Program Information
Quantification of Neurochemical Changes in Hippocampus of High Fat Diet Induced Mice by in Vivo MR Spectroscopy
S Lim*, K Song , C Yoo , B Choe , The Catholic University of Korea, College of Medicine, Seoul, Republic of Korea
Presentations
TU-C1-GePD-IT-2 (Tuesday, August 1, 2017) 9:30 AM - 10:00 AM Room: Imaging ePoster Theater
Purpose: In this study, we investigated the neurochemical alterations in mouse hippocampus using in vivo magnetic resonance spectroscopy (MRS). We also examine the effect of high-fat diet on the levels of abdominal fat, plasma leptin, and corticosterone.
Methods: Fourteen male, 4 week-old, C57BL/6 mice were arbitrarily assigned into two groups: low fat (LF; n = 7) and high fat (HF; n = 7). LF and HF groups were fed diets consisting of 10% and 60% fat, respectively, for 10 weeks and weighed once per week. MRS scans were conducted following 10 weeks for each group. In vivo 1H MRS spectra were acquired using point resolved spectroscopy (PRESS) pulse sequences applied to the hippocampus with variable power and optimized relaxation delays. Parameters were as follows: TR = 5000 ms, TE = 13.40 ms, spectral width = 5.0 kHz, average = 384, number of data points = 2048, voxel size = 1.2*1.5*2.0 mm. Abdominal fat MRI scans were performed 3 days following the brain MRS scan. T1-weighted images were acquired using the following parameters: TR = 900 ms, Average = 4, TE = 9.14 ms. Abdominal fat quantification was performed using ImageJ.
Results: At week 10, mIns levels in the HF group were significantly lower than those in the LF group (p = 0.007). Total choline levels were also significantly lower in the HF group than in the LF group (p = 0.015). The average amount of abdominal fat in HF diet mice was significantly higher than that in LF diet mice (p < 0.000). Plasma analysis revealed that both corticosterone and leptin levels in HF mice were significantly higher than those in LF mice (p = 0.03, p = 0.000 respectively).
Conclusion: We suggest that diets rich in saturated fats induce a stress-related response through metabolic disturbance and HPA axis dysfunction.
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