Methods: Groups of female adult Wistar rats were fed with either standard rat chow or soya bean ad libitum for 7 days. Devazepide, a CCK antagonist (1mg/kg s.c. twice daily), Camostate, a trypsin inhibitor (200 mg/kg, i.g.) or propranolol, a β-adrenerg blocking agent (14mg/100ml drinking water) was used in combination with soya feeding. At the end of the experiments, animals were sacrificed, their pancreata as well as the parotid and submandibular glands were excised. Tissue weight, DNA content and at the propranolol treatment caspase 3/7 activity were determined. Values are given as mean ± S.D.
Results: Soya feeding resulted in increases of both pancreatic and parotid tissue weight and DNA content indicating that this treatment induces hypertrophy as well as hyperplasia in these glands. There was no changes in the submandibular gland. Devazepide blocked the pancreatic effect of soya but it did not inhibit the trophic action of soya feeding on the parotid gland. Camostate treatment increased pancreatic weight and DNA content but did not affect these values in the parotid glands. Propranolol treatment was without effect on pancreatic growth but inhibited parotid enlargement by 60%.
Conclusion: Our results suggest that endogenous CCK release has no determinant effect on the parotid hypertrophy/hyperplasia unlike on the pancreas. β-adrenergic effects play important roles in the parotid enlargement elicited by soya feeding.
Supported by: OTKA T-046511, ETT 247/2003-5