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The effect of an unsaturated-fat diet on cataract formation in streptozotocin-induced diabetic rats

Published online by Cambridge University Press:  10 January 2017

J. C. Hutton
Affiliation:
School of Biochemistry, University of New South Wales, Kensington, NSW 2033, Australia
P. J. Schofield
Affiliation:
School of Biochemistry, University of New South Wales, Kensington, NSW 2033, Australia
J. F. Williams
Affiliation:
School of Biochemistry, University of New South Wales, Kensington, NSW 2033, Australia
H. L. Regtop
Affiliation:
School of Biochemistry, University of New South Wales, Kensington, NSW 2033, Australia
F. C. Hollows
Affiliation:
School of Biochemistry, University of New South Wales, Kensington, NSW 2033, Australia
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1. Cataract formation in streptozotocin-induced diabetes in rats was reduced by approximately 85% when a diet rich in maize oil (300 g/kg diet) (fat diet) was given, thus confirming results of earlier studies. However, the concentration of sorbitol in the lens of diabetic animals remained high, the values for diabetic rats given the standard diet and the fat diet being 65 and 40 μmol/g protein respectively.

2. With the standard diet, the fatty acid profile of the triglycerides of the epididymal fat pads was characterized by a greater relative proportion of saturated fatty acids for the diabetic animals compared to that for the normal animals. The fat diet moderated the tendency towards saturation in the diabetic animals.

3. The fat diet had other effects on the diabetic animals; these included a reduced mortality rate, increased body-weight, a decrease in the daily water intake, and in the daily urinary excretion of glucose and urea.

4. In the diabetic animals the fat diet had no effect on the specific activities in the liver of hexokinase (EC 2.7.1.1), glucokinase (EC 2.7.1.2), phosphofructokinase (EC 2.7.1.11) and pyruvate kinase (EC 2.7.1.40). However, the specific activity of glucose-6-phosphatase (EC 3.1.3.9) was reduced, while that of malate dehydrogenase (decarboxylating) (NADP) (EC 1.1.1.40) was increased. The NAD+: NADH ratio, as calculated from liver pyruvate and lactate concentrations, tended to increase.

5. The results suggested that the fat diet moderated the long-term metabolic effects of diabetes.

Type
Papers of direct relevance to Clinical and Human Nutrition
Copyright
Copyright © The Authors 1976

References

Beale, R. N. & Croft, D. (1961). J. clin. Pathol. 14, 418.CrossRefGoogle Scholar
Benjamin, W. & Gellhorn, A. (1964). J. biol. Chem. 239, 64.CrossRefGoogle Scholar
Bucher, T., Czok, R., Lamprecht, W. & Latzko, E. (1965). In Methods of Enzymatic Analysis, p. 253 [Bergmeyer, H. U., editor]. New York: Academic Press.CrossRefGoogle Scholar
Chylack, L. T. & Kinoshita, J. H. (1969). Invest. Ophthal. 8, 401.Google Scholar
Dole, V. P. & Meinertz, H. (1960). J. biol. Chem. 235, 2595.CrossRefGoogle Scholar
Estrich, D., Ravnik, A., Schlierf, G., Fukayama, G. & Kinsell, L. (1967). Diabetes 16, 232.CrossRefGoogle Scholar
Fechner, W. & L’Age, M. (1972). Acta endocr. Copenh. 159, Suppl., 89.Google Scholar
Folch, J., Lees, M. & Sloane Stanley, G. H. (1957). J. biol. Chem. 226, 497.CrossRefGoogle Scholar
Gumaa, K. A., McLean, P. & Greenbaum, A. L. (1971). In Essays in Biochemistry, vol. 7, p. 39 [Campbell, P. N. and Dickens, F., editors]. London: Academic Press.Google Scholar
Harper, A. E. (1965). In Methods of Enzymatic Analysis, p. 788 [Bergmeyer, H. U., editor]. New York: Academic Press.CrossRefGoogle Scholar
Ho, R. J. (1970). Analyt. Biochem. 36, 105.CrossRefGoogle Scholar
Hohorst, H. J. (1965). In Methods of Enzymatic Analysis, p. 266 [Bergmeyer, H. U., editor]. New York: Academic Press.CrossRefGoogle Scholar
Hsu, R. Y. & Lardy, H. A. (1969). Meth. Enzym. 13, 230.CrossRefGoogle Scholar
Huggett, A. St G. & Nixon, D. A. (1957). Biochem. J. 66, 12P.Google Scholar
Hutton, J. C., Schofield, P. J., Williams, J. F. & Hollows, F. C. (1974). Aust.J. exp. Biol. med. Sci. 52, 361.CrossRefGoogle Scholar
Kinoshita, J. H. (1965 a). Invest. Ophthal. 4, 786.Google Scholar
Kinoshita, J. H. (1965 b). Invest. Ophthal. 4, 619.Google Scholar
Kinoshita, J. H., Futterman, S., Satoh, K. & Merola, L. O. (1963). Biochim. biophys. Acta 74, 340.CrossRefGoogle Scholar
Kuck, J. F. R. (1966). Invest. Ophthal. 5, 65.Google Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). J. biol. Chem. 193, 265.CrossRefGoogle Scholar
McCarthy, R. D. & Duthie, A. H. (1962). Lipid Res. 3, 117.CrossRefGoogle Scholar
Mansford, K. R. L. & Opie, L. (1968). Lancet i, 670.CrossRefGoogle Scholar
Patterson, J. W. (1953). A. J. Physiol. 172, 77.CrossRefGoogle Scholar
Patterson, J. W. (1955). Proc. Soc. exp. Biol. Med. 90, 706.CrossRefGoogle Scholar
Patterson, J. W., Patterson, M. E. & Bunting, K. W. (1962). Exp. Eye Res. 1, 411.CrossRefGoogle Scholar
Patterson, J. W., Patterson, M. E., Kinsey, E. V. & Reddy, D. V. N. (1965). Invest. Ophthal. 4, 98.Google Scholar
Sharma, C., Manjeshwar, R. & Weinhouse, S. (1963). J. biol. Chem. 238, 3840.CrossRefGoogle Scholar
Shonk, C. E. & Boxer, G. E. (1964). Cancer Res. 24, 709.Google Scholar
Stewart, M. A., Sherman, W. R., Kurien, M. M., Moonsammy, G. I. & Wisgerhof, M. (1967). J. Neurochem. 14, 1057.CrossRefGoogle Scholar
van Heyningen, R. (1959). Nature, Lond. 184, 194.CrossRefGoogle Scholar
van Heyningen, R. (1965). Biochem. J. 96, 419.CrossRefGoogle Scholar
Williamson, D. H., Lund, P. & Krebs, H. A. (1967). Biochem. J. 103, 514.CrossRefGoogle Scholar