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Resistant starch is more effective than cholestyramine as a lipid-lowering agent in the rat

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Lipids

Abstract

Amylase-resistant starch (RS) represents a substrate for the bacterial flora of the colon, and the question arises as whether RS shares with soluble fibers common mechanisms for their lipid-lowering effects. It is uncertain whether a cholesterol-lowering effect depends basically on an enhanced rate of steroid excretion or whether colonic fermentations also play a role in this effect. In the present study, the effect of RS (25% raw potato starch), of a steroid sequestrant (0.8% cholestyramine), or both were compared on bile acid excretion and lipid metabolism in rats fed semipurified diets. RS diets led to a marked rise in cecal size and the cecal pool of short-chain fatty acids (SCFA), as well as SCFA absorption; cholestyramine did not noticeably affect cecal fermentation. Whereas cholestyramine was particularly effective at enhancing bile acid excretion, RS was more effective in lowering plasma cholesterol (−32%) and triglycerides (−29%). The activity of 3-hydroxy-3-methylglutaryl-CoA reductase was increased fivefold by cholestyramine and twofold by RS. This induction in rats fed RS diets was concomittant to a depressed fatty acid synthase activity. In rats fed the RS diet, there was a lower concentration of cholesterol in all lipoprotein fractions, especially the (d=1.040−1.080) fraction high-density lipoprotein (HDL1), while those fed cholestyramine had only a significant reduction of HDL1 cholesterol. In contrast to cholestyramine, RS also depressed the concentration of triglycerides in the triglyceride-rich lipoprotein fraction. There was no noticeable synergy between the effects of RS and cholestyramine when both were present in the diet. This suggests that the cholesterol-lowering effect of RS is not limited to its capacity to enhance bile acids excretion. The difference between RS and cholestyramine could relate to the capacity of fermentation end-products to counteract the upregulation of cholesterol and bile acid biosynthesis. Thus, in the absence of fermentation in the large intestine, a high rate of bile acids excretion is not always sufficient to elicit a cholesterol-lowering effect.

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Abbreviations

ANOVA:

analysis of variance

FAS:

fatty acid synthase

HDL:

high-density lipoprotein

HMG-CoA:

3-hydroxy-3-methylglutaryl-CoA

RS:

resistant starch

SCFA:

short-chain fatty acid

TGRLP:

triglyceride-rich lipoprotein

References

  1. Stedronsky, E.R. (1994)Biochim. Biophys. Acta 1210, 255–287.

    PubMed  CAS  Google Scholar 

  2. Anderson, I.H., Levine, A.S., and Lewitt, M.D. (1981)N. Engl. J. Med. 304, 891–892.

    Article  PubMed  CAS  Google Scholar 

  3. Englyst, H.N., and Cummings, J.H. (1985)Am. J. Clin. Nutr. 42, 778–787.

    PubMed  CAS  Google Scholar 

  4. Fluorie, B., Leblond, A., Florent, C., Rautureau, M., Bisalli A., and Rambaud, J.C. (1988)Gastroenterology 95, 356–363.

    Google Scholar 

  5. Carroll, K.K., Hamilton, R.M.G., Huff, M.W., and Falloner, A.D. (1978)Am. J. Clin. Nutr. 31, S203-S207.

    PubMed  CAS  Google Scholar 

  6. Demigné, C., and Rémésy, C. (1982)J. Nutr. 112, 2227–2234.

    PubMed  Google Scholar 

  7. Sacquet, E., Leprince, C., and Riottot, M. (1983)Reprod. Nutr. Dev. 23, 783–792.

    PubMed  CAS  Google Scholar 

  8. Asp, N.G., Björck, I., Holm, J., Nyman, M., and Siljetröm, M. (1987)Scand. J. Gastroenterol. 22, 29–32.

    Google Scholar 

  9. Mathé, D., Riottot, M., Rostaqui, N., Sacquet, E., Navarro, N., Lécuyer, B., and Lutton, C. (1993)J. Clin. Biochem. Nutr. 14, 17–24.

