Non-Alcoholic Fatty Liver Disease, and the Underlying Altered Fatty Acid Metabolism, Reveals Brain Hypoperfusion and Contributes to the Cognitive Decline in APP/PS1 Mice.
Alzheimer disease mouse model
NAFLD
amyloïd Beta
brain hypoperfusion
inflammation
liver-to-brain axis
polyunsaturated fatty acids
senescence
untargeted and targeted lipidomics
Journal
Metabolites
ISSN: 2218-1989
Titre abrégé: Metabolites
Pays: Switzerland
ID NLM: 101578790
Informations de publication
Date de publication:
25 May 2019
25 May 2019
Historique:
received:
29
04
2019
revised:
16
05
2019
accepted:
21
05
2019
entrez:
28
5
2019
pubmed:
28
5
2019
medline:
28
5
2019
Statut:
epublish
Résumé
Non-alcoholic fatty liver disease (NAFLD), the leading cause of chronic liver disease, is associated with cognitive decline in middle-aged adults, but the mechanisms underlying this association are not clear. We hypothesized that NAFLD would unveil the appearance of brain hypoperfusion in association with altered plasma and brain lipid metabolism. To test our hypothesis, amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mice were fed a standard diet or a high-fat, cholesterol and cholate diet, inducing NAFLD without obesity and hyperglycemia. The diet-induced NAFLD disturbed monounsaturated and polyunsaturated fatty acid (MUFAs, PUFAs) metabolism in the plasma, liver, and brain, and particularly reduced n-3 PUFAs levels. These alterations in lipid homeostasis were associated in the brain with an increased expression of
Identifiants
pubmed: 31130652
pii: metabo9050104
doi: 10.3390/metabo9050104
pmc: PMC6572466
pii:
doi:
Types de publication
Journal Article
Langues
eng
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