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Research Article| Volume 193, ISSUE 1, P86-93, July 2007

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A green tea extract lowers plasma cholesterol by inhibiting cholesterol synthesis and upregulating the LDL receptor in the cholesterol-fed rabbit

  • Christina A. Bursill
    Affiliations
    Wellcome Trust Centre of Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, United Kingdom

    CSIRO, Health Sciences and Nutrition, Adelaide, SA 5000, Australia

    University of Adelaide, SA 5000, Australia
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  • Mavis Abbey
    Affiliations
    CSIRO, Health Sciences and Nutrition, Adelaide, SA 5000, Australia
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  • Paul D. Roach
    Correspondence
    Corresponding author. Tel.: +61 2 4348 4129; fax: +61 2 4348 4145.
    Affiliations
    University of Newcastle, School of Environmental and Life Sciences, P.O. Box 127, Ourimbah, NSW 2258, Australia

    CSIRO, Health Sciences and Nutrition, Adelaide, SA 5000, Australia
    Search for articles by this author

      Abstract

      Green tea extracts enriched in catechins decrease plasma cholesterol in hamsters, mice and rats. The aims of this study were to determine whether a catechin-enriched extract of green tea could lower plasma cholesterol in the cholesterol-fed rabbit and to determine the mechanism of action. Four groups of six New Zealand White rabbits were initially made hypercholesterolaemic by feeding a 0.25% (w/w) cholesterol diet for 2 weeks before the diet was supplemented with a catechin extract from green tea at 0, 0.5, 1 or 2% (w/w) for 4 weeks. Administration of the crude catechin extract from green tea significantly (p < 0.05) lowered cholesterol in plasma (−60%), VLDL + IDL (−70%), LDL (−80%), liver (total by −25% and unesterified by −15%) and aorta (−25%) compared to control. There was a significant reduction in the cholesterol synthesis index (−60%) and a significant increase in hepatic LDL receptor activity (+80%) and protein (+70%) but there was no change in the intrinsic capacity to absorb cholesterol from the intestines. These results suggest that green tea catechins lowered plasma, liver and aortic cholesterol in the cholesterol-fed rabbit by lowering cholesterol synthesis and upregulating the hepatic LDL receptor.

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