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- Axelson, Jan, et al.
(författare)
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The changes in the rat parotid glands following total parenteral nutrition and pancreatico-biliary diversion are not mediated by cholecystokinin
- 1996
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Ingår i: International Journal of Pancreatology. - 0169-4197. ; 20:2, s. 109-118
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Tidskriftsartikel (refereegranskat)abstract
- CONCLUSIONS: The results of the present study suggest that the pancreas and parotid glands both respond with hypoplasia during absence of food in the digestive tract and with hyperplasia following pancreatico-biliary diversion (PBD). Factors other than cholecystokinin (CCK) are, however, involved in the effects on the parotid glands, since infusion of CCK-8S and devazepide was without influence. BACKGROUND AND AIM: Total parenteral nutrition (TPN) causes reduced pancreatic weight, whereas PBD evokes hyperCCKemia and enlargement of the rat pancreas. The pancreas and parotid glands have in part similar morphology and function. Therefore, we studied the possible presence of alterations also in the parotid glands during TPN, after PBD and during infusion of sulfated cholecystokinin (CCK-8S) and the CCK-A receptor antagonist devazepide, respectively. MATERIALS AND RESULTS: Rats either received TPN for 7 d, or were kept under otherwise identical conditions with free access to food and water. TPN markedly reduced both pancreatic and parotid wet weight and thereby also the protein and amylase contents, and pancreatic DNA content was decreased. There was a significant correlation between the pancreas and parotid glands when comparing these parameters. The concentration of plasma CCK was unaffected by TPN. PBD caused a sevenfold increase in plasma CCK and a three fold increase in the pancreatic weight compared to control rats 28 d after the operation. The protein and DNA contents in the pancreas were found to be increased. The parotid glands increased twofold in weight, but their protein and amylase contents were not affected. There was a significant correlation between the pancreas and parotid glands when comparing weight, and protein and amylase concentrations. Infusion of CCK-8S during 28 d caused a marked increase in pancreatic wet wt and protein and DNA contents. The CCK-A receptor antagonist devazepide induced a reduction in protein and DNA contents in the pancreas. The parotid glands were not affected by either treatment. No effect on the labeling index of serous and ductal cells of the parotid gland was seen at 36 h, 3, 7, and 28 d of infusion with CCK-8S or devazepide.
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| 2. |
- Roth, Bengt, et al.
(författare)
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Lipid deposition in Kupffer cells after parenteral fat nutrition in rats: a biochemical and ultrastructural study
- 1996
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Ingår i: Intensive Care Medicine. - 0342-4642. ; 22:11, s. 1224-1231
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To study fat metabolism and evaluate lipid deposition in hepatocytes and Kupffer cells during parenteral nutrition (PN) with or without fat. DESIGN: 20 male Sprague-Dawley rats, divided into four groups, were investigated. Rats fed orally were used as a reference group and compared to three groups of rats receiving PN either without fat or with 33% of non-protein energy as fat or with 66% of non-protein energy as fat. The PN regimens were equicaloric and administered continuously via a jugular catheter for 7 days. INTERVENTIONS: After suffocation, blood was collected for determination of serum lipids. Epididymal fat and heart were collected for analysis of lipoprotein lipase activities, and pieces of liver were saved for analyses of liver triglyceride concentration and hepatic lipase activity. Light and electron microscopy were used for examination of lipid deposition in Kupffer cells. RESULTS: Directly after termination of parenteral feeding, the serum levels of triglycerides were similar in all PN groups, while the levels of non-high-density lipoprotein (HDL) cholesterol and non-HDL phospholipids were significantly increased in parallel with increased doses of fat. Lipid-free PN resulted in significantly less liver steatosis than high-fat PN. Lipid PN also resulted in downregulated hepatic lipase activity, signs of lipid accumulation in Kupffer cells and hepatocytes and an increased number of phagosomes in Kupffer cells. CONCLUSIONS: Fat vacuoles were found in Kupffer cells after lipid PN, although serum levels of triglycerides were not elevated and lipoprotein lipase activity were not depressed. The cells were distended by fat vacuoles after administration of PN solutions with a high fat concentration. Morphological signs of increased Kupffer cell activity were also found, suggesting that intravenous fat emulsions may activate macrophages.
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