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The changes in the rat parotid glands following total parenteral nutrition and pancreatico-biliary diversion are not mediated by cholecystokinin

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Summary

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 pancreactico-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 threefold 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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References

  1. Young JA, Cook DI, van Lennep EW, Roberts M. Secretion of the major salivary glands, inPhysiology of the Gastrointestinal Tract, vol. 7, Johnson LR, ed., Raven, New York, 1987: pp. 73–815.

    Google Scholar 

  2. Skude G, Ihse I. Salivary amylase in duodenal aspirates.Scand J Gastroenterol 1976; 11: 17–20.

    PubMed  CAS  Google Scholar 

  3. Lankisch PG, Otto J. Salivary isoamylase in duodenal aspirates.Dig Dis Sci 1986; 31: 1299–1302.

    Article  PubMed  CAS  Google Scholar 

  4. Axelson J, Hakanson R, Ihse I, Lija I, JRehfeld JF, Sundler F. Effects of endogenous cholecystokinin and of infusion with the cholecystokinin antagonist L-364,718 on pancreatic and gastro-intestinal growth.Scand J Gastroenterol 1990; 25: 471–480.

    Article  PubMed  CAS  Google Scholar 

  5. Saikatsu S, Ikeno K, Hanada Y, Ikeno T. Intravenous injection of cerulein or cholecystokinin increases the parotid-type amylase in the serum of rats. Shika Kiso Igakkai Zasshi 1989; 31: 592–596.

    PubMed  CAS  Google Scholar 

  6. Grimmel K, Rossbach G, Kasper H. Amylase activity of parotid saliva in acute and chronic pancreatitis.Acta Hepatogastroenterol 1976; 23: 334–344.

    CAS  Google Scholar 

  7. Hirano T, Manabe T, Tobe T. Cellular alterations of parotid gland of rats with acute pancreatitis induced by cerulein.Int J Pancreatol 1991; 10: 217–227.

    PubMed  CAS  Google Scholar 

  8. Miazza BM, Turberg Y, Guillaume P, Hahne W, Chayvialle JA, Loizeau E. Mechanism of pancreatic growth induced by pancreatico-biliary diversion in the rat.Scand J Gastroenterol 1985; 20: 75–83.

    Article  Google Scholar 

  9. Fölsch UR, Cantor P, Wilms HM, Schafmayer A, Becker HD, Creutzfeldt W. Role of cholecystokinin in the negative feedback control of pancreatic enzyme secretion in conscious rats.Gastroenterology, 1987; 92: 449–458.

    PubMed  Google Scholar 

  10. Hughes CA, Breuer RS, Ducker DA, Hatoff DE, Dowling RH. The effect of cholecystokinin and secretin on intestinal and pancreatic structure and function, inMechanisms of Intestinal Adaptation, Robinson JWL, Dowling RH, Riecken EO, eds., MTP, Lancaster, 1981: pp. 435–450.

    Google Scholar 

  11. Miazza BM, van Hung L, Vaja S, Dowling RH. Pancreatic hyperplasia after pancreatico biliary diversion (PBD) in orally and parenterally fed rats, inMechanisms of Intestinal Adaptation, Robinson JWL, Dowling RH, Riecken EO, eds., MTP, Lancaster, 1981: pp. 481–490.

    Google Scholar 

  12. Nylander AG, Chen D, Ihse I, Rehfeld JF, Håkanson R. Pancreatic atrophy in rats produced by the cholecystokinin-A receptor antagonist devazepide.Scand J Gastroenterol 1992; 27: 743–747.

    Article  PubMed  CAS  Google Scholar 

  13. Solomon TE, Yamada T, Elashoff J, Wood J, Beglinger C. Bioactivity of cholecystokinin analogues: CCK-8 is not more potent than CCK-33.Am J Physiol 1984; 253: 4016–4021.

    Google Scholar 

  14. Ohlsson B, Axelson J, Sternby B, Rehfeld JF, Ihse I. Time course of the pancreatic changes following long-term stimulation or inhibition of the CCK-A receptor.Int J Pancreatol 1995; 18: 59–66.

    PubMed  CAS  Google Scholar 

  15. Rehfeld JF. Immunochemical studies on cholecystokinin. I. Development of sequence-specific radioimmunoassays for porcine triacontratriapeptide cholecystokinin.J Biol Chem 1978; 253: 4016–4021.

    PubMed  CAS  Google Scholar 

  16. Cantor P. Evaluation of a radioimmunoassay for cholecystokinin in human plasma.Scand J Lab Invest 1986; 46: 213–221.

    Article  CAS  Google Scholar 

  17. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the folin phenol reagent.J Biol Chem 1951; 193: 265–275.

