scholarly journals Fermentation of Resistant Starch Is Not a Predictor of Very High or Low Serum TMAO in Rats, but Results in Greater Serum TMAO than Controls

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 386-386
Author(s):  
Diana Coulon ◽  
Ryan Page ◽  
Justin Guice ◽  
Anne Raggio ◽  
Brian Marx ◽  
...  
Keyword(s):  
Resistant Starch ◽  
Control Diet ◽  
Human Study ◽  
Cleveland Clinic ◽  
Mass Spectrometry Data ◽  
Gut Health ◽  
Sprague Dawley ◽  
High Fat ◽  
Risk Of Death ◽  
Sprague Dawley Rats

Abstract Objectives Consumption of resistant starch (RS) has positive gut health benefits, but RS has been associated with increased serum trimethylamine oxide (TMAO). Increased serum TMAO has been linked to enhanced risk of cardiovascular death. A human study found that RS and a high fat (41% of energy) diet resulted in higher TMAO levels compared to a low RS diet, but this was not seen in a high carbohydrate diet (27% energy as fat). We wanted to ascertain serum TMAO in rats fed a high-RS diet with moderate (MF) or high fat (HF) diets compared to controls. Methods Twenty-four male, Sprague-Dawley rats (n = 6) were fed either 23% RS type 2, high-amylose diet or a control diet using 100% amylopectin with either MF (30% energy) or HF (42% energy) levels. A 2X choline amount had been used in the AIN-93M diets as substrate for ultimate production of TMAO. After six weeks, serum TMAO was measured using stable isotope dilution liquid chromatography tandem mass spectrometry. Data were analyzed as a 2 × 2 factorial followed by Tukey test (P < 0.05). Serum TMAO is assessed for risk of death over a seven-year period into quadrants. Quadrants 3 (4.28–7.89 µM) and 4 (7.91-186.1 µM) have greater risk. Quadrants 1 (0.12–2.55 µM) and 2 (2.56–4.27 µM) had much lower risk. Results Average TMAO level for rats fed RS HF was 2.94 ± 0.4, and RS MF was 2.42 ± 0.4. The control HF was 1.53 ± 0.17, and control MF was 1.06 ± 0.17. Rats fed RS had significantly greater TMAO levels of 2.68 ± 0.28, quadrant 2, while the control rats had an average of 1.3 ± 0.12, quadrant 1. There was no significant increased effect for MF vs. HF. However, the variability was similar for the two RS groups with values in quadrants 1–3. Amount of fermentation was not associated with TMAO amounts. For example, the RS rat with the lowest serum TMAO (0.87 µM) had an empty cecum weight (ECW) of 2.40 g, while the highest (4.41 µM) had an ECW of 2.29 g. Conclusions Sprague-Dawley rats fed either MF or HF had increased TMAO with consumption of RS. Data indicate amount of fermentation is not the reason for increased TMAO. Possible differences in gut bacteria that produce trimethylamine from choline may be cause of TMAO production in the rats. Funding Sources LSU AgCenter and Lerner Research Institute (Dr Stan Hazen) of Cleveland Clinic for analysis of serum TMAO, and starches were gifted from Ingredion Incorporated.

scholarly journals The Impact of DJOS Surgery, a High Fat Diet and a Control Diet on the Enzymes of Glucose Metabolism in the Liver and Muscles of Sprague-Dawley Rats

2019 ◽  
Vol 10 ◽  
Author(s):  
Dominika Stygar ◽  
Dorian Andrare ◽  
Barbara Bażanów ◽  
Elżbieta Chełmecka ◽  
Tomasz Sawczyn ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
High Fat Diet ◽  
Control Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
The Impact

Adrenal medulla as a mediator of diet-induced hypertension

1993 ◽  
Vol 265 (1) ◽  
pp. R1-R6 ◽  
Author(s):  
L. N. Kaufman ◽  
H. Y. Li ◽  
M. M. Peterson ◽  
A. K. Gilardy
Keyword(s):  
Adrenal Medulla ◽  
Dietary Fat ◽  
Control Diet ◽  
Surgical Removal ◽  
Sprague Dawley ◽  
Urinary Catecholamine ◽  
High Fat ◽  
Diet Treatment ◽  
Sprague Dawley Rats ◽  
And Control