    Google Scholar 

  10. Behall, K.M., Scholfield, D.J., Yuhaniak, I., and Canary, J. (1989)Am. J. Clin. Nutr. 49, 337–344.

    PubMed  CAS  Google Scholar 

  11. De Deckere, E.A.M., Kloots, W.J., and Van Amelsvoort, J.M.M. (1993)J. Nutr. 123, 2142–2151.

    PubMed  Google Scholar 

  12. Würsch, P. (1989) inNutritional Value of Cereal Products, Beans and Starches (Bourne, G.H., ed.) pp. 199–256, Karger, Amsterdam, The Netherlands.

    Google Scholar 

  13. Abadie, C., Hug, M., Kübli, C., and Gains, N., (1994)Biochem. J. 299, 725–730.

    PubMed  CAS  Google Scholar 

  14. Rémésy, C., and Demigné, C. (1974)Biochem. J. 141, 85–91.

    PubMed  Google Scholar 

  15. Turley, S.D., and Dietschy, J.M. (1978)J. Lipid Res. 19, 924–928.

    PubMed  CAS  Google Scholar 

  16. Sérougne, C., Férézou, J., and Rukaj, A. (1987)Biochim. Biophys. Acta 921, 522–530.

    PubMed  Google Scholar 

  17. Wilce, P.A., and Kroone, P.A. (1992) inLipoprotein Analysis, A Pratical Approach (Converse, C.A., Skinner, E.R., eds.) pp. 203–214, Oxford University Press, United Kingdom.

    Google Scholar 

  18. Hsu, R.Y., Butterworth, P.H.W., and Porter, J.W. (1969) inMethods Enzymol (Lowenstein, J.M., ed.) Vol. 14, pp. 230–235, Academic Press, New York.

    Google Scholar 

  19. Morand, C., Rémésy, C., Levrat, M.A., and Demigné, C. (1992)J. Nutr. 122, 345–354.

    PubMed  CAS  Google Scholar 

  20. Rémésy, C., Levrat, M.-A., Gamet, L., and Demigné, C. (1993)Am. J. Physiol. 264, G855-G862.

    PubMed  Google Scholar 

  21. Nagengast, F.M. (1992) inDietary Fibre—A Component of Food (Schweitzer, T.F., and Edwards, C.A., eds.) pp. 217–232, Springer, London.

    Google Scholar 

  22. MacFarlane, G.T., and Cummings, J.H. (1991) inThe Large Intestine: Physiology, Pathophysiology and Disease (Phillips, S.F., Pemberton, J.H., and Shorter, R.G., eds.) pp. 51–92, Raven Press, New York.

    Google Scholar 

  23. McBurney, M.L., Cuff, D.J., and Thompson, L.U. (1990)J. Sci. Food Agric. 50, 79–88.

    Article  CAS  Google Scholar 

  24. Levrat, M.A., Rémésy, C., and Demigné, C. (1991)J. Nutr. Biochem. 2, 31–36.

    Article  CAS  Google Scholar 

  25. Moundras, C., Behr, S.R., Demigné, C., Mazur, A., and Rémésy, C. (1994)J. Nutr. 124, 2179–2188.

    PubMed  CAS  Google Scholar 

  26. White, B.A., Caccapuoti, A.F., Fricke, R., Whitehead, T., Moshbach, E., and Hylemon, P.B. (1981)J. Lipid Res. 22, 891–898.

    PubMed  CAS  Google Scholar 

  27. Younes, H., Levrat, M.A., Demigné, C., and Rémésy, C. (1993)Ann. Nutr. Metab. 37, 311–319.

    PubMed  CAS  Google Scholar 

  28. Grundy, S.M., Ahrens, E.H., and Salen, L.G. (1971)J. Lab. Clin. Med. 78, 94–121.

    PubMed  CAS  Google Scholar 

  29. Vahouny, G.V., Roy, T., Gallo, L.L., Story, J.A., Kritchevsky, D., and Cassidy, M. (1980)Am. J. Clin. Nutr. 33, 2182–2191.