    PubMed  CAS  Google Scholar 

  18. Dahlqvist A. A method for the determination of amylase in intestinal content.Scand J Clin Lab Invest 1962; 14: 145–151.

    Article  PubMed  CAS  Google Scholar 

  19. Nagy I, Pap A, Varró V. Time-course of changes in pancreatic size and enzyme composition in rats during starvation.Int J Pancreatol 1989; 5: 35–45.

    PubMed  CAS  Google Scholar 

  20. Iovanna JL, Dusetti NJ, Cadenas MB, Mallmann MC, Calco EL. Changes in pancreatic trophism and gene expression during a prolonged fasting period in rats.Int J Pancreatol 1991; 8: 177–186.

    Article  PubMed  CAS  Google Scholar 

  21. Koop I, Kimmich T, Koop H, Armold R. Effect of food deprivation on the function of intestinal cholecystokinin-producing cell in the rat.Digestion 1987; 38: 114–123.

    Article  PubMed  CAS  Google Scholar 

  22. Nealon WH, Upp JR, Jr., Alexander RW, Gomez G, Townsend CM, Thompson JC. Intravenous amino acids induce human gallbladder contraction.Am J Physiol 1990; 259: G173-G178.

    PubMed  CAS  Google Scholar 

  23. Adler G, Beglinger C, Braun U, Reinshagen M, Koop I, Schafmayer A, Rovati L, Arnold R. Interaction of the cholinergic system and cholecystokinin in the regulation of endogenous and exogenous stimulation of pancreatic secretion in humans.Gastroenterology 1991; 100: 537–543.

    PubMed  CAS  Google Scholar 

  24. Schneyer CA, Hall HD. Amylase and electrolyte changes after postganglionic parasympathectomy of parotid gland.Am J Physiol 1964; 207: 308–312.

    PubMed  CAS  Google Scholar 

  25. Jaworek J, Konturek SJ, Bielanski W, Bilski J, Hladij M. Release and binding of epidermal growth factor in the pancreas of rats.Int J Pancreatol 1992; 11: 19–17.

    Article  Google Scholar 

  26. Ino M, Ushiro K, Ino C, Yamashita T, Kumazawa T. Kinetics of epidermal growth factor in saliva.Acta Otolaryngol Suppl Stockh 1993; 500: 126–130.

    Article  PubMed  CAS  Google Scholar 

  27. Dembinski A, Gregory H, Konturek SJ, Polanski M. Trophic action of epidermal growth factor on the pancreas and gastrointestinal mucosa in rats.J Physiol 1982; 325: 35–42.

    PubMed  CAS  Google Scholar 

  28. Ohlsson B, Jansen C, Ihse I, Axelson J. Epidermal growth factor induces cell proliferation in mouse pancreas and salivary glands.Pancreas 1996, in press.

  29. Gasslander T, Chu M, Smeds S, Ihse I. Proliferative response of different exocrine pancreatic cells following surgical pancreatico-biliary diversion.Scand J Gastroenterol 1991; 26: 399–404.

    Article  PubMed  CAS  Google Scholar 

  30. Chu M, Borch K, Lilja I, Blomqvist, Rehfeld JF, Ihse I. Endogenous hypercholecystokininemia model in the hamster: trophic effect on the exocrine pancreas.Pancreas 1992; 7: 220–225.

    Article  PubMed  CAS  Google Scholar 

  31. Gasslander T, Axelson J, Håkanson R, Ihse I, Lilja I, Rehfeld JF. Cholecystokinin is responsible for growth of the pancreas following pancreatico-biliary diversion in rats.Scand J Gastroenterol 1990; 25: 1060–1065.

    Article  PubMed  CAS  Google Scholar 

  32. Schick J, Kern H, Scheele G. Hormonal stimulation in the exocrine pancreas results in coordinate and anticoordinate regulation of protein synthesis.J Cell Biol 1984; 99: 1569–1574.

    Article  PubMed  CAS  Google Scholar 

  33. Fölsch UR, Winckler K, Wormsley KG. Influence of repeated administration of cholecystokinin and secretin on the pancreas of the rat.Scand J Gastroenterol 1978; 13: 663–671.

    Article  PubMed  Google Scholar 

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Axelson, J., Fan, B.G., Ohlsson, B. et al. The changes in the rat parotid glands following total parenteral nutrition and pancreatico-biliary diversion are not mediated by cholecystokinin. Int J Pancreatol 20, 109–118 (1996). https://doi.org/10.1007/BF02825509

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  • DOI: https://doi.org/10.1007/BF02825509

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