Male Sprague-Dawley rats fed either a high-fat or glucose-enriched diet for 10 wk developed higher blood pressure (BP) and higher urinary catecholamine excretion than rats fed a control diet. After 10 wk of diet treatment, systolic BP was 164 +/- 3, 156 +/- 2, and 145 +/- 4 mmHg in rats fed the high-fat, glucose, and control diets, respectively (P < 0.02 vs. control). During weeks 7-9 of diet treatment, excretion of epinephrine and norepinephrine was increased in hypertensive rats (those fed the high-fat or glucose diet) when compared with rats fed the control diet (P < 0.001). The purpose of this study was to determine whether the hypertensive response to nutrients could be prevented by prior surgical removal of the adrenal medulla. Adrenal demedullation nearly abolished epinephrine excretion, attenuated norepinephrine excretion, and completely blocked the hypertensive response to dietary fat and glucose. These findings suggest that adrenal medullary catecholamines play a role in the hypertensive response to nutrients.

scholarly journals Effects of Diet-Induced Obesity and Deficient in Vitamin D on Spermatozoa Function and DNA Integrity in Sprague-Dawley Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
O. Merino ◽  
R. Sánchez ◽  
B. M. Gregorio ◽  
F. J. Sampaio ◽  
J. Risopatrón
Keyword(s):  
Vitamin D ◽  
Dna Fragmentation ◽  
High Fat Diet ◽  
Control Diet ◽  
Sperm Function ◽  
Sprague Dawley ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
The Impact

Obesity has adverse effects on male fertility and usually is diagnosed with a prevalence of vitamin D deficiency (VD-). Discussion on the impact of obesity/VD- on sperm function has been limited. This study analyzed the effects of diet-induced obesity/VD- on viability and plasma membrane integrity (PMI), superoxide anion (O2-) level, and DNA fragmentation (DNAfrag) in sperm Sprague-Dawley rats. The males were randomized into four groups and fed for a period of 12 weeks: G1: control diet with vitamin D (C/VD+), G2: control diet without vitamin D (C/VD-), G3: high-fat diet with vitamin D (HF/VD+), and G4: high-fat diet without vitamin D (HF/VD-). Sperm function parameters were analyzed by flow cytometry. PMI percentages and O2- levels were not affected by any of the diets. DNA fragmentation was increasing significantly (p<0.05) in the spermatozoa of animals with diets vitamin D deficient (G2) and diet-induced obesity (G4). Our results allow us to point out that diet-induced obesity and VD- produce greater damage in DNA sperm of rats. The use of nutraceuticals containing vitamin D could be reducing the risk of fragmentation of DNA in spermatozoa.

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.

scholarly journals The Effects of Duodenojejunal Omega Switch in Combination with High-Fat Diet and Control Diet on Incretins, Body Weight, and Glucose Tolerance in Sprague-Dawley Rats

2017 ◽  
Vol 28 (3) ◽  
pp. 748-759 ◽  
Author(s):  
Dominika Stygar ◽  
Tomasz Sawczyn ◽  
Bronisława Skrzep-Poloczek ◽  
Aleksander J. Owczarek ◽  
Natalia Matysiak ◽  
...  
Keyword(s):  
Body Weight ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Control Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
And Control

scholarly journals Characterization of the microbiome of Down syndrome mouse model (Ts65Dn) in standard and high-fat diet.

2020 ◽  
Author(s):  
Ilona Ewa Grabowicz ◽  
Marta Fructuoso ◽  
Ilario De Toma ◽  
Mara Dierssen ◽  
Bartek Wilczynski
Keyword(s):  
Down Syndrome ◽  
High Fat Diet ◽  
Control Diet ◽  
Neurodevelopmental Disorder ◽  
Human Study ◽  
Chromosome 21 ◽  
Genotypic Differences ◽  
Gut Health ◽  
High Fat ◽  
Host Genotype

The intestinal microbiota is known to affect its host in numerous ways and can be altered by many factors including the host genotype and high-calorie diets. Down syndrome (DS) is a genetic neurodevelopmental disorder caused by the total or partial triplication of chromosome 21. Recently, a human study reported microbiota differences between DS and euploid humans. To further explore the differences due to the genotype, we here investigated the microbiome of trisomic mice (Ts65Dn). In trisomic mice we found a significant enrichment in abundances of bacteria: Bacteroides ovatus, B. thetaiotaomicron, and Akkermansia muciniphila - the mucus-degrading and gut-health promoting species. Since diet composition has an effect on microbiota species, we studied the effect of a high-fat diet on the observed genotypic differences. Our study provides evidence that microbiomes of trisomic mice on the control diet present more inter-individual differences than WT mice. Moreover, we observed that the high-fat diet led to increased differences between individuals and this effect was even more pronounced in the trisomic than in WT mice. We validated the results obtained with widely used 16rRNA gene sequencing with the sequencing of the total RNA.

