β-Amyloid or its precursor protein is found in epithelial cells of the small intestine and is stimulated by high-fat feeding

Galloway, Susan; Jian, Le; Johnsen, R.; Chew, Stewart; Mamo, John

doi:10.1016/j.jnutbio.2006.07.003

Cited by 78 publications

(88 citation statements)

References 38 publications

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“…Enterocytic Ab is enhanced in animals given high-fat diets, consistent with the possibility that chylomicron production is increased. 24 Alternatively, increased apo B48 in the postabsorptive state may be due Figure 4 A comparison of beta-amyloid (Ab) isoforms distributed in plasma lipoproteins isolated from subjects with Alzheimer's disease and mild cognitive impairment vs. age-matched control subjects. The triglyceride-rich lipoprotein fraction includes chylomicrons, VLDLs and their remnants (r , 1.109 g/mL); LDL (1.063-1.019 g/mL) and HDL (1.064 -1.21 g/mL) are indicated.…”

Section: Discussionmentioning

confidence: 99%

Plasma lipoprotein β-amyloid in subjects with Alzheimer's disease or mild cognitive impairment

et al. 2008

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Background: Plasma amyloid b-peptide (Ab) can compromise the blood-brain barrier, contributing to cerebrovascular alterations and amyloid angiopathy in Alzheimer's disease (AD). The objectives of this study were to investigate the distribution of lipoprotein-bound plasma-Ab isoforms.Methods: This involved a case-control study of subjects with AD or amnestic mild cognitive impairment (MCI) versus controls. Lipoprotein Ab distribution was determined in fasted plasma. For assessment of chylomicron homeostasis in the postabsorptive state, subjects were bled 4 h after a low-fat meal. The main outcome measures were plasma lipoprotein Ab isoform distribution and lipid homeostasis. Results: We found the majority of plasma Ab to be associated with triglyceride-rich lipoproteins (TRLs) encompassing chylomicrons, VLDL and IDL. For all lipoprotein groups, Ab 1 -40 was the predominant isoform, accounting for approximately 50% of the total. Thereafter, equivalent amounts of the isoforms 1 -42, 2-40, 1 -38, 1-37 and 1 -39 were found. Ab 1 -37 , Ab 1 -38 and Ab 2 -40 isoforms were significantly enriched within the TRL fraction of AD/MCI subjects and similar trends were observed for isoforms Ab 1 -39 , Ab 1 -40 and Ab 1 -42 . Lipoprotein-Ab was inversely associated with plasma total-and LDL cholesterol. AD/MCI subjects were not dyslipidaemic, however, there was evidence of accumulation of chylomicrons in the postabsorptive state. Conclusions: Our data show that Ab was found to be associated with plasma lipoproteins, especially those enriched with triglyceride. We find that Ab may be increased in normolipidaemic AD subjects, commensurate with possible disturbances in postprandial lipoprotein homeostasis.

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Section: Discussionmentioning

confidence: 99%

Plasma lipoprotein β-amyloid in subjects with Alzheimer's disease or mild cognitive impairment

et al. 2008

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“…These associations remain during lipolysis and tissue uptaking processes [9]. Therefore, it can be proposed that an increased plasmatic amount of such proteins containing Aβ could produce an imbalance and could even be delivered in brain contributing to cerebral amyloidosis, one of the responsible events related to Alzheimer's disease [9,10]. The natural question is: how can we increase the amount of Aβ associated to postprandial lipids?…”

Section: Findings On Amyloid-β Production Induced By Saturated Fat DImentioning

confidence: 99%

“…Another organ where it has been documented that Aβ is produced is the small intestine. Given the evidence that Aβ is associated to postprandial lipoproteins, chylomicrons, Galloway et al [10] followed this line of evidence and studied small intestinal epithelial cells (where the chylomicrons are produced). They fed wild-type mice with low-or high-fat diet.…”

Section: Findings On Amyloid-β Production Induced By Saturated Fat DImentioning

confidence: 99%

High-Fat and Cholesterol Intake Affects Brain Homeostasis and Could Accelerate the Development of Dementia: A Systemic View

Meraz-Ríos¹,

Leal-Galicia²

2016

Update on Dementia

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Alzheimer's disease is the most common type of dementia in occidental countries. The majority of the cases develop the disease for no genetic reasons; therefore, it is crucial to establish which environmental factors trigger the development of the disease. It has been proposed that nutritional habits, especially main components of Western countries' diet such as saturated fat or cholesterol, increase the risk for development of Alzheimer's disease (AD) and/or accelerate the onset of the disease, which is a big concern in countries where obesity is a public health problem. It is crucial to understand the links between alimentary habits and the development of AD and other types of dementia. A possible mechanism is the disruption of blood-brain barrier (BBB), which is the protection of the brain from circulating blood. Such disruptions can result from consuming high-fat diet (HFD) or high-cholesterol diet (HCD) and inflammation produced by alteration in brain vasculature resulted for chronic consumption of such type of diets. What has named a "Systemic view" comprises the idea that; what happens outside of the brain environment does affect brain functioning and the modifications experienced in the brain environment resulted from the influence of external factors will affect the entire body. In the current chapter, we will review the state of the art in the studies of the impact of a diet rich in fat or cholesterol on the brain and how the alterations induced in other organs can impact brain functioning increasing the susceptibility of development of dementia.

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“…This study utilized an in vivo high-fat (HF) feeding model previously shown to stimulate enterocytic abundance of A, to determine if Probucol modulates the secretion of apo B lipoprotein-A from absorptive epithelial cells of the small intestine, a major site of A biosynthesis [28][29][30].…”

Section: Introductionmentioning

confidence: 99%

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

Pallebage-Gamarallage

Galloway

Takechi

et al. 2011

Lipids

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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 the intestinal apo B and Aβ abundance. We found that apo B is found in both 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 changes in the net villi abundance. On the other hand, HF induced enterocytic perinuclear Aβ was significantly attenuated by Probucol. No significant changes of Aβ were observed within the lacteals. The findings of this study support the notion that Probucol suppresses dietary fat induced stimulation of A biosynthesis and attenuate availability of apo B lipoprotein-Aβ for secretion.

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β-Amyloid or its precursor protein is found in epithelial cells of the small intestine and is stimulated by high-fat feeding

Cited by 78 publications

References 38 publications

Plasma lipoprotein β-amyloid in subjects with Alzheimer's disease or mild cognitive impairment

Plasma lipoprotein β-amyloid in subjects with Alzheimer's disease or mild cognitive impairment

High-Fat and Cholesterol Intake Affects Brain Homeostasis and Could Accelerate the Development of Dementia: A Systemic View

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

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