Naringenin alleviates cognition deficits in high‐fat diet‐fed SAMP8 mice

2020 ◽  
Vol 44 (9) ◽  
Author(s):  
Tao Zhou ◽  
Long Liu ◽  
Qiulian Wang ◽  
Ying Gao
Keyword(s):  
High Fat ◽  
2018 ◽  
Vol 21 (8) ◽  
pp. 755-760 ◽  
Author(s):  
Yehua Rui ◽  
Shengyi Yang ◽  
Li-hua Chen ◽  
Li-qiang Qin ◽  
Zhongxiao Wan

2018 ◽  
Vol 59 ◽  
pp. 64-75 ◽  
Author(s):  
Miao-miao Zhou ◽  
Lin Ding ◽  
Min Wen ◽  
Hong-xia Che ◽  
Jia-qi Huang ◽  
...  

2019 ◽  
Author(s):  
Chyi-Huey Bai ◽  
Javad Alizargar ◽  
Jia-Ping Wu

AbstractSarcopenic obesity is a progressive loss of skeletal muscle mass and strength with increases in adiposity. The aim of this study was to investigate the effects of resveratrol on obesity or sarcopenia to potential therapy risk for skeletal muscle declines in physical function. C57BL/6J male mice were fed either a high-fat diet for 4 weeks and resveratrol (low-, middle-, and high-dose) for 8 weeks to express the obesity effect. Samp8 mice sarcopenia skeletal muscle functional deterioration expressed an age-associated decline. Resveratrol (150 mg/Kg BW, daily) was administered by oral gavage two times a week one month of the experimental period. Exercise training based on adaptations in the muscle is training twice a week for 4 weeks. The skeletal muscles from mice in each group were analyzed by H&E staining, TUNEL and western blot analysis to determine mitochondrial function expression, apoptosis and relative fibrosis signaling. Results of the present study indicate that resveratrol in obesity skeletal muscle is linked to an increase in the expression of mitochondrial function involved in Bcl-2 and PI3K/AKT. On the other hand, resveratrol attenuates sarcopenia Samp8 mice, the age-related loss of skeletal muscle mass and mitochondrial function involved in Bad, caspase 3 and IL-6/ERK1. However, exercise training not find a significant difference in sarcopenia skeletal muscles SAMP8 mice. Exercise training didn’t induce sarcopenia skeletal muscle hypertrophy in sarcopenic SAMP8 mice. Therefore, we suggest that resveratrol as a therapeutic potential in the combination of sarcopenia and obesity, the state called sarcopenic obesity.


Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 1084 ◽  
Author(s):  
Yehua Rui ◽  
Menglian Lv ◽  
Jie Chang ◽  
Jiaying Xu ◽  
Liqiang Qin ◽  
...  

Background: Chia seed is an ancient seed with the richest plant source of α-linolenic acid, which has been demonstrated to improve metabolic syndrome associated risk factors. Under high fat diet (HFD) condition, the senescence-accelerated mouse-prone 8 (SAMP8) mice demonstrated worsen Alzheimer’s disease (AD) related pathology compared to low fat diet fed SAMP8 mice. Objective: To explore whether chia seed supplementation might improve cognitive impairment under aging and metabolic stress via high fat diet (HFD) fed SAMP8 mice as a model. Design: SAMP8 mice and senescence-accelerated mouse-resistant 1 (SAMR1) were randomized into 4 groups, i.e., SAMR1 low fat diet group (SAMR1-LFD), SAMP8-HFD and SAMP8-HFD group supplemented with 10% chia seed (SAMP8-HFD+Chia). At the end of the intervention, cognitive function was measured via Morris water maze (MWM) test. Hippocampus and parietal cortex were dissected for further analysis to measure key markers involved AD pathology including Aβ, tau and neuro-inflammation. Results: During navigation trials of MWM test, mice in SAMP8-LFD group demonstrated impaired learning ability compared to SAMR1-LFD group, and chia seed had no effect on learning and memory ability for HFD fed SAMP8 mice. As for Alzheimer’s disease (AD) related pathology, chia seed not only increased α-secretase such as ADAM10 and insulin degrading enzyme (IDE), but also increased β-secretase including beta-secretase 1 (BACE1) and cathepsin B, with an overall effects of elevation in the hippocampal Aβ42 level; chia seed slightly reduced p-Tauser404 in the hippocampus; while an elevation in neuro-inflammation with the activation of glial fibrillary acidic protein (GFAP) and Ibα-1 were observed post chia seed supplementation. Conclusions: Chia seed supplementation did not improve cognitive impairment via MWM in HFD fed SAMP8 mice. This might be associated with that chia seed increased key enzymes involved both in non-amyloidogenic and amyloidogenic pathways, and neuro-inflammation. Future studies are necessary to confirm our present study.


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