scholarly journals Impact of a High-fat Diet on the Development of Chronic Inflammation in Heart of Wistar rats

Folia Medica ◽  
2019 ◽  
Vol 61 (3) ◽  
pp. 404-410
Author(s):  
Iliyan V. Dimitrov ◽  
Vassil I. Kamenov ◽  
Nikolay P. Boyadjiev ◽  
Katerina N. Georgieva ◽  
Anelia V. Bivolarska ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Interleukin 4 ◽  
Laboratory Animals ◽  
Control Group ◽  
Low Grade ◽  
High Fat ◽  
Amyloid A ◽  
Anti Inflammatory

Introduction: Obesity is linked to the development of low-grade, chronic inflammation. Obesity-related inflammation appears to be a different type of inflammation, mainly due to excessive food intake and unusual homeostasis. It can be evaluated by measuring the concentration of pro- and anti-inflammatory marker molecules &ndash; C-reactive protein (CRP), serum amyloid-A (SAA) and interleukin-4. Aim: The aim of the present study is to evaluate the rate of the inflammatory process in heart, provoked by the consumption of a high-fat diet. Materials and methods: Sixty 8-week-old male Wistar rats were used in this experiment. The laboratory animals were fed orally with two different types of rodent food for 14 or 18 weeks &ndash; a high-fat diet (experimental groups) and standard rodent food (control groups). They all were kept under standard housing conditions. The levels of the pro- and anti-inflammatory markers in tissue homogenates from heart were analyzed using ELISA. Their expression in tissue samples was detected immunohistochemically by the biotin-streptavidin-peroxidase method. The total protein concentration was determined by the Lawry method. Results: CRP levels showed no significant differences when the control group was compared with the groups fed with a high-fat diet (p>0.05). The SAA levels detected were also insignificantly changed. Only the IL-4 tissue levels showed tendency to increase (p<0.05) in the high-fat diet group. Conclusions: Our experiment indicates that there is a specific reaction of the heart to a high-fat diet. It also refers to the existence of adaptive mechanisms allowing the heart to counteract the development of dietary induced inflammation.

Particular Matter of Motor Vehicle Exposure and High-Fat Diet Effects on Kidney Histopathology, Creatinine, and Malondialdehyde (MDA) Levels in Wistar Rats

2021 ◽  
Vol 5 (3) ◽  
pp. 124-128
Author(s):  
Rizka Veni ◽  
Awal Prasetyo ◽  
Muflihatul Muniroh
Keyword(s):  
High Fat Diet ◽  
Wistar Rats ◽  
Motor Vehicle ◽  
Histopathological Change ◽  
Normal Diet ◽  
Control Group ◽  
High Fat ◽  
Control Group Design ◽  
Treatment Groups ◽  
Significant Difference

This study aims to analyze the effect of combination of motor vehicle particular matter exposure and high-fat diet in kidney histopathology, creatinine levels, and MDA levels in Wistar rats. This study used a posttest-only control group design. Eighteen healthy male Wistar rats were divided into three groups. The intervention groups received motor vehicle fume exposure for 100 s with normal diet (X1) or high-fat diet (X2), and the control group received no exposure (C). Data analysis was processed with a SPSS 25.0 computer program by using the one-way ANOVA test followed by post hoc LSD. The degree of kidney histopathological damage showed significant differences between the X1 and X2 groups when compared with the control group (p < 0.05). The results of the creatinine level examination found a significant difference between the X2 and C groups (p < 0.05) and the treatment groups X1 and X2 (p < 0.05). The results of kidney MDA level examination showed a significant difference between the treatment groups (X1 and X2) and the control group (p < 0.05). The combination of particular matter of motor vehicle fumes exposure and high-fat diet could induce kidney damage through histopathological change and increased creatinine levels and kidney MDA levels in Wistar rats.

scholarly journals Effects of a Mixed Limosilactobacillus fermentum Formulation with Claimed Probiotic Properties on Cardiometabolic Variables, Biomarkers of Inflammation and Oxidative Stress in Male Rats Fed a High-Fat Diet

