Hostname: page-component-586b7cd67f-rdxmf Total loading time: 0 Render date: 2024-11-29T04:42:08.691Z Has data issue: false hasContentIssue false
  • English
  • Français

Effect of riboflavin deficiency on lipid metabolism of liver and brown adipose tissue of sucking rat pups

Published online by Cambridge University Press:  07 March 2008

Julia M. Duerden  and
C. J. Bates
Julia M. Duerden
Affiliation:
Dunn Nutritional Laboratory, Downham's Lane, Milton Road, Cambridge CB4 1XJ
C. J. Bates
Affiliation:
Dunn Nutritional Laboratory, Downham's Lane, Milton Road, Cambridge CB4 1XJ
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. An increase in 1iver:body-weight and in hepatic triacylglycerol content, together with changes in the fatty acid profiles of hepatic phospholipids, were observed as a result of moderate riboflavin deficiency in sucking rat pups. Oxygen consumption by hepatic mitochondria, with palmitoyl L-carnitine as substrate, was not significantly impaired.

2. Mitochondria from interscapular brown adipose tissue, however, showed a marked impairment of O2 Consumption, with palmitoyl L-carnitine as substrate, in the riboflavin-deficient pups. This impairment was also apparent after uncoupling with carbonyl cyanide p-trifluoromethoxyphenylhydrazone, but was not consistently observed after the addition of GDP to suppress uncoupled oxidation. It was much less evident, and did not reach statistical significance, for the mitochondria of brown adipose tissue of the corresponding deficient dams.

3. Binding of 3H-labe11ed GDP by brown adipose tissue mitochondria was unaffected by riboflavin deficiency in the pups, suggesting that the effect on O2 consumption is more likely to be due to impaired integrity of the mitochondrial respiratory chain, than to impairment of the specific capacity for uncoupling of respiration which is characteristic of brown adipose tissue mitochondria. Total cytochrome c oxidase (EC 1.9.3.1) activity of the brown adipose tissue of riboflavin-deficient pups was not significantly reduced.

4. A small but significant impairment was observed in the stimulation ofwhole-body O2consumption by injected noradrenaline in the riboflavin-deficient pups, suggesting that the impairment of brown adipose tissue mitochondrial function may be accompanied by impaired physiological capacity in vivo.

Type
Papers on General Nutrition
Information
British Journal of Nutrition , Volume 53 , Issue 1 , January 1985 , pp. 107 - 115
Copyright
Copyright © The Nutrition Society 1985

References

REFERENCES

Bates, C. J., Prentice, A. M., Paul, A. A., Prentice, A., Sutcliffe, B. & Whitehead, R. G. (1982). Transactions of the Royal Society of Tropical Medicine and Hygiene 76, 253–258.CrossRefGoogle Scholar
Bensadoun, A. & Weinstein, D. (1976). Analytical Biochemistry 70, 241–250.CrossRefGoogle Scholar
Cannon, B. & Johansson, B. (1980). Molecular Aspects of Medicine, vol. 3, pp. 119–223. Oxford: Pergamon Press.Google Scholar
Cannon, B. & Lindberg, O. (1979). Methods in Enzymology 55, 65–78.CrossRefGoogle Scholar
Chance, B. & Williams, G. R. (1955). Journal of Biological Chemistry 217, 409–427.CrossRefGoogle Scholar
Drahota, Z., Hahn, P. & Honova, E. (1965–66). Biologia Neonutorum 9, 124–131.CrossRefGoogle Scholar
Duerden, J. M. & Bates, C. J. (1985). British Journal of Nutrition 53, 95–105.Google Scholar
Goodbody, A. E. & Trayhurn, P. (1981). Biochemical Journal 194, 1019–1022.CrossRefGoogle Scholar
Hahn, P. & Koldovsky, O. (1966). Utilization of Nutrients During Postnatal Development. Oxford: Pergamon Press.Google Scholar
Hoppel, C. L., DiMarco, J. P. & Tandler, B. (1979). Journal of Biological Chemistry 254, 4164–4170.CrossRefGoogle Scholar
Lowry, O. H., Rosebrough, N. J., Farr, A. L. & Randall, R. J. (1951). Journal of Biological Chemistry 193, 265–275.CrossRefGoogle Scholar
Nicholls, D. G. (1979). Biochimica Biophysica Acta 549, 1–29.CrossRefGoogle Scholar
Norton, W. N., Daskal, I., Savage, H. E., Seibert, R. A. & Lane, M. (1976). American Journal of Pathology 85, 651–660.Google Scholar
Olpin, S. E. & Bates, C. J. (1982 a). British Journal of Nutrition 47, 577–588.CrossRefGoogle Scholar
Olpin, S. E. & Bates, C. J. (1982 b). British Journal of Nutrition 47, 589–596.CrossRefGoogle Scholar
Phillips, P. H. & Engel, R. W. (1938). Journal of Nutrition 16, 451–462.CrossRefGoogle Scholar
Shaw, J. H. & Phillips, P. H. (1941). Journal of Nutrition 22, 345–358.CrossRefGoogle Scholar
Stock, M. J. (1975). Journal of Applied Biology 37, 849–850.Google Scholar
Street, H. R., Cowgill, G. R. & Zimmerman, H. M. (1941). Journal of Nutrition 22, 7–24.CrossRefGoogle Scholar
Sundin, U., Herron, D. & Cannon, B. (1981). Biologia Neonatorurn 39, 141.CrossRefGoogle Scholar
Tandler, B. & Hoppel, C. L. (1972). In. Methods and Achievements in Experimental Pathology, vol. 6, pp. 2548 [Bajusz, E. and Jasmin, G., editors]. Basel: Karger.Google Scholar
Tandler, B. & Hoppel, C. L. (1980). Anatomical Record 196, 183–190.CrossRefGoogle Scholar
Yeh, Y.-Y. &Zee, P. (1979). Archives of Biochemistry and Biophysics 199, 560–569.CrossRefGoogle Scholar
Yonetani, T. & Ray, G. S. (1965). Journal of Biological Chemistry 240, 3392–3398.CrossRefGoogle Scholar