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Alteration of regression of cholesterol accumulation in rats by dietary pectin

Published online by Cambridge University Press:  09 March 2007

James N. Thomas ,
Michael J. Kelley  and
Jon A. Story
James N. Thomas
Affiliation:
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907, USA
Michael J. Kelley
Affiliation:
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907, USA
Jon A. Story
Affiliation:
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907, USA
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Abstract

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1. Male, Wistar rats (50–74 g) were given a semi-purified diet containing cholesterol (10 g/kg diet) for 4 weeks, groups of control and experimental animals killed, and the remainder of the cholesterol-fed animals given either a semi-purified cholesterol-free diet without a fibre source or a similar diet with pectin (50 g/kg diet) for 8 weeks. Animals were killed at 2-week intervals and serum and liver cholesterol and triglycerides, faecal neutral steroids and acidic steroids measured.

2. Animals given pectin had significantly lower serum cholesterol levels than animals given the basal diet after 4 and 6 weeks.

3. Both experimental groups efficiently decreased their liver cholesterol levels during regression.

4. Bile acid excretion was elevated in both groups, especially in rats receiving pectin, but neutral steroid excretion was unchanged.

5. The increase in bile acid excretion was primarily in the form of chenodeoxycholic acid and its metabolites.

6. This increased bile acid excretion is postulated to result from stimulation of the normal mechanism for increased steroid excretion in the rat, i.e. a change in the value of cholic: chenodeoxycholic acid or from a mechanism not yet elucidated.

Type
Papers of direct relevance to Clinical and Human Nutrition
Information
British Journal of Nutrition , Volume 51 , Issue 3 , May 1984 , pp. 339 - 345
Copyright
Copyright © The Nutrition Society 1984

References

REFERENCES

Beher, W. T., Beher, M. E. & Rao, B. (1967). Life Sciences 6, 863–866.CrossRefGoogle Scholar
Birkner, H. J. & Kern, F. Jr (1974). Gastroenterology 67, 237–244.CrossRefGoogle Scholar
Brydon, W. G., Tadesse, K., Smith, D. M. & Eastwood, M. A. (1979). Journal of Chromatography 172, 450–452.CrossRefGoogle Scholar
Chang, M. L. W. & Johnson, M. A. (1980). Nutrition Reports International 22, 91–99.Google Scholar
Cohen, B. I., Raicht, R. R. & Mosbach, E. H. (1977). Journal of Lipid Research 18, 223–231.CrossRefGoogle Scholar
Cummings, J. H., Southgate, D. A. T., Branch, W. J. & Wiggins, H. S. (1979). British Journal of Nutrition 41, 477–485.CrossRefGoogle Scholar
Eastwood, M. A. & Hamilton, D. (1968). Biochimica et Biophysica Acta 152, 165–173.CrossRefGoogle Scholar
Grundy, S. M., Ahrens, E. H. Jr & Miettinen, T. A. (1965). Journal of Lipid Research 6, 397–409.CrossRefGoogle Scholar
Gustafsson, B. E., Angelin, B., Einarsson, K. & Gustafsson, J.-A. (1977). Journal of Lipid Research 18, 717–721.CrossRefGoogle Scholar
Gustafsson, B. E., Einarsson, K. & Gustafsson, J.-A. (1975). Journal of Biological Chemistry 250, 8496–8502.CrossRefGoogle Scholar
Jenkins, D. J. A., Newton, C., Leeds, A. R. & Cummings, J. H. (1975). Lancet i, 116–117.Google Scholar
Karvinen, E. & Miettinen, M. (1968). Acta Physiologica Scandinavica 72, 62–64.CrossRefGoogle Scholar
Kay, R. M., Strasberg, S. M., Pertunka, C. N. & Wayman, M. (1979). Dietary Fibers: Chemistry and Nutrition pp. 57–65 [Inglett, G. E. and Falkehag, S. I., editors]. New York: Academic Press.CrossRefGoogle Scholar
Kay, R. M. & Truswell, S. W. (1977). American Journal of Clinical Nutrition 30, 171–175.CrossRefGoogle Scholar
Kern, J. Jr, Birkner, H. J. & Ostrower, V. S. (1978). American Journal of Clinical Nutrition 31, S175–S179.CrossRefGoogle Scholar
Miettinen, T. S. & Tarpila, S. (1977). Clinica Chimica Acta 79, 471–477.CrossRefGoogle Scholar
Palmer, G. H. & Dixon, D. G. (1966). American Journal of Clinical Nutrition 18, 437–442.CrossRefGoogle Scholar
Reddy, B. S., Watamabe, K. & Sheinfil, A. (1980). Journal of Nutrition 110, 1247–1254.CrossRefGoogle Scholar
Rudel, L. L. & Morris, M. D. (1973). Journal of Lipid Research 14, 364–366.CrossRefGoogle Scholar
Ryan, W. G. & Rasho, O. M. (1967). Clinical Chemistry 13, 769–772.CrossRefGoogle Scholar
Shefer, S., Hauser, D., Lapar, V. & Mosbach, E. H. (1973). Journal of Lipid Research 14, 573–580.CrossRefGoogle Scholar
Spritz, N., Ahrens, E. H. Jr & Grundy, S. (1965). Journal of Clinical Investigation 44, 1482–1493.CrossRefGoogle Scholar
Story, J. A., Baldino, A., Czarnecki, S. K. & Kritchevsky, D. (1981 a). Nutrition Reports International 24, 1213–1219.Google Scholar
Story, J. A., Czarnecki, S. K., Tepper, S. A. & Kritchevsky, D. (1981 b). Nutrtion Reports International 24, 465–470.Google Scholar
Thomas, J. N., Kelley, M. J. & Story, J. A. (1980). Federation Proceedings of the American Societies for Experimental Biology 39, 784.Google Scholar
Uchida, K., Nomura, Y. & Takeuchi, N. (1980). Journal of Biochemistry 87, 187–194.CrossRefGoogle Scholar
Vahouny, G. V., Roy, T., Gallo, L. L., Story, J. A., Kritchevsky, D. & Cassidy, M. M. (1980). American Journal of Clinical Nutrition 33, 2182–2191.CrossRefGoogle Scholar
Van Handel, E. V. & Zilversmit, D. B. (1957). Journal of Laboratory and Clinical Medicine 50, 152–157.Google Scholar
Wells, A. F. & Ershoff, B. H. (1961). Journal of Nutrition 74, 87–92.CrossRefGoogle Scholar
Wilson, J. D. & Lindsey, C. A. Jr (1965). Journal of Clinical Investigation 44, 1805–1814.CrossRefGoogle Scholar