scholarly journals High-fructose diet initially promotes increased aortic wall thickness, liver steatosis, and cardiac histopathology deterioration, but does not increase body fat index

2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Dian Handayani ◽  
Erlinda Febrianingsih ◽  
Adelya Desi Kurniawati ◽  
Inggita Kusumastuty ◽  
Shafira Nurmalitasari ◽  
...  

Background: Dietary fats and fructose have been responsible for inducing obesity and body tissues damage due to the consequence of metabolic syndrome through several mechanisms. The body fat index (BFI) is one of the anthropometric measures used to detect obesity in rats. This study aims to examine the correlation between high-fat high-fructose diet and liver steatosis cell count, early atherosclerosis characteristics, and BFI in Sprague Dawley Rats.Design and methods: This was an experimental design using 2 groups of 12-weeks-old Sprague Dawley (SD) rats. The control group received a standard diet and tap water beverages for 17 weeks. The intervention group was fed with high-fat diet from modified AIN 93-M and additional 30% fructose drink. We analyzed the foam cell count, aortic wall thickness, cardiac histopathology, and liver steatosis cell count after the sacrifice process.Results: The rats in the intervention group had a higher aortic wall thickness, liver steatosis, and foam cell count (+125%, p<0.01; +317%, p<0.01 and +165%, p<0.01 respectively) compared to the control group. The intervention group also showed higher mononuclear inflammatory and hypertrophic cell count. A significant positive correlation was found between dietary fructose with premature atherosclerosis by increasing foam cell count (r=0.66) and aortic wall thickness (r=0.68). In addition, 30% dietary fructose increased liver steatosis (r =0.69) and mononuclear inflammatory cardiac cell count (r=0.61). Interestingly, the intervention had no effect on BFI (p>0.5; r=0.13).Conclusions: Dietary fat and fructose consumption for 17 weeks promote atherosclerosis, liver steatosis, and cardiac histopathology alteration without increasing BFI.

Author(s):  
Rokhima Lusiantari ◽  
Miranti Dewi Pramaningtyas ◽  
Titis Nurmasitoh ◽  
Rachmi Hidayati Pattimura ◽  
Anggita Dewanti

Background<br />Shortening is widely used as raw material for bread and other foods. Hypercholesterolemia increases aortic arch foam cell formation and abdominal aortic wall thickness. This study aimed to determine the effect of shortening on the number of aortic arch foam cells and abdominal aortic wall thickness in rats.<br /><br />Methods<br />This study was of experimental posttest control group design. Twenty four male Wistar rats were randomized into 4 groups. The negative control group (C-) received standard feed, the positive control group (C+) standard high-fat feed, group T1 shortening and standard feed at a ratio of 1:5 and group T2 shortening and standard feed at a ratio of 1:10. The interventions were given for 6 weeks through gavage. The foam cell count in the aortic arch and the thickness of the abdominal aortic wall were measured. One-way ANOVA test was used to analyze the data. <br /><br />Results<br /><p>There was no significant difference in the mean foam cell count of the aortic arch between the four groups C- (7.17 ± 4.17), C + (9.33 ± 7.01), T1 (11.83 ± 4.88) and T2 (9.33 ± 6.80) (p=0.598). The mean thickness of the abdominal aortic wall between the four groups C- (741.98 ± 60.67μm), C + (714.29 ± 90.59μm), T1 (838.90 ± 75.86 μm), and T2 (749.88 ± 99.37μm) also was not significantly different (p=0.110).</p><br />Conclusion <br />Shortening tends to increase the foam cell count of the aortic arch and the thickness of the abdominal aortic wall of rats.


2020 ◽  
Vol 33 (1) ◽  
pp. 50-55
Author(s):  
Andressa Moreira ◽  
Alessandra Nicolini ◽  
Eduardo Gaio ◽  
Fernanda Visioli ◽  
Cassiano Rösing ◽  
...  

