scholarly journals High fat feeding promotes sympathetic axon outgrowth and cardiac hyperinnervation in male Sprague‐Dawley rats

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Belinda H. McCully ◽  
Cole T. Streiff ◽  
Beth A. Habecker ◽  
Virginia L. Brooks
Keyword(s):  
Axon Outgrowth ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Sympathetic Axon ◽  
Fat Feeding

The Effects of Maternal High Fat Diet on the Lingual CD36 Lipid Sensors of the Offspring Sprague Dawley Rats

Metabolism ◽  
2021 ◽  
Vol 116 ◽  
pp. 154497
Author(s):  
Elif Günalan ◽  
Meyli Ezgi Karagöz ◽  
Bayram Yılmaz ◽  
Burcu Gemici
Keyword(s):  
High Fat Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Lipid Sensors

scholarly journals Short-Term High Fat Intake Does Not Significantly Alter Markers of Renal Function or Inflammation in Young Male Sprague-Dawley Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Catherine Crinigan ◽  
Matthew Calhoun ◽  
Karen L. Sweazea
Keyword(s):  
Kidney Disease ◽  
Renal Mass ◽  
Early Stage ◽  
Young Male ◽  
Protective Effects ◽  
Sprague Dawley ◽  
High Fat ◽  
Short Term ◽  
Sprague Dawley Rats ◽  
The Impact

Chronic high fat feeding is correlated with diabetes and kidney disease. However, the impact of short-term high fat diets (HFD) is not well-understood. Six weeks of HFD result in indices of metabolic syndrome (increased adiposity, hyperglycemia, hyperinsulinemia, hyperlipidemia, hyperleptinemia, and impaired endothelium-dependent vasodilation) compared to rats fed on standard chow. The hypothesis was that short-term HFD would induce early signs of renal disease. Young male Sprague-Dawley rats were fed either HFD (60% fat) or standard chow (5% fat) for six weeks. Morphology was determined by measuring changes in renal mass and microstructure. Kidney function was measured by analyzing urinary protein, creatinine, and hydrogen peroxide (H2O2) concentrations, as well as plasma cystatin C concentrations. Renal damage was measured through assessment of urinary oxDNA/RNA concentrations as well as renal lipid peroxidation, tumor necrosis factor alpha (TNFα), and interleukin 6 (IL-6). Despite HFD significantly increasing adiposity and renal mass, there was no evidence of early stage kidney disease as measured by changes in urinary and plasma biomarkers as well as histology. These findings suggest that moderate hyperglycemia and inflammation produced by short-term HFD are not sufficient to damage kidneys or that the ketogenic HFD may have protective effects within the kidneys.

Abstract 382: Anti-MAA Antibodies in Sprague Dawley Rats are Increased in Response to a High Fat Western Diet

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Michael J Duryee ◽  
Anand Dusad ◽  
Scott W Shurmur ◽  
Michael D Johnston ◽  
Robert P Garvin ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Normal Diet ◽  
Western Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Stable Plaque ◽  
Circulating Antibodies ◽  
Modified Proteins ◽  
Progression Of Atherosclerosis

Introduction Malondialdehyde/Acetaldehyde (MAA) modified proteins have been suggested to play a role in the development/progression of atherosclerosis. Circulating antibodies directed against these proteins have recently been shown to be associated with the severity of the disease. More specifically, the isotype of the antibody to MAA correlated with either an acute MI (IgG) or stable plaque formation (IgA) formation. MAA is thought to form as a result of the oxidation of fat(s) and thus the concentration and antibody response should reflect the amount of fat in the diet. Objective The purpose of this study was to evaluate the antibody responses to MAA modified proteins following immunization and high fat western diet feeding in rats. Methods Male Sprague Dawley rats were immunized with MAA-modified protein weekly for 5 weeks and then assayed for antibodies to these proteins. Animals were then separated into the following groups: chow sham, chow MAA immunized, high fat sham, and high fat MAA immunized. The high fat animals were fed a Western diet with 2-thiouracil for 12 weeks, bled every 3 weeks, and serum assayed for the presence of circulating MAA antibodies. Results Prior to feeding with high fat diet, rats immunized with MAA-modified protein had a significant increase (P<0.001) in serum antibodies directed against these modified proteins compared to controls (N of 4 per group). Following feeding of high fat diet antibody concentrations increased 6 fold in the high fat MAA immunized group compared to the chow MAA immunized group (P<0.05). Antibodies in the high fat sham and chow sham had only minimal increases in antibodies to these proteins. Conclusions These data demonstrate that following immunization with MAA-modified proteins, circulating antibodies are produced that increase following consumption of a high fat Western diet. It suggests that MAA-modified proteins are produced at low levels following normal diet, producing antibodies which act as a normal clearance method for altered protein. When high fat consumption increases these antibody levels are increased in response to the oxidative stress. Implications Use of these antibodies as a biomarker in the future may help predict the onset or progression of atherosclerosis.

scholarly journals High-Fat-High-Fructose Diet Decreases Hippocampal Neuron Number in Male Rats

2020 ◽  
Vol 12 (1) ◽  
pp. 1-7
Author(s):  
Inggita Kusumastuty ◽  
Frinny Sembiring ◽  
Sri Andarini ◽  
Dian Handayani
Keyword(s):  
Cell Death ◽  
Nerve Cell ◽  
Hippocampal Neurons ◽  
Sprague Dawley ◽  
High Fat ◽  
Group I ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Group Ii ◽  
Nerve Cell Death

BACKGROUND: Consumption of foods and drinks high in energy, fat, and/or sugar beyond the recommended quantities can cause obesity, which triggers the incidence of brain nerve cell death related to oxidative stress, high levels of tumor necrosis factor (TNF)-α and triglycerides, and low high-density lipoprotein (HDL) levels. Progressive nerve cell death causes decreasing cognitive performance. This study aims to prove that an American Institute of Nutrition committee in 1993 (AIN-93M) diet modified with high-fat-high-fructose (HFHF) can decrease the number of hippocampal neurons. A decrease in the number of hippocampal neurons indicates progressive nerve cell death.METHODS: An experimental study using a post-test control group design was carried out using male Sprague Dawley rats. Samples were selected using simple random sampling to divide them into two groups, Group I was AIN-93M-modified HFHF diet (n=14) and Group II was AIN-93M standard (n=16). The number of visible neurons was measured in the hippocampus area of Sprague Dawley rats’ brains, stained with haemotoxylin and eosin (H&E) and scanned under 400x magnification. Neurons were counted in 10 visual fields using the "Cell_Count" application.RESULTS: The data were analysed by Pearson’s correlation test using SPSS. The results show that rats in Group I had a greater weight gain and fewer neurons than those in the Group II (p=0.023, r=-0.413).CONCLUSION: The consumption of foods high in fat and fructose can cause an increase in nerve cell death, as shown by the decrease in the number of hippocampal neurons.KEYWORDS: brain nerve cells, high fat, high fructose, increased body weight

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