Hostname: page-component-78c5997874-lj6df Total loading time: 0 Render date: 2024-11-05T10:40:00.128Z Has data issue: false hasContentIssue false
  • English
  • Français

Effect of reduced dietary zinc intake on carbohydrate and Zn metabolism in the genetically diabetic mouse (C57BL/KsJ db+/db+)

Published online by Cambridge University Press:  09 March 2007

Susan Southon ,
Z. Kechrid ,
A. J. A. Wright  and
Susan J. Fairweather-Tait
Susan Southon
Affiliation:
AFRC Institute of Food Research Norwich, Colney Lane, Norwich NR4 7UA
Z. Kechrid
Affiliation:
AFRC Institute of Food Research Norwich, Colney Lane, Norwich NR4 7UA
Susan J. Fairweather-Tait
Affiliation:
AFRC Institute of Food Research Norwich, Colney Lane, Norwich NR4 7UA
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. Male, 4–5-week-old, genetically diabetic mice (C57BL/KsJ db/db) and non-diabetic heterozygote litter-mates (C57BL/KsJ db/+)were fed on a diet containing 1 mg zinc/kg (low-Zn groups) or 54 mg Zn/kg (control groups) for 27 d. Food intakes and body-weight gain were recorded regularly. On day 28, after an overnight fast, animals were killed and blood glucose and insulin concentrations, liver glycogen, and femur and pancreatic Zn concentrations were determined.

2. The consumption of the low-Zn diet had only a minimal effect on the Zn status of the mice as indicated by growth rate, food intake and femur and pancreatic Zn concentrations. In fact, diabetic mice fed on the low-Zn diet had a higher total food intake than those fed on the control diet. The low-Zn diabetic mice had higher fasting blood glucose and liver glycogen levels than their control counterparts. Fasting blood insulin concentration was unaffected by dietary regimen.

3. A second experiment was performed in which the rate of loss of 65Zn, injected subcutaneously, was measured by whole-body counting in the two mouse genotypes over a 28 d period, from 4 to 5 weeks of age. The influence of feeding low-Zn or control diets was also examined. At the end of the study femur and pancreatic Zn and non-fasting blood glucose levels were determined.

4. All mice fed on the low-Zn diet showed a marked reduction in whole-body 65Zn loss compared with those animals fed on the control diet. In the low-Zn groups, the loss of 65Zn from the diabetic mice was significantly greater than that from heterozygote mice. This difference was not observed in the control groups. Blood glucose levels were elevated in the low-Zn groups. Possible reasons for these observations are discussed.

5. The present study demonstrates an adverse effect of reduced dietary Zn intake on glucose utilization in the genetically diabetic mouse, which occurred before any significant tissue Zn depletion became apparent.

Type
Other Studies Relevant to Human Nutrition
Information
British Journal of Nutrition , Volume 60 , Issue 3 , November 1988 , pp. 499 - 507
Copyright
Copyright © The Nutrition Society 1988

References

American Institute of Nutrition (1977) Journal of Nutrition 107, 1340–1348.CrossRefGoogle Scholar
Boquist, L. & Lernmark, A. (1969) Acta Pathalogica et Microbiologica Scandinavica 76, 215–228.CrossRefGoogle Scholar
Brown, E. D., Penhos, J. C., Recant, L. & Smith, J. C. (1975) Proceedings of the Society for Experimental Biology and Medicine 150, 557–560.CrossRefGoogle Scholar
Coleman, D. L. & Hummel, K. P. (1967) Diabetologia 3, 238–248.CrossRefGoogle Scholar
Huber, A. M. & Gershoff, S. N. (1970) Journal of Nutrition 100, 949–954.CrossRefGoogle Scholar
Huber, A. M. & Gershoff, S. N. (1973) Journal of Nutrition 103, 1739–1744.CrossRefGoogle Scholar
Jackson, M. J., Jones, D. A. & Edwards, R. H. T. (1984) British Journal of Nutrition 51, 199–208.CrossRefGoogle Scholar
Keppler, D. & Decker, K. (1974). In Methods of Enzymatic Analysis, Vol. 3, pp. 1127–1131. [H. U. Bergmeyer, editor]. New York and London: Academic Press.Google Scholar
Kinlaw, W. B., Levine, A. S., Morley, J. E., Silvis, S. E. & McClain, C. J. (1983) American Journal of Medicine 75, 273–277.CrossRefGoogle Scholar
Levine, A. S., McClain, C. J., Handwerger, B. S., Brown, D. M. & Morley, J. E. (1983) American Journal of Clinical Nutrition 37, 382–386.CrossRefGoogle Scholar
Mills, C. F., Quarterman, J., Chesters, J. K., Williams, R. B. & Dalgarno, A. C. (1969) American Journal of Clinical Nutrition 22, 1240–1249.CrossRefGoogle Scholar
Mooradian, A. D. & Morley, J. E. (1987) American Journal of Clinical Nutrition 45, 877–895.CrossRefGoogle Scholar
Quarterman, J., Mills, C. F. & Humphries, W. R. (1966) Biochemical and Biophysics Research Communications 25, 354–359.CrossRefGoogle Scholar
Reeves, P. G. & O'Dell, B. L. (1983) British Journal of Nutrition 49, 441–452.CrossRefGoogle Scholar
Scott, D. A. & Fisher, A. M. (1938) Journal of Clinical Investigation 17, 725–728.CrossRefGoogle Scholar
Southon, S., Fairweather-Tait, S. J. & Williams, C. M. (1988 a) British Journal of Nutrition 59, 315–322.CrossRefGoogle Scholar
Southon, S., Gee, J. M. & Johnson, I. T. (1984) British Journal of Nutrition 52, 371–380.CrossRefGoogle Scholar
Southon, S., Wright, A. J. A., Price, K. R., Fairweather-Tait, S. J. & Fenwick, G. R. (1988 b) British Journal of Nutrition 59, 49–55.CrossRefGoogle Scholar
Wada, L., Turnland, J. R. & King, J. (1985) Journal of Nutrition 115, 1345–1354.CrossRefGoogle Scholar
Williams, R. B. & Mills, C. F. (1970) British Journal of Nutrition 24, 989–1003.CrossRefGoogle Scholar