scholarly journals Long-Term High-Fat Diet Consumption Depletes Glial Cells and Tyrosine Hydroxylase–Containing Neurons in the Brain of Middle-Aged Rats

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 295
Author(s):  
Mei-Chuan Chou ◽  
Hsiang-Chun Lee ◽  
Yen-Chin Liu ◽  
Patrick Szu-Ying Yen ◽  
Ching-Kuan Liu ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Glial Cells ◽  
High Fat Diet ◽  
Pyramidal Neurons ◽  
High Fat ◽  
Middle Aged ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto ◽  
The Brain

Epidemiologic studies have indicated that dyslipidemia may facilitate the progression of neuronal degeneration. However, the effects of chronic dyslipidemia on brain function, especially in older individuals, remain unclear. In this study, middle-aged 37-week-old male Wistar-Kyoto rats were fed a normal diet (ND) or a 45% high-fat diet (HFD) for 30 weeks (i.e., until 67 weeks of age). To study the effects of chronic dyslipidemia on the brain, we analyzed spontaneous locomotor activity, cognitive function, and brain tissues in both groups of rats after 30 weeks. Compared with age-matched rats fed a ND, Wistar-Kyoto rats fed a HFD had dyslipidemia and showed decreased movement but normal recognition of a novel object. In our brain analyses, we observed a significant decrease in astrocytes and tyrosine hydroxylase–containing neurons in the substantia nigra and locus coeruleus of rats fed a HFD compared with rats fed a ND. However, hippocampal pyramidal neurons were not affected. Our findings indicate that the long-term consumption of a HFD may cause lipid metabolism overload in the brain and damage to glial cells. The decrease in astrocytes may lead to reduced protection of the brain and affect the survival of tyrosine hydroxylase–containing neurons but not pyramidal neurons of the hippocampus.

Preventive effect of Eucommia leaf extract on aortic media hypertrophy in Wistar-Kyoto rats fed a high-fat diet

2017 ◽  
Vol 40 (6) ◽  
pp. 546-551 ◽  
Author(s):  
Shingo Hosoo ◽  
Masahiro Koyama ◽  
Akira Watanabe ◽  
Ryuya Ishida ◽  
Tetsuya Hirata ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Leaf Extract ◽  
Preventive Effect ◽  
High Fat ◽  
Wistar Kyoto Rats ◽  
Aortic Media ◽  
Wistar Kyoto

scholarly journals Tocotrienols Influence Body Weight Gain and Brain Protein Expression in Long-Term High-Fat Diet-Treated Mice

2020 ◽  
Vol 21 (12) ◽  
pp. 4533
Author(s):  
Yugo Kato ◽  
Yoshinori Aoki ◽  
Koji Fukui
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Cognitive Dysfunction ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
High Fat ◽  
Parkinson’S Diseases ◽  
Antioxidative Effects ◽  
The Brain

Obesity induces serious diseases such as diabetes and cardiovascular disease. It has been reported that obesity increases the risk of cognitive dysfunction. Cognitive dysfunction is a characteristic symptom of Alzheimer’s and Parkinson’s diseases. However, the detailed mechanisms of obesity-induced cognitive dysfunction have not yet been elucidated. The onset and progression of obesity-induced severe secondary diseases such as diabetes, cardiovascular events, and hypertension are deeply connected to oxidative stress. We hypothesized that obesity induces cognitive dysfunction via acceleration of reactive oxygen species (ROS) production. Vitamin E, which is a lipophilic vitamin, has strong antioxidative effects and consists of two groups: tocopherols and tocotrienols. Recently, it has been demonstrated that tocotrienols have strong neuroprotective and anti-obesity effects. In this study, we fed mice a high-fat diet (HFD) from 9 to 14 months of age and assessed the effect of tocotrienols treatment on body weight, brain oxidation levels, and cognitive function. The results revealed that treatment with tocotrienols inhibited body weight gain; further, tocotrienols reached the brain and attenuated oxidation in HFD-treated mice. These results indicate that tocotrienols have anti-obesity effects and inhibit obesity-induced brain oxidation.

Lactobacillus paracasei ameliorates cognitive impairment in high-fat induced obese mice via insulin and neuroinflammation signaling pathway

2021 ◽  
Author(s):  
yaoyao ji ◽  
Xinsong Lang ◽  
Wei Wang ◽  
Shengnan Li ◽  
Changhui Zhao ◽  
...  
Keyword(s):  
Nervous System ◽  
Cognitive Impairment ◽  
Lipid Metabolism ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders ◽  
The Brain

Long-term consumption of high-fat diet (HFD) can cause glucose and lipid metabolism disorders, damage the brain nervous system and result in cognitive impairment. The objective of this study was to...

scholarly journals High-Fat Diet Leads to Reduced Protein O-GlcNAcylation and Mitochondrial Defects Promoting the Development of Alzheimer’s Disease Signatures

2021 ◽  
Vol 22 (7) ◽  
pp. 3746
Author(s):  
Ilaria Zuliani ◽  
Chiara Lanzillotta ◽  
Antonella Tramutola ◽  
Eugenio Barone ◽  
Marzia Perluigi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
High Fat Diet ◽  
Mitochondrial Activity ◽  
High Fat ◽  
Hexosamine Biosynthetic Pathway ◽  
Neurodegenerative Process ◽  
The Brain

The disturbance of protein O-GlcNAcylation is emerging as a possible link between altered brain metabolism and the progression of neurodegeneration. As observed in brains with Alzheimer’s disease (AD), flaws of the cerebral glucose uptake translate into reduced protein O-GlcNAcylation, which promote the formation of pathological hallmarks. A high-fat diet (HFD) is known to foster metabolic dysregulation and insulin resistance in the brain and such effects have been associated with the reduction of cognitive performances. Remarkably, a significant role in HFD-related cognitive decline might be played by aberrant protein O-GlcNAcylation by triggering the development of AD signature and mitochondrial impairment. Our data support the impairment of total protein O-GlcNAcylation profile both in the brain of mice subjected to a 6-week high-fat-diet (HFD) and in our in vitro transposition on SH-SY5Y cells. The reduction of protein O-GlcNAcylation was associated with the development of insulin resistance, induced by overfeeding (i.e., defective insulin signaling and reduced mitochondrial activity), which promoted the dysregulation of the hexosamine biosynthetic pathway (HBP) flux, through the AMPK-driven reduction of GFAT1 activation. Further, we observed that a HFD induced the selective impairment of O-GlcNAcylated-tau and of O-GlcNAcylated-Complex I subunit NDUFB8, thus resulting in tau toxicity and reduced respiratory chain functionality respectively, highlighting the involvement of this posttranslational modification in the neurodegenerative process.

Sign in / Sign up

Export Citation Format

Share Document