scholarly journals Partial Replacement of Dietary Fat with Krill Oil or Coconut Oil Alleviates Dyslipidemia by Partly Modulating Lipid Metabolism in Lipopolysaccharide-Injected Rats on a High-Fat Diet

2022 ◽  
Vol 19 (2) ◽  
pp. 843
Author(s):  
Hee-Kyoung Son ◽  
Bok-Hee Kim ◽  
Jisu Lee ◽  
Seohyun Park ◽  
Chung-Bae Oh ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Coconut Oil ◽  
Partial Replacement ◽  
Krill Oil ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Phosphate Buffered Saline

This study investigated the effects of partial replacement of dietary fat with krill oil (KO) or coconut oil (CO) on dyslipidemia and lipid metabolism in rats fed with a high-fat diet (HFD). Sprague Dawley rats were divided into three groups as follows: HFD, HFD + KO, and HFD + CO. The rats were fed each diet for 10 weeks and then intraperitoneally injected with phosphate-buffered saline (PBS) or lipopolysaccharide (LPS) (1 mg/kg). The KO- and CO-fed rats exhibited lower levels of serum lipids and aspartate aminotransferases than those of the HFD-fed rats. Rats fed with HFD + KO displayed significantly lower hepatic histological scores and hepatic triglyceride (TG) content than rats fed with HFD. The KO supplementation also downregulated the adipogenic gene expression in the liver. When treated with LPS, the HFD + KO and HFD + CO groups reduced the adipocyte size in the epididymal white adipose tissues (EAT) relative to the HFD group. These results suggest that KO and CO could improve lipid metabolism dysfunction.

Hypertension and sympathetic hyperactivity induced in rats by high-fat or glucose diets

1991 ◽  
Vol 260 (1) ◽  
pp. E95-E100 ◽  
Author(s):  
L. N. Kaufman ◽  
M. M. Peterson ◽  
S. M. Smith
Keyword(s):  
Dietary Fat ◽  
High Fat Diet ◽  
Control Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Hypertensive Rats ◽  
Diet Treatment ◽  
Sprague Dawley Rats ◽  
Sympathetic Nervous ◽  
And Control

Male Sprague-Dawley rats fed either a high-fat diet or a glucose-enriched diet developed higher blood pressure (BP) than rats fed a control diet. After 8 wk of diet treatment systolic BP was 11% higher (P less than 0.01) in fat-fed rats and 7% higher (P less than 0.05) in glucose-fed rats when compared with rats fed the control diet. Rats fed the high-fat diet developed hypertension only when they were allowed to overeat and become obese and hyperinsulinemic. But when their feeding was restricted to prevent obesity and hyperinsulinemia, they remained normotensive. In contrast, elevated BP developed in rats consuming the glucose diet in the absence of obesity or hyperinsulinemia. After 7 wk of diet treatment, urinary norepinephrine excretion was 1.9 +/- 0.1, 1.9 +/- 0.1, and 1.5 +/- 0.1 micrograms/day in rats fed the high-fat, glucose, and control diets, respectively (P less than 0.05 vs. control). Higher norepinephrine excretion in hypertensive rats suggests that increased sympathetic nervous system (SNS) activity might participate in mediating the effects of dietary fat or glucose on BP. In addition, insulin may contribute to raising BP in rats fed the high-fat diet, either directly or indirectly through its stimulatory effect on the SNS. We conclude that chronic feeding of diets high in fat or glucose increases BP and enhances SNS activity in rats.

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

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 diet alters gut microbiota but not spatial working memory in early middle-aged Sprague Dawley rats

PLoS ONE ◽  
2019 ◽  
Vol 14 (5) ◽  
pp. e0217553 ◽  
Author(s):  
Nikita Girish Deshpande ◽  
Juhi Saxena ◽  
Tristan G. Pesaresi ◽  
Casey Dylan Carrell ◽  
Grayson Breneman Ashby ◽  
...  
Keyword(s):  
Working Memory ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Spatial Working Memory ◽  
Sprague Dawley ◽  
High Fat ◽  
Middle Aged ◽  
Sprague Dawley Rats

Attenuation of circadian rhythms of food intake and respiration in aging diabetes-prone BHE/Cdb rats

2000 ◽  
Vol 279 (1) ◽  
pp. R230-R238 ◽  
Author(s):  
Clayton E. Mathews ◽  
Kathie Wickwire ◽  
Wiliam P. Flatt ◽  
Carolyn D. Berdanier
Keyword(s):  
Food Intake ◽  
High Fat Diet ◽  
Diet Composition ◽  
Stock Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Daily Rhythms ◽  
Sprague Dawley Rats ◽  
Typical Day ◽  
Food Intake Patterns

The hypothesis that BHE/Cdb rats with mutations in their mitochondrial genome might accommodate this mutation by changing their food intake patterns was tested. Four experiments were conducted. Experiments 1 and 2examined food intake patterns of BHE/Cdb rats fed a stock diet or BHE/Cdb and Sprague-Dawley rats fed a high-fat diet from weaning. Experiment 3 examined the daily rhythms of respiration and heat production in these rats at 200 days of age. Experiment 4 examined the effects of diet composition on these measurements at 50-day intervals. The Sprague-Dawley rats, regardless of diet, had the typical day-night rhythms of feeding and respiration. In contrast, the BHE/Cdb rats fed the high-fat diet showed normal rhythms initially, but with age, these rhythms were attenuated. The changes in rhythms preceded the development of glucose intolerance.

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