scholarly journals ER stress contributes to high-fat diet-induced decrease of thyroglobulin and hypothyroidism

2019 ◽  
Vol 316 (3) ◽  
pp. E510-E518 ◽  
Author(s):  
Xiaohan Zhang ◽  
Shanshan Shao ◽  
Lifang Zhao ◽  
Rui Yang ◽  
Meng Zhao ◽  
...  
Keyword(s):  
Er Stress ◽  
Thyroid Function ◽  
High Fat Diet ◽  
Control Diet ◽  
Underlying Mechanism ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Rat Thyroid

Recent studies revealed the emerging role of excess uptake of lipids in the development of hypothyroidism. However, the underlying mechanism is largely unknown. We investigated the effect of high-fat diet (HFD) on thyroid function and the role of endoplasmic reticulum (ER) in HFD-induced hypothyroidism. Male Sprague-Dawley rats were fed with HFD or control diet for 18 wk. HFD rats showed an impaired thyroid function, with decreased thyroglobulin (Tg) level. We found the ER stress was triggered in HFD rat thyroid glands and palmitate-treated thyrocytes. Luminal swelling of ER in thyroid epithelial cells of HFD rats was also observed. The rate of Tg degradation increased in palmitate-treated thyrocytes. In addition, applying 4-phenyl butyric acid to alleviate ER stress in HFD rats improved the decrease of Tg and thyroid function. Withdrawal of the HFD improved thyroid function . In conclusion, we demonstrate that ER stress mediates the HFD-induced hypothyroidism, probably by impairing the production of Tg, and attenuation of ER stress improves thyroid function. Our study provides the understanding of how HFD induces hypothyroidism.

scholarly journals Dietary obesity increases NO and inhibits BKCa-mediated, endothelium-dependent dilation in rat cremaster muscle artery: association with caveolins and caveolae

2012 ◽  
Vol 302 (12) ◽  
pp. H2464-H2476 ◽  
Author(s):  
Lauren Howitt ◽  
T. Hilton Grayson ◽  
Margaret J. Morris ◽  
Shaun L. Sandow ◽  
Timothy V. Murphy
Keyword(s):  
Control Diet ◽  
Cremaster Muscle ◽  
Sprague Dawley ◽  
High Fat ◽  
Caveolin 1 ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Dependent Component ◽  
Obese Rats ◽  
Dietary Obesity

Obesity is a risk factor for hypertension and other vascular disease. The aim of this study was to examine the effect of diet-induced obesity on endothelium-dependent dilation of rat cremaster muscle arterioles. Male Sprague-Dawley rats (213 ± 1 g) were fed a cafeteria-style high-fat or control diet for 16–20 wk. Control rats weighed 558 ± 7 g compared with obese rats 762 ± 12 g ( n = 52–56; P < 0.05). Diet-induced obesity had no effect on acetylcholine (ACh)-induced dilation of isolated, pressurized (70 mmHg) arterioles, but sodium nitroprusside (SNP)-induced vasodilation was enhanced. ACh-induced dilation of arterioles from control rats was abolished by a combination of the KCa blockers apamin, 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34), and iberiotoxin (IBTX; all 0.1 μmol/l), with no apparent role for nitric oxide (NO). In arterioles from obese rats, however, IBTX had no effect on responses to ACh while the NO synthase (NOS)/guanylate cyclase inhibitors Nω-nitro-l-arginine methyl ester (l-NAME; 100 μmol/l)/1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 μmol/l) partially inhibited ACh-induced dilation. Furthermore, NOS activity (but not endothelial NOS expression) was increased in arteries from obese rats. l-NAME/ODQ alone or removal of the endothelium constricted arterioles from obese but not control rats. Expression of caveolin-1 and -2 oligomers (but not monomers or caveolin-3) was increased in arterioles from obese rats. The number of caveolae was reduced in the endothelium of arteries, and caveolae density was increased at the ends of smooth muscle cells from obese rats. Diet-induced obesity abolished the contribution of large-conductance Ca2+-activated K+ channel to ACh-mediated endothelium-dependent dilation of rat cremaster muscle arterioles, while increasing NOS activity and inducing an NO-dependent component.

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