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Metabolic changes associated with the occurrence of fatty liver and kidney syndrome in chicks

Published online by Cambridge University Press:  09 March 2007

C. C. Whitehead ,
D. W Bannister  and
Maureen E. Cleland
C. C. Whitehead
Affiliation:
Agricultural Research Council's Poultry Research Centre, King's Buildings, West Mains Road, Edinburgh EH9 3JS
D. W Bannister
Affiliation:
Agricultural Research Council's Poultry Research Centre, King's Buildings, West Mains Road, Edinburgh EH9 3JS
Maureen E. Cleland
Affiliation:
Agricultural Research Council's Poultry Research Centre, King's Buildings, West Mains Road, Edinburgh EH9 3JS
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Abstract

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1. The changes in a number of metabolic measurements brought about by low-biotin diets associated with high and low incidences of fatty liver and kidney syndrome (FLKS) were studied in healthy 4-week-old broiler chicks.

2. Liver pyruvate carboxylase (pyruvate: CO2 ligase (ADP); EC 6.4.1.1) activity was low in birds fed on a diet causing a high incidence of FLKS but the addition of fat or protein to this diet, to decrease the incidence of FLKS, increased enzyme activity.

3. Liver weights, blood lactate concentrations, plasma lactate dehydrogenase (l-lactate:NAD oxidoreductase; EC 1.1.1.27) activities and values for C16:1:C18:0 fatty acid in liver, adipose tissue and plasma triglyceride were highest in birds fed on the high-FLKS diet and all measurements were negatively correlated with pyruvate carboxylase activity.

4. Birds with high plasma lactate dehydrogenase activity or triglyceride C16:1:C18:0 values were the most likely to develop FLKS when fasted.

5. There was no evidence that increased liver weight was associated with increased activities of certain other liver enzymes.

6. It is concluded that FLKS occurs in birds with little or no hepatic gluconeogenic capacity via pyruvate carboxylase as a result of a dietary insufficiency of biotin but that the initiation of the syndrome is probably associated with the inhibition of other pathways of gluconeogenesis.

Type
Papers on General Nutrition
Information
British Journal of Nutrition , Volume 40 , Issue 2 , September 1978 , pp. 221 - 234
Copyright
Copyright © The Nutrition Society 1978

References

Balnave, D., Cumming, R. B. & Sutherland, T. M. (1976). Aust. vet. J. 52, 433.CrossRefGoogle Scholar
Balnave, D. & Pearce, J. (1976). Br. Poult. Sci. 17, 627.CrossRefGoogle Scholar
Bannister, D. W. (1976 a). Comp. Biochem. Physiol. 53B, 575.Google Scholar
Bannister, D. W. (1976 b). Biochem. J. 156, 167.CrossRefGoogle Scholar
Bannister, D. W. & Cleland, M. E. (1977). Int. J. Biochem. 8, 89.Google Scholar
Bannister, D. W., Evans, A. J. & Whitehead, C. C. (1975). Res. vet. Sci. 18, 149.CrossRefGoogle Scholar
Bergmeyer, H. U. & Bernt, E. (1974). In Methods of Enzymatic Analysis, p. 574 [Bergmeyer, H. U., editor]. London and New York: Academic Press.CrossRefGoogle Scholar
Blair, R. & Whitehead, C. C. (1974). Proc. XV Wld's Poult. Congr., New Orleans, p. 380.Google Scholar
Christie, W. W., Noble, R. C. & Moore, J. H. (1970). Analyst, London. 95, 940.CrossRefGoogle Scholar
Czok, R. & Lamprecht, W. (1970). In Methoden der enzymatischen Analyse, 2nd ed., p. 1407 [Bergmeyer, H. U., editor]. Neinheim: Verlag Chemie.Google Scholar
Evans, A. J., Bannister, D. W., Whitehead, C. C., Siller, W. G. & Wight, P. A. L. (1977). Res. vet. Sci. 23, 275.CrossRefGoogle Scholar
Folch, J., Lees, N. & Sloane Stanley, G. H. (1957). J. biol. Chem. 226, 497.CrossRefGoogle Scholar
Hohorst, H. J. (1963). In Methods of Enzymatic Analysis, p. 266 [Bergmeyer, H. U., editor]. London and New York: Academic Press.Google Scholar
Hood, R. L., Johnson, A. R., Fogarty, A. C. & Pearson, J. A. (1976). Aust. J. biol. Sci. 29, 429.CrossRefGoogle Scholar
Lohr, J. E. (1975). N.Z. vet. J. 23, 167.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). J. biol. Chem. 193, 265.CrossRefGoogle Scholar
Morley, G., Dawson, A. & Marks, V. (1968). Proc. Ass. clin. Biochem. 5, 42.Google Scholar
Payne, G. G., Gilchrist, P., Pearson, J. A. & Hemsley, L. A. (1974). Br. Poult. Sci. 15, 489.CrossRefGoogle Scholar
Sutherland, E. W. & Waselait, W. D. (1956). J. biol. Chem. 218, 459.CrossRefGoogle Scholar
Whitehead, C. C. (1975). Res. vet. Sci. 18, 32.CrossRefGoogle Scholar
Whitehead, C. C., Bannister, D. W., Evans, A. J., Siller, W. G. & Wight, P. A. L. (1976). Br. J. Nutr. 35, 115.CrossRefGoogle Scholar
Whitehead, C. C. & Blair, R. (1974). Wld's Poult. Sci. J. 30, 231.Google Scholar
Whitehead, C. C. & Blair, R. (1976). Res. vet. Sci. 21, 141.CrossRefGoogle Scholar
Whitehead, C. C., Blair, R., Bannister, D. W. & Evans, A. J. (1975). Res. vet. Sci. 18, 100.CrossRefGoogle Scholar
Whitehead, C. C., Blair, R., Bannister, D. W., Evans, A. J. & Jones, R. M. (1976). Res. vet. Sci. 20, 180.CrossRefGoogle Scholar
Wight, P. A. L. & Siller, W. G. (1975). Res. vet. Sci. 19, 173.CrossRefGoogle Scholar
Wise, E. M. & Ball, E. G. (1964). Proc. natn. Acad. Sci. USA 52, 1255.CrossRefGoogle Scholar
Wright, L. D. & Skeggs, H. R. (1944). Proc. soc. exp. Biol. Med. 56, 95.CrossRefGoogle Scholar
Yeh, Y.-Y. & Leveille, G. A. (1969). J. Nutr. 98, 356.CrossRefGoogle Scholar
Yeh, Y.-Y., Leveille, G. A. & Wiley, J. H. (1970). J. Nutr. 100, 917.CrossRefGoogle Scholar