Effects of short‐term Western diet on cerebral oxidative stress and diabetes related factors in APP × PS1 knock‐in mice

A chronic high fat Western diet (WD) promotes a variety of morbidity factors although experimental evidence for short‐term WD mediating brain dysfunction remains to be elucidated. The amyloid precursor protein and presenilin‐1 (APP × PS1) knock‐in mouse model has been demonstrated to recapitulate so...

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Bibliographic Details
Published in:Journal of neurochemistry 2009-02, Vol.108 (4), p.860-866
Main Authors: Studzinski, Christa M., Li, Feng, Bruce‐Keller, Annadora J, Fernandez‐Kim, Sun Ok, Zhang, Le, Weidner, Adam M., Markesbery, William R., Murphy, M. Paul, Keller, Jeffrey N.
Format: Article
Language:English
Subjects:
adipokine
Alzheimer’s disease
amyloid‐β
Biochemistry
Diabetes
Diet
Neurological disorders
Neurology
Oxidation
protein oxidation
Rodents
Western diet
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Summary:A chronic high fat Western diet (WD) promotes a variety of morbidity factors although experimental evidence for short‐term WD mediating brain dysfunction remains to be elucidated. The amyloid precursor protein and presenilin‐1 (APP × PS1) knock‐in mouse model has been demonstrated to recapitulate some key features of Alzheimer’s disease pathology, including amyloid‐β (Aβ) pathogenesis. In this study, we placed 1‐month‐old APP × PS1 mice and non‐transgenic littermates on a WD for 4 weeks. The WD resulted in a significant elevation in protein oxidation and lipid peroxidation in the brain of APP × PS1 mice relative to non‐transgenic littermates, which occurred in the absence of increased Aβ levels. Altered adipokine levels were also observed in APP × PS1 mice placed on a short‐term WD, relative to non‐transgenic littermates. Taken together, these data indicate that short‐term WD is sufficient to selectively promote cerebral oxidative stress and metabolic disturbances in APP × PS1 knock‐in mice, with increased oxidative stress preceding alterations in Aβ. These data have important implications for understanding how WD may potentially contribute to brain dysfunction and the development of neurodegenerative disorders such as Alzheimer’s disease.
ISSN:0022-3042
1471-4159
DOI:10.1111/j.1471-4159.2008.05798.x