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Hexose absorption from jejunal loops in situ in zinc-deficient and Zn-supplemented rats

Published online by Cambridge University Press:  09 March 2007

Susan Southon
Affiliation:
AFRC Food Research Institute Norwich, Colney Lane, Norwich NR4 7UA
Jennifer M. Gee
Affiliation:
AFRC Food Research Institute Norwich, Colney Lane, Norwich NR4 7UA
I. T. Johnson
Affiliation:
AFRC Food Research Institute Norwich, Colney Lane, Norwich NR4 7UA
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Abstract

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1. Immature, male Wistar rats were given a low-zinc semi-synthetic diet (2 mg Zn/kg) for 22–28 d. Control groups received a similar diet supplemented with 58 mg Zn/kg either ad lib., or in amounts matched to the consumption of the Zn-deficient group. There was a rapid onset of reduced food consumption and growth retardation in the Zn-depleted animals.

2. Serosal surface area of small intestines taken from Zn-deficient rats was significantly reduced compared with that of control animals. Villi, dissected from samples of proximal jejunum, were markedly smaller than those of control rats and were present in greater numbers per unit area of serosa.

3. Luminal loss of galactose from jejunal loops in situ was significantly greater in the Zn-deficient rats compared with controls when expressed in terms of unit dry weight of intestine and serosal or villous surface area. Since only a small proportion of the total galactose remained in the mucosal tissue and associated extracellular space, this loss could only be accounted for by an increased efficiency of net transepithelial transport. Differences in total galactose absorption per unit length of jejunum were not so marked.

4. This intestinal adaptation to Zn-deficiency allows the maintenance of normal, and possibly increased, rates of hexose transfer into the body of animals exhibiting severe growth retardation, reduced food utilization and abnormal glucose metabolism.

Type
Papers on General Nutrition
Copyright
Copyright © The Nutrition Society 1986

References

REFERENCES

Boquist, L. & Lernmark, A. (1969). Acta Pathologica et Microbiologica Scandinavica 6, 215228.CrossRefGoogle Scholar
Brown, E. D., Penhos, J. C., Recant, L. & Smikthy, J. C. Jr (1975). Proceedings of the Society for Experimental Biology and Medicine 150, 557560.CrossRefGoogle Scholar
Ghishan, F. K. (1984). Journal of Pediatric Gastroenterology and Nutrition 3, 608612.Google Scholar
Hendricks, D. G. & Mahoney, A. W. (1972). Journal of Nutrition 102, 10791084.CrossRefGoogle Scholar
Hove, E., Elvehjem, C. A. & Hart, E. B. (1937). American Journal of Physiology 119, 768775.CrossRefGoogle Scholar
Huber, A. M. & Gershoff, S. N. (1973). Journal of Nutrition 103, 17391744.CrossRefGoogle Scholar
Levin, R. J. (1967). British Medical Bulletin 23, 209212.CrossRefGoogle Scholar
Lorenz-Meyer, H., Thiel, F., Menge, H., Gottesburen, H. & Ricken, E. O. (1977). Research in Experimental Medicine 170, 8999.CrossRefGoogle Scholar
Quarterman, J. & Florence, E. (1972). British Journal of Nutrition 28, 7579.CrossRefGoogle Scholar
Quarterman, J., Mills, C. F. & Humphries, W. R. (1966). Biochemical and Biophysical Research Communications 25, 354359.CrossRefGoogle Scholar
Reeves, P. G. & O'Dell, B. L. (1983). British Journal of Nutrition 49, 441452.CrossRefGoogle Scholar
Southon, S., Gee, J. M. & Johnson, I. T. (1984). British Journal of Nutrition 52, 371380.CrossRefGoogle Scholar
Southon, S., Livesey, G., Gee, J. M. & Johnson, I. T. (1985). British Journal of Nutrition 53, 595603CrossRefGoogle Scholar