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BioMed Research International
Volume 2015 (2015), Article ID 759803, 7 pages
Research Article

Effects of Caloric Intake on Learning and Memory Function in Juvenile C57BL/6J Mice

1Central Laboratory, Xuanwu Hospital, Capital Medical University, Key Laboratory for Neurodegenerative Disease of Ministry of Education, Beijing Geriatric Medical Research Center, No. 45 Changchun Street, Xicheng District, Beijing 100053, China
2Department of Neurology, Beijing Anzhen Hospital, Capital Medical University, No. 2 Anzhen Road, Chaoyang District, Beijing 100029, China
3Center of Alzheimer’s Disease, Beijing Institute for Brain Disorders, Capital Medical University, Beijing 100069, China

Received 1 September 2014; Revised 13 January 2015; Accepted 14 January 2015

Academic Editor: Aijun Wang

Copyright © 2015 Bao-Lei Xu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Dietary composition may influence neuronal function as well as processes underlying synaptic plasticity. In this study, we aimed to determine the effect of high and low caloric diets on a mouse model of learning and memory and to explore mechanisms underlying this process. Mice were divided into three different dietary groups: normal control , high-caloric (HC) diet , and low-caloric (LC) diet . After 6 months, mice were evaluated on the Morris water maze to assess spatial memory ability. We found that HC diet impaired learning and memory function relative to both control and LC diet. The levels of SIRT1 as well as its downstream effectors p53, p16, and peroxisome proliferator-activated receptor γ (PPARγ) were decreased in brain tissues obtained from HC mice. LC upregulated SIRT1 but downregulated p53, p16, and PPARγ. The expressions of PI3K and Akt were not altered after HC or LC diet treatment, but both LC and HC elevated the levels of phosphorylated-cAMP response element-binding protein (p-CREB) and IGF-1 in hippocampal CA1 region. Therefore, HC diet-induced dysfunction in learning and memory may be prevented by caloric restriction via regulation of the SIRT1-p53 or IGF-1 signaling pathways and phosphorylation of CREB.