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Effect of diet on disaccharidase activity in the chick

Published online by Cambridge University Press:  09 February 2010

R. C. Siddons
Affiliation:
National Institute for Research in Dairying, Shinjield, Reading RG2 9AT
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Abstract

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1. The influence of diets, particularly dietary carbohydrate, on the development of the intestinal disaccharidases of the chick was studied.

2. The maltase activity in the small intestine was similar in groups of 25-d-old chicks that had been fed, from hatching, on diets containing either starch, glucose, maltose, sucrose, or a mixture of 50% glucose + 50% lactose, as the source of carbohydrate. The sucrase activity in the small intestine was also similar in the different groups, as was the palatinase (the enzyme that hydrolyses palatinose, i.e. 6-o-α-D-glucopyranosyl-D-fructose) activity. The maltase activity in the large intestine of the group receiving the starch-containing diet was significantly increased. The lactase activity in the large intestine was significantly higher in the group receiving the 50% glucose + 50% lactose and in the group receiving glucose than in the other groups. Body- weights were similar with all the diets.

3. The fasting of chicks for a period of 3 d caused a marked decrease in the activity of the disaccharidases and in the protein content of the homogenates of the small intestine.

4. The maltase activity was similar in the small intestine of chicks that had been fasted for 3 d and subsequently given diets containing either starch, glucose, maltose, sucrose or fructose for 5 d. The sucrase activity, the isomaltase activity and the palatinase activity were also similar in the small intestine of the chicks given the different diets. Feeding with a fat-free or protein-free diet did not affect the development of disaccharidases in the small intestine, but feeding with a carbohydrate-free diet resulted in reduced disaccharidase activity.

5. The results suggest that, in the chick, dietary carbohydrate is necessary for the development of the disaccharidases but the form of the carbohydrate is not important. None of the sugars tested had a specific effect on a particular disaccharidase.

Type
General Nutrition
Copyright
Copyright © The Nutrition Society 1972

References

Alvarez, A. & Sas, J. (1961). Nature, Lond. 190, 826.CrossRefGoogle Scholar
Asp, N. G. & Dahlqvist, A. (1968). Biochem. J. 106, 841.CrossRefGoogle Scholar
Bayless, T. M. & Huang, S. (1969). Am. J. clin. Nutr. 22, 250.CrossRefGoogle Scholar
Blair, D. G. R., Yakimets, W. & Tuba, J. (1963). Can. J. Biochem. 41, 917.Google Scholar
Bolin, T. D., Pirola, R. C. & Davis, A. E. (1969). Gustroevzterology 57, 406.CrossRefGoogle Scholar
Cevini, G., Giovannini, M. & Careddu, P. (1962). Mivzerva paediat. 14, 831.Google Scholar
Cuatrecasas, P., Lockwood, D. H. & Caldwell, J. R. (1965). Lancet i, 14.CrossRefGoogle Scholar
Dahlqvist, A. (1964). Analyt. Biochem. 7, 18.CrossRefGoogle Scholar
Deren, J. J., Broitman, S. A. & Zamcheck, N. (1967). J. clin. Innest. 46, 186.CrossRefGoogle Scholar
Doell, R. G. & Rretchmer, N. (1962). Biochint. biophys. Acta 62, 353.CrossRefGoogle Scholar
Gray, G. M. & Santiago, N. A. (1969). J. clin. Innest. 48, 716.CrossRefGoogle Scholar
Gray, G. M., Santiago, N. A., Colver, E. H. & Genel, M. (1969). J. clin. Innest. 48, 729.CrossRefGoogle Scholar
Keusch, G. T., Troncale, F. J., Thavaramara, B., Prinyanont, P., Anderson, P. R. & Bhamarapravathi, N. (1969). Am. J. clin. Nutr. 22, 638.CrossRefGoogle Scholar
Koldovský, O. & Chytil, F. (1965). Biochem. J. 94, 266.CrossRefGoogle Scholar
Prosper, J., Murray, R. L. & Kern, F. (1968). Gastroenterology 55, 223.CrossRefGoogle Scholar
Reddy, B. S., Pleasants, J. R. & Wostmann, B. S. (1968). J. Nutr. 95, 413.CrossRefGoogle Scholar
Rosensweig, N. S. & Herman, R. H. (1968 a). J. clin. Invest. 47, 2253.CrossRefGoogle Scholar
Rosensweig, N. S. & Herman, R. H. (1968 b). Am. J. clin. Nutr. 21, 536.Google Scholar
Rubino, A., Zimbalatti, F. & Auricchio, S. (1964). Biochim. biophys. Acta 92, 305.Google Scholar
Siddons, R. C. (1969). Biochem. J. 112, 51.CrossRefGoogle Scholar
Siddons, R. C. (1970). Biochem. J. 116, 71.CrossRefGoogle Scholar
Siddons, R. C. & Coatcs, M. E. (1972). Br. J. Nutr. 27, 101.CrossRefGoogle Scholar
Solimano, G., Burgess, E. A. & Levin, B. (1967). Br. J. Nutr. 21, 55.CrossRefGoogle Scholar
Stanfield, J. P., Hutt, M. S. R. & Tunnicliffe, R. (1965). Lancet ii, 519.CrossRefGoogle Scholar
Welsh, J. D. & Walker, A. (1965). Proc. Soc. exp. Biol. Med. 120, 525.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). J. biol. Chem. 193, 265.CrossRefGoogle Scholar