The purpose of this study was to evaluate aortic wall thickness after periodontal disease and/or obesity induction in a Wistar rat model.Sixty male Wistar rats were randomly divided into four groups: control (CT), periodontal disease (PD), obesity (OB), and obesity plus periodontal disease (OB+PD). Groups OB and OB+PD received cafeteria diet for 17 weeks. After they had acquired obesity (week 12), periodontal disease was induced by placing a silk ligature on the maxillary right second molar of groups PD and OB+PD. During the experimental period, body weight and Lee index were assessed. Mean alveolar bone loss (ABL) was evaluated, and aortas were prepared for histometric analysis of the aortic wall by ImageJ software. Body weight and Lee index increased in rats exposed to cafeteria diet. Mean ABL was higher in Groups PD and OB+PD than in control and OB (p<0.05). ABL was 18% higher in Group OB+PD than in Group PD, with statistically significant difference (p<0.001). Aortas were thicker in Groups OB and OB+PD than in control and PD groups, respectively (2.31mm ± 0.28 and 2.33 ± 0.29 vs. 2.18 ± 0.26 and 2.14 ± 0.27). Group OB differed significantly from the control group (p=0.036), and OB+PD and OB differed significantly from PD (p=0.004 and p= 0.001, respectively). Obesity alters aortic wall thickness in Wistar rats. However, the presence of periodontal disease did not affect the aortic wall thickness under the conditions of the present study.


2014 ◽  
Vol 73 (Suppl 2) ◽  
pp. 1119.3-1120
Author(s):  
A. Nakhleh ◽  
D. Rimar ◽  
I. Rukhkyan ◽  
V. Wolfson ◽  
I. Rosner ◽  
...  

2015 ◽  
Vol 61 (4) ◽  
pp. 1034-1040 ◽  
Author(s):  
Eric K. Shang ◽  
Eric Lai ◽  
Alison M. Pouch ◽  
Robin Hinmon ◽  
Robert C. Gorman ◽  
...  

2006 ◽  
Vol 111 (4) ◽  
pp. 281-287 ◽  
Author(s):  
Michael R. Skilton ◽  
Alison K. Gosby ◽  
Ben J. Wu ◽  
Lisa M. L. Ho ◽  
Roland Stocker ◽  
...  

Epidemiological studies suggest a link between fetal/early infant nutrition and adult coronary artery disease. In the present study, we examined the effects of altering nutrition during gestation, lactation and juvenile life on aortic structure and function in rats. Wistar rat dams were fed either a control or low-protein diet throughout pregnancy, or a low-protein diet for the final 7 days of gestation only. At 21 days post-partum, male pups were weaned on to a control, low-protein or high-fat diet. At 12 weeks, the offspring rats were killed. In 46 rats, aortic sections were mounted and stained to assess media thickness and elastin content. In a further 38 rats, aortic rings were suspended in an organ bath and vascular reactivity was tested with dose–response curves to the endothelium-dependent dilator acetylcholine and the endothelium-independent dilator sodium nitroprusside. Rats exposed to maternal protein restriction while in utero had a significantly decreased aortic wall thickness compared with control rats (P=0.005). Total elastin content of the aorta was also decreased by both maternal low-protein (P=0.02) and early postnatal low-protein (P=0.01) diets. Neither maternal nor postnatal low-protein or high-fat diets, however, resulted in any significant changes in arterial dilator function. In conclusion, fetal undernutrition in rats, induced via a maternal low-protein diet, causes a decrease in aortic wall thickness and elastin content without altering aortic dilator function. These changes in vascular structure may amplify aging-related changes to the vasculature and contribute to the pathophysiology of the putative link between impaired fetal growth and adult cardiovascular disease.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Jacob W Groenendyk ◽  
Parag Shukla ◽  
Youssef A Elnabawi ◽  
Joshua P Rivers ◽  
Aditya Goyal ◽  
...  

