Impairment of hippocampal-dependent memory induced by juvenile high-fat diet intake is associated with enhanced hippocampal inflammation in rats.
Brain, Behavior, and Immunity. 2014-08-01; 40: 9-17
DOI: 10.1016/j.bbi.2014.03.005
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1. Brain Behav Immun. 2014 Aug;40:9-17. doi: 10.1016/j.bbi.2014.03.005. Epub 2014
Mar 22.
Impairment of hippocampal-dependent memory induced by juvenile high-fat diet
intake is associated with enhanced hippocampal inflammation in rats.
Boitard C(1), Cavaroc A(1), Sauvant J(1), Aubert A(1), Castanon N(1), Layé S(1),
Ferreira G(2).
Author information:
(1)INRA, Nutrition and Integrative Neurobiology, UMR 1286, 33076 Bordeaux,
France; Université de Bordeaux, Nutrition and Integrative Neurobiology, UMR 1286,
33076 Bordeaux, France.
(2)INRA, Nutrition and Integrative Neurobiology, UMR 1286, 33076 Bordeaux,
France; Université de Bordeaux, Nutrition and Integrative Neurobiology, UMR 1286,
33076 Bordeaux, France. Electronic address: .
In addition to metabolic and cardiovascular disorders, obesity pandemic is
associated with chronic low-grade inflammation as well as adverse cognitive
outcomes. However, the existence of critical periods of development that differ
in terms of sensitivity to the effects of diet-induced obesity remains
unexplored. Using short exposure to a high-fat diet (HFD) exerting no effects
when given to adult mice, we recently found impairment of hippocampal-dependent
memory and plasticity after similar HFD exposure encompassing adolescence (from
weaning to adulthood) showing the vulnerability of the juvenile period (Boitard
et al., 2012). Given that inflammatory processes modulate hippocampal functions,
we evaluated in rats whether the detrimental effect of juvenile HFD (jHFD) on
hippocampal-dependent memory is associated with over-expression of hippocampal
pro-inflammatory cytokines. jHFD exposure impaired long-term spatial reference
memory in the Morris water maze without affecting acquisition or short-term
memory. This suggests an effect on consolidation processes. Moreover, jHFD
consumption delayed spatial reversal learning. jHFD intake did neither affect
basal expression of pro-inflammatory cytokines at the periphery nor in the brain,
but potentiated the enhancement of Interleukin-1-beta and Tumor Necrosis
Factor-alpha expression specifically in the hippocampus after a peripheral immune
challenge with lipopolysaccharide. Interestingly, whereas the same duration of
HFD intake at adulthood induced similar weight gain and metabolic alterations as
jHFD intake, it did neither affect spatial performance (long-term memory or
reversal learning) nor lipopolysaccharide-induced cytokine expression in the
hippocampus. Finally, spatial reversal learning enhanced Interleukin-1-beta in
the hippocampus, but not in the frontal cortex and the hypothalamus, of jHFD-fed
rats. These results indicate that juvenile HFD intake promotes exaggerated
pro-inflammatory cytokines expression in the hippocampus which is likely to
contribute to spatial memory impairment.
Copyright © 2014 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.bbi.2014.03.005
PMID: 24662056 [Indexed for MEDLINE]