involvement of the insulin-pancreatic acinar axis. Rats were kept at 34 degrees C and a relative humidity of 40% for 2 weeks with or without insulin administration. Control rats were housed at the thermoneutral temperature of 25 degrees C. By using isolated acini, secretory function was examined at the cellular level. 2. Without insulin treatment, acinar amylase concentration, expressed per microgram of cellular protein, was increased by heat exposure, while trypsinogen concentration, expressed per microgram of acinar DNA, decreased. The ratio of acinar amylase to trypsinogen increased significantly from 2.82 to 5.69 by prolonged heat exposure. With insulin treatment, the heat-induced increase in amylase activity was lessened but the decrease in trypsinogen remained unchanged. The ratio was somewhat lessened to 4.66. 3. In acini from saline-treated rats, amylase release in response to varying concentrations of cholecystokinin octapeptide or carbamylcholine was significantly augmented by prolonged heat exposure. As a result, the dose-response curve shifted upwards. However, in acini from insulin-treated rats, the increase in secretory response was lessened, similar to the effect on acinar content. On the other hand, changes in trypsinogen release were not as notable as those in amylase release. The ratio of amylase to trypsinogen in pancreatic juice released by 100 pM-cholecystokinin octapeptide increased from 1.56 to 3.04 in saline-treated rats and from 1.60 to 2.34 in insulin-treated rats. 4. In heat-exposed, saline-treated rats the plasma concentrations of glucose and insulin were significantly elevated, while in insulin-treated rats these increases were lessened and the elevation of plasma insulin concentration was no longer significant. 5. It is suggested that heat exposure elevates resting plasma glucose concentration, probably because of decreased metabolic activity, which results in a concomitant rise in plasma insulin concentration. This hormonal change most likely is a major cause of augmentation of acinar amylase synthesis and of the resultant potentiation of stimulus-secretion coupling via an insulin-pancreatic acinar axis. Heat exposure modified pancreatic exocrine function in the opposite direction to what occurred in cold-exposed animals. It was confirmed that changes in pancreatic exocrine function via a modification of the insulin-pancreatic acinar axis can actually occur under normal physiological circumstances. From the nutritional point of view, this modification by ambient temperature should be taken into consideration.
Habara
Y
Y
Department of Physiology, Asahikawa Medical College, Japan.
D000681:Amylases / Q000378:metabolism*; D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D006358:Hot Temperature; D008297:Male; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D012844:Sincalide / Q000494:pharmacology*; D014362:Trypsinogen / Q000378:metabolism
D002217:Carbachol; D014362:Trypsinogen; D000681:Amylases; D012844:Sincalide