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    Probucol Suppresses Enterocytic Accumulation of Amyloid-β Induced by Saturated Fat and Cholesterol Feeding

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    Access Status
    Open access
    Authors
    Pallebage-Gamarallage, Menuka
    Galloway, Susan
    Takechi, Ryusuke
    Dhaliwal, Satvinder
    Mamo, John
    Date
    2011
    Type
    Journal Article
    
    Metadata
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    Citation
    Pallebage-Gamarallage, Menuka and Galloway, Susan and Takechi, Ryusuke and Dhaliwal, Satvinder and Mamo, John. 2011. Probucol Suppresses Enterocytic Accumulation of Amyloid-β Induced by Saturated Fat and Cholesterol Feeding. Lipids. 47 (1): pp. 27-34.
    Source Title
    Lipids
    ISSN
    00244201
    School
    School of Public Health
    Remarks

    The final publication is available at link.springer.com

    URI
    http://hdl.handle.net/20.500.11937/36581
    Collection
    • Curtin Research Publications
    Abstract

    Amyloid-β (Aβ) is secreted from lipogenic organs such as intestine and liver as an apolipoprotein of nascent triacylglycerol rich lipoproteins. Chronically elevated plasma Aβ may compromise cerebrovascular integrity and exacerbate amyloidosis—a hallmark feature of Alzheimer’s disease (AD). Probucol is a hypocholesterolemic agent that reduces amyloid burden in transgenic amyloid mice, but the mechanisms for this effect are presently unclear. In this study, the effect of Probucol on intestinal lipoprotein-Aβ homeostasis was explored. Wild-type mice were fed a control low-fat diet and enterocytic Aβ was stimulated by high-fat (HF) diet enriched in 10% (w/w) saturated fat and 1% (w/w) cholesterol for the duration of 1 month. Mice treated with Probucol had the drug incorporated into the chow at 1% (w/w). Quantitative immunofluorescence was utilised to determine intestinal apolipoprotein B (apo B) and Aβ abundance. We found apo B in both the perinuclear region of the enterocytes and the lacteals in all groups. However, HF feeding and Probucol treatment increased secretion of apo B into the lacteals without any change in net villi abundance. On the other hand, HF-induced enterocytic perinuclear Aβ was significantly attenuated by Probucol. No significant changes in Aβ were observed within the lacteals. The findings of this study support the notion that Probucol suppresses dietary fat induced stimulation of Aβ biosynthesis and attenuate availability of apo B lipoprotein-Aβ for secretion.

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