    PubMed  CAS  Google Scholar 

  30. Reddy, B.S., Watanabe, K., and Sheinfil, A. (1980)J. Nutr. 110, 1247–1247.

    PubMed  CAS  Google Scholar 

  31. Vahouny, G.V., Satchithanandam, S., Chen, I., Tepper, S.A., Kritchevsky, D., Lightfoot, F.G., and Cassidy, M.M. (1988)Am. J. Clin. Nutr. 47, 201–206.

    PubMed  CAS  Google Scholar 

  32. Wright, R.S., Anderson, J.W., and Bridges, S.R. (1990)Proc. Exp. Biol. Med. 195, 26–29.

    CAS  Google Scholar 

  33. Illman, R.J., Topping, D.L., McIntosh, G.H., Trimble, R.P., Storer, G.B., Taylor, M.N., and Cheng, B.Q. (1988)Ann. Nutr. Metab. 32, 97–107.

    Article  CAS  Google Scholar 

  34. Beaulieu, K.E., and McBurney, M.I. (1992)J. Nutr. 122, 241–245.

    PubMed  CAS  Google Scholar 

  35. Nishina, P.M., and Freedland, R.A. (1990)J. Nutr. 120, 668–673.

    PubMed  CAS  Google Scholar 

  36. Morand, C., Besson, C., Demigné, C., and Rémésy, C. (1994)Arch. Biochem. Biophys. 309, 254–260.

    Article  PubMed  CAS  Google Scholar 

  37. Demigné, C., Morand, C., Levrat, M.A., Besson, C., Moundras, C., and Rémésy, C. (1995)Br. J. Nutr. 74 (in press).

  38. Eason, R.A., and Zammit, V.A. (1985)Biochem. J. 230, 747–752.

    Google Scholar 

  39. Morand, C., Levrat, M.A., Besson, C., Demigné, C., and Rémésy, C. (1994)J. Nutr. Biochem. 5, 138–144.

    Article  CAS  Google Scholar 

  40. Haave, N.C., and Innis, S.M. (1991)J. Nutr. 121, 1529–1535.

    PubMed  CAS  Google Scholar 

  41. Lusk, L.T., Walker, L.F., Dubien, L.H., and Getz, G.S. (1979)Biochem. J. 183, 83–90.

    PubMed  CAS  Google Scholar 

  42. Lee, C.C., and Koo, S.I. (1988)Atherosclerosis 70, 205–215.

    Article  PubMed  CAS  Google Scholar 

  43. Rudling, M. (1992)J. Lip. Res. 33, 493–501.

    CAS  Google Scholar 

  44. Spady, D.K., Turley, S.D., and Dietschy, J.M. (1985)J. Lipid Res. 26, 465–472.

    PubMed  CAS  Google Scholar 

  45. Eisenberg, S. (1980)Ann. N. Y. Acad. Sci. 348, 30–47.

    PubMed  CAS  Google Scholar 

  46. Annison, G., and Topping, D.L. (1994)Ann. Rev. Nutr. 14, 298–320.

    Google Scholar 

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Authors and Affiliations

  1. Laboratoire des Maladies Métaboliques, INRA de Clermont-Ferrand/Theix, 63122, St-Genès-Champanelle, France

    Hassan Younes, Marie-Anne Levrat, Christian Demigné & Christian Rémésy

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  1. Hassan Younes
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  2. Marie-Anne Levrat
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  3. Christian Demigné
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  4. Christian Rémésy
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Younes, H., Levrat, MA., Demigné, C. et al. Resistant starch is more effective than cholestyramine as a lipid-lowering agent in the rat. Lipids 30, 847–853 (1995). https://doi.org/10.1007/BF02533961

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  • DOI: https://doi.org/10.1007/BF02533961

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