Hostname: page-component-586b7cd67f-g8jcs Total loading time: 0 Render date: 2024-11-29T07:59:33.906Z Has data issue: false hasContentIssue false
  • English
  • Français

Dietary effects on pancreatic lesions induced by excess arginine in rats

Published online by Cambridge University Press:  09 March 2007

Shigeyuki Takama  and
Yasuo Kishino
Shigeyuki Takama
Affiliation:
Department of Nutrition, School of Medicine, The University of Tokushima, Tokushima 770, Japan
Yasuo Kishino
Affiliation:
Department of Nutrition, School of Medicine, The University of Tokushima, Tokushima 770, Japan
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. The effect of nutrition on the incidence of pancreatic damage was studied. Injection of excess arginine was found to cause more massive necrosis of the acinar cells after 24 h in malnourished rats (those given 50 g casein/kg diet) than in well-nourished rats (those given 200 g casein/kg diet).

2. Ultrastructural examination showed that whorl formation of the endoplasmic reticulum, decreases in the number of zymogen granules and formation of vacuoles in the cytoplasm were more marked in rats given 50 g casein/kg diet. Degradation of zymogen granules within vacuoles in the damaged cells was frequently observed in rats given 200 g casein/kg diet.

3. Necrosis of adipose tissue was associated with pancreatic damage more frequently in rats given 200 g casein/kg diet; rats with large amounts of zymogen granules in the acinar cells showed particularly severe necrosis of adipose tissue. Rats given 50 g casein/kg diet did not show necrosis of adipose tissue.

4. These results indicate that in the malnourished state there were more marked arginine lesions of the pancreas in which to study cellular and histologic changes than in the well-nourished state and that the occurrence of necrosis of adipose tissue may be related to a high content of zymogen granules in the acinar cells before pancreatic damage.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 54 , Issue 1 , July 1985 , pp. 37 - 42
Copyright
Copyright © The Nutrition Society 1985

References

Greenbaum, L. M., Hirshkowitz, A. & Shoichet, I. (1959). Journal of Biological Chemistry 234, 2885–2890.CrossRefGoogle Scholar
Grossman, M. I., Greengard, H. & Ivy, A. C. (1942). American Journal of Physiology 138, 676–682.CrossRefGoogle Scholar
Herman, L. & Fitzgerald, P. J. (1962). Journal of Cell Biology 12, 277–296.CrossRefGoogle Scholar
Ibrahim, S. A., Sanders, H. & Thompson, R. H. S. (1964). Biochemical Journal 93, 588–594.CrossRefGoogle Scholar
Kishino, Y. & Kawamura, S. (1984). Virchows Archiv B Cell Pathology 47, 147–155.CrossRefGoogle Scholar
Lee, P. C., Nakashima, Y., Appert, H. E. & Howard, J. M. (1979). Surgery, Gynecology and Obstetrics 148, 39–44.Google Scholar
Magee, D. F. & White, T. T. (1958). American Journal of Physiology 193, 21–24.CrossRefGoogle Scholar
Maki, T., Kakizaki, G., Sato, T., Saito, Y., Suda, Y., Onuma, T. & Hayasaka, N. (1967). Tohoku Journal of Experimental Medicine 92, 301–309.CrossRefGoogle Scholar
Mizunuma, T., Kawamura, S. & Kishino, Y. (1984). Journal of Nutrition 114, 467–471.CrossRefGoogle Scholar
Neal, M. P. & Ellis, M. M. (1930). Southern Medical Journal 23, 313–320.CrossRefGoogle Scholar
O'Brien, J. S. (1967). Journal of Theoretical Biology 15, 307–324.CrossRefGoogle Scholar
Ouaqued, M., Saraux, B., Girard-Globa, A. & Bourdel, G. (1980). Journal of Nutrition 110, 2302–2309.CrossRefGoogle Scholar
Panabokké, R. G. (1958). Journal of Pathology and Bacteriology 75, 319–331.CrossRefGoogle Scholar
Sarles, H. (1973). Digestion 9, 389–403.CrossRefGoogle Scholar
Storck, G. (1971). Acta Chirurgica Scandinavica 417 (Suppl.), 1–36.Google Scholar
van Deenen, L. L. M. (1966). Annals of New York Academy of Sciences 137, 717–730.CrossRefGoogle Scholar