Differential effects of a short-term high-fat diet in an animal model of depression in rats treated with the 5-HT3 receptor antagonist, ondansetron, the 5-HT3 receptor agonist, 2-methyl-5-HT, and the SSRI, fluoxetine

2016 ◽  
Vol 144 ◽  
pp. 78-84 ◽  
Author(s):  
Isabel C. Sumaya ◽  
Dee Bailey ◽  
Susan L. Catlett
Keyword(s):  
Animal Model ◽  
Receptor Antagonist ◽  
High Fat Diet ◽  
Receptor Agonist ◽  
High Fat ◽  
Short Term ◽  
Differential Effects ◽  
Animal Model Of Depression

scholarly journals Induced Short-term Hearing Loss due to Stimulation of Age-related Factors by Intermittent Hypoxia, High-Fat Diet, and Galactose Injection

2020 ◽  
Author(s):  
Dong Jun Park ◽  
Sunmok Ha ◽  
Jin Sil Choi ◽  
Su Hoon Lee ◽  
Jeong-Eun Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Cellular Aging ◽  
High Fat ◽  
Short Term ◽  
Related Factors ◽  
Age Related

Age-related hearing loss (ARHL) is the most common sensory disorder in the elderly. It is associated with aging and hair cell death due to oxidative stress-induced mitochondrial dysfunction. Although transgenic mice and long-term cultures for induction of aging have been used to study ARHL, there are presently no ARHL animal models stimulated by intermittent environmental change for aging. In this study, an ARHL animal model was established by inducing continuous oxidative stress to promote short-term aging of cells, determined based on the expression of the hearing loss-induced phenotype and aging related factors in the short term. The incidence of hearing loss was significantly different among the groups subjected to intermittent hypoxic environment, high-fat diet (HFD), and injection with D-galactose. Continuous oxidative stress and HFD were factors that accelerated cellular aging. Increase in UCP2 affected oxidative stress and mitochondrial dysfunction. CDH23, SLC26A4, KCNQ4, Myo7a, and Myo6, which are ARHL-related factors, were modified by oxidative stress in cells of the hearing organ. We found that intermittent hypoxic, HFD, and galactose injection accelerated cellular aging in the short term. Thus, we anticipate that the development of this hearing loss animal model, which reflects intermittent environmental changes, will benefit future research on ARHL.

scholarly journals Effects of 12 Weeks of Exercise on Hepatic TNF-α and PPARα in an Animal Model of High-Fat Diet-Induced Nonalcoholic Steatohepatitis

2009 ◽  
Vol 7 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Haifeng Zhang ◽  
Yuxiu He ◽  
Pak Kwong Chung ◽  
Tom K. Tong ◽  
Frank H. Fu ◽  
...  
Keyword(s):  
Animal Model ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
High Fat ◽  
Tnf Α

Regional determinants of arterial endothelial phenotype dominate the impact of gender or short-term exposure to a high-fat diet

2005 ◽  
Vol 332 (1) ◽  
pp. 142-148 ◽  
Author(s):  
Anthony G. Passerini ◽  
Congzhu Shi ◽  
Nadeene M. Francesco ◽  
Peiying Chuan ◽  
Elisabetta Manduchi ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Short Term ◽  
Short Term Exposure ◽  
Endothelial Phenotype ◽  
The Impact

scholarly journals Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet

2010 ◽  
Vol 299 (4) ◽  
pp. R1082-R1090 ◽  
Author(s):  
Jill K. Morris ◽  
Gregory L. Bomhoff ◽  
John A. Stanford ◽  
Paige C. Geiger
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Model ◽  
Locomotor Activity ◽  
Substantia Nigra ◽  
High Fat Diet ◽  
Model Assessment ◽  
High Fat

Despite numerous clinical studies supporting a link between type 2 diabetes (T2D) and Parkinson's disease (PD), the clinical literature remains equivocal. We, therefore, sought to address the relationship between insulin resistance and nigrostriatal dopamine (DA) in a preclinical animal model. High-fat feeding in rodents is an established model of insulin resistance, characterized by increased adiposity, systemic oxidative stress, and hyperglycemia. We subjected rats to a normal chow or high-fat diet for 5 wk before infusing 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our goal was to determine whether a high-fat diet and the resulting peripheral insulin resistance would exacerbate 6-OHDA-induced nigrostriatal DA depletion. Prior to 6-OHDA infusion, animals on the high-fat diet exhibited greater body weight, increased adiposity, and impaired glucose tolerance. Two weeks after 6-OHDA, locomotor activity was tested, and brain and muscle tissue was harvested. Locomotor activity did not differ between the groups nor did cholesterol levels or measures of muscle atrophy. High-fat-fed animals exhibited higher homeostatic model assessment of insulin resistance (HOMA-IR) values and attenuated insulin-stimulated glucose uptake in fast-twitch muscle, indicating decreased insulin sensitivity. Animals in the high-fat group also exhibited greater DA depletion in the substantia nigra and the striatum, which correlated with HOMA-IR and adiposity. Decreased phosphorylation of HSP27 and degradation of IκBα in the substantia nigra indicate increased tissue oxidative stress. These findings support the hypothesis that a diet high in fat and the resulting insulin resistance may lower the threshold for developing PD, at least following DA-specific toxin exposure.

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