OBJECTIVE: To comparatively analyze the ultrastructural changes in the submandibular and parotid glands and in the exocrine pancreas following diabetes induced by Streptozotocin exposure and the effects of fasting and insulin treatment on these alterations. METHODS: For experimental procedure, we included 48 Sprague-Dawley type rats in July 2001-March 2002 at Gazi University, Turkey. We divided the rats into 8 groups following the infusion of Streptozotocin. RESULTS: While the degeneration manifested itself as accumulation of secretions within the mucous cells in the submandibular gland, lipid droplets were absent, being replaced by vacuolar structures. The parotid gland and exocrine pancreas, having similar properties, were affected similarly. Diabetes-induced loss of granules was observed in the serous cells in both glands. There was diffuse lipid accumulation within these cells. Regarding granule content, we observed the most prominent degenerative changes in the parotid gland. While cellular loss was observed in neither the submandibular, nor the parotid gland, we noted presence of apoptotic cells was noted in the pancreas. State of fasting was found to cause alterations within the glands indicating increased activity. While insulin treatment was seen to restore the structure to normal in general in both of the 3 glands. CONCLUSION: This study demonstrated that both of the 3 glands are affected by diabetes and concomitant fasting, and this effect manifests itself via the granule content.
OBJECTIVE: To comparatively analyze the ultrastructural changes in the submandibular and parotid glands and in the exocrine pancreas following diabetes induced by Streptozotocin exposure and the effects of fasting and insulin treatment on these alterations. METHODS: For experimental procedure, we included 48 Sprague-Dawley type rats in July 2001-March 2002 at Gazi University, Turkey. We divided the rats into 8 groups following the infusion of Streptozotocin. RESULTS: While the degeneration manifested itself as accumulation of secretions within the mucous cells in the submandibular gland, lipid droplets were absent, being replaced by vacuolar structures. The parotid gland and exocrine pancreas, having similar properties, were affected similarly. Diabetes-induced loss of granules was observed in the serous cells in both glands. There was diffuse lipid accumulation within these cells. Regarding granule content, we observed the most prominent degenerative changes in the parotid gland. While cellular loss was observed in neither the submandibular, nor the parotid gland, we noted presence of apoptotic cells was noted in the pancreas. State of fasting was found to cause alterations within the glands indicating increased activity. While insulin treatment was seen to restore the structure to normal in general in both of the 3 glands. CONCLUSION: This study demonstrated that both of the 3 glands are affected by diabetes and concomitant fasting, and this effect manifests itself via the granule content.