Introduction: Patients with psoriasis (PSO), an inflammatory skin disease, experience increased cardiovascular disease and obesity. Traditional measures of obesity, such as BMI and waist-to-hip ratio (WHR), do not fully capture the increased cardiovascular risk. Assessment of adipose tissue distribution via CT scan enables characterization of visceral adiposity (VAT) versus subcutaneous adiposity (SAT), which is clinically useful as excess VAT is known to be associated with cardiovascular events. Aortic Wall Thickness (AWT) is a validated measure of subclinical atherosclerosis. However, the relationship between adiposity distribution and AWT is unknown. Hypothesis: We hypothesized that VAT, but not SAT, BMI, or WHR, would be associated with increased AWT in PSO patients. Methods: Consecutive PSO patients (n=164) underwent quantification of VAT and SAT via CT, and AWT via MRI of the descending aorta. Interrelationships were analyzed via multivariable regression. Results: Patients were middle-aged (mean 50.4), predominantly male (56%), and were at low cardiovascular risk (median Framingham risk 3), despite high prevalence of hyperlipidemia (47%). VAT was significantly associated with AWT (β=0.18, p=0.04), SAT, BMI, or WHR did not demonstrate similar association. This association persisted beyond adjustment for SAT, Framingham score, insulin resistance, and systolic BP (β=0.30, p=0.03). Conclusions: Visceral adiposity demonstrated an association with AWT, a marker of early atherosclerosis, whereas subcutaneous adiposity, BMI, and WHR did not. These findings add to a growing body of literature that visceral fat and its assessment may provide incremental data for risk of subclinical CVD.


2011 ◽  
Vol 300 (6) ◽  
pp. F1431-F1436 ◽  
Author(s):  
Keith Ng ◽  
Cara M. Hildreth ◽  
Jacqueline K. Phillips ◽  
Alberto P. Avolio

Increased aortic pulse-wave velocity (PWV) reflects increased arterial stiffness and is a strong predictor of cardiovascular risk in chronic kidney disease (CKD). We examined functional and structural correlations among PWV, aortic calcification, and vascular remodeling in a rodent model of CKD, the Lewis polycystic kidney (LPK) rat. Hemodynamic parameters and beat-to-beat aortic PWV were recorded in urethane-anesthetized animals [12-wk-old hypertensive female LPK rats ( n = 5)] before the onset of end-stage renal disease and their age- and sex-matched normotensive controls (Lewis, n = 6). Animals were euthanized, and the aorta was collected to measure calcium content by atomic absorption spectrophotometry. A separate cohort of animals ( n = 5/group) were anesthetized with pentobarbitone sodium and pressure perfused with formalin, and the aorta was collected for histomorphometry, which allowed calculation of aortic wall thickness, medial cross-sectional area (MCSA), elastic modulus (EM), and wall stress (WS), size and density of smooth muscle nuclei, and relative content of lamellae, interlamellae elastin, and collagen. Mean arterial pressure (MAP) and PWV were significantly greater in the LPK compared with Lewis (72 and 33%, respectively) animals. The LPK group had 6.8-fold greater aortic calcification, 38% greater aortic MCSA, 56% greater EM/WS, 13% greater aortic wall thickness, 21% smaller smooth muscle cell area, and 20% less elastin density with no difference in collagen fiber density. These findings demonstrate vascular remodeling and increased calcification with a functional increase in PWV and therefore aortic stiffness in hypertensive LPK rats.


1973 ◽  
Vol 11 (1) ◽  
pp. 39-42 ◽  
Author(s):  
A. E. Marble ◽  
W. Hilliard ◽  
A. S. MacDonald ◽  
C. H. Miller ◽  
J. G. Holland ◽  
...  

2019 ◽  
Vol 17 ◽  
pp. 205873921985855
Author(s):  
Kaijian Hou ◽  
Wansheng Ke ◽  
Jianping Xiong

This study was designed to investigate the effect of metformin on the improvement of prostate cancer in diabetic rats. A total of 20 Sprague Dawley (SD) rats were equally divided into control and intervention groups. The intervention group received intragastric metformin 200 mg/kg, while the control group was given intragastric drinking water for 4 weeks. Tumor volumes were compared, all tumor specimens underwent routine pathological examination, immunohistochemical detection of E-cadherin and N-cadherin, and western blot assay. The tumor volume of control and intervention group was 462.15 ± 45.67 and 23.46 ± 5.32 mm3, respectively. Hematoxylin and eosin (HE) staining showed partial visible glandular structure with deepened nuclear staining in the intervention group. Immunohistochemistry showed high expression (6.5 ± 0.28 vs 3.8 ± 0.26, P < 0.05) of E-cadherin and low expression (3.4 ± 0.12 vs 7.8 ± 0.34, P < 0.05) of N-cadherin in the intervention group. Western blot assay showed higher expression of E-cadherin, while low N-cadherin in the intervention group. Metformin can effectively alleviate lesion extent of prostate cancer and mechanism may be related to upregulation of E-cadherin and downregulation of N-cadherin expression.


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