Foods ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2202
Author(s):  
Micaelle Oliveira de Luna Freire ◽  
Luciana Caroline Paulino do Nascimento ◽  
Kataryne Árabe Rimá de Oliveira ◽  
Alisson Macário de Oliveira ◽  
Thiago Henrique Napoleão ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Control Diet ◽  
Male Rats ◽  
Control Group ◽  
Low Grade ◽  
Probiotic Properties ◽  
High Fat ◽  
Low Grade Inflammation ◽  
And Oxidative Stress

High-fat diet (HFD) consumption has been linked to dyslipidemia, low-grade inflammation and oxidative stress. This study investigated the effects of a mixed formulation with Limosilactobacillusfermentum 139, L. fermentum 263 and L. fermentum 296 on cardiometabolic parameters, fecal short-chain fatty acid (SCFA) contents and biomarkers of inflammation and oxidative stress in colon and heart tissues of male rats fed an HFD. Male Wistar rats were grouped into control diet (CTL, n = 6), HFD (n = 6) and HFD with L. fermentum formulation (HFD-Lf, n = 6) groups. The L.fermentum formulation (1 × 109 CFU/mL of each strain) was administered twice a day for 4 weeks. After a 4-week follow-up, biochemical parameters, fecal SCFA, cytokines and oxidative stress variables were evaluated. HFD consumption caused hyperlipidemia, hyperglycemia, low-grade inflammation, reduced fecal acetate and propionate contents and increased biomarkers of oxidative stress in colon and heart tissues when compared to the CTL group. Rats receiving the L. fermentum formulation had reduced hyperlipidemia and hyperglycemia, but similar SCFA contents in comparison with the HFD group (p < 0.05). Rats receiving the L. fermentum formulation had increased antioxidant capacity throughout the colon and heart tissues when compared with the control group. Administration of a mixed L. fermentum formulation prevented hyperlipidemia, inflammation and oxidative stress in colon and heart tissues induced by HFD consumption.

scholarly journals Histologi Lumen Dan Endotelium Arteri Dorsal Penis Tikus Wistar (Rattus Novergicus) Yang Diinduksi Pakan Tinggi Lemak

2020 ◽  
Vol 7 (1) ◽  
pp. 73
Author(s):  
I Wayan Rosiana ◽  
I Gede Widhiantara
Keyword(s):  
Treatment Group ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Wistar Rat ◽  
Lumen Diameter ◽  
Control Group ◽  
High Fat ◽  
Arterial Lumen ◽  
Male Wistar Rats ◽  
The Difference

This study aims to look at the histopathological picture of the dorsal arteries of the penis of the hiperlipidemic wistar rats (Rattus novergicus) induction by high-fat diet that seen in terms of lumen diameter and thickness of the arterial endotelium wall. Hyperlipidemia is a risk factor for ateriosclerosis in the penile arteries causing erectile dysfunction in men. This study is an experimental study with a randomized posttest only control goup design. The sample are  10 individuals adult male wistar rats aged 3-4 months with a range of body weight 150-200 grams. Before treatment, adaptation was carried out for 7 days. After that the sample rats in the treatment group were made hyperlidemic by feeding lard for 50 days. Then surgery is performed for histopathological preparations at the posttest. To determine the differences in endotelium thickness and arterial lumen diameter in the two groups, an independent t-test was used. Thick diameter data of the endotelium and dorsal arteries of the penis of the wistar rat between the lower treatment group and the control group. The difference that occurred was statistically significant (p <0.05). So it can be concluded that the provision of high-fat diet (hyperlipidemia) decreases the lumen diameter and endotelium thickness of dorsal arteries penis. Keywords: Dorsal arteries, high-fat diet, Wistar rats

scholarly journals Empagliflozin reverses obesity and insulin resistance through fat browning and alternative macrophage activation in mice fed a high-fat diet

2019 ◽  
Vol 7 (1) ◽  
pp. e000783 ◽  
Author(s):  
Liang Xu ◽  
Naoto Nagata ◽  
Guanliang Chen ◽  
Mayumi Nagashimada ◽  
Fen Zhuge ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Chronic Inflammation ◽  
Plasma Levels ◽  
High Fat Diet ◽  
Macrophage Activation ◽  
Low Grade ◽  
Obese Mice ◽  
High Fat

ObjectiveWe reported previously that empagliflozin—a sodium-glucose cotransporter (SGLT) 2 inhibitor—exhibited preventive effects against obesity. However, it was difficult to extrapolate these results to human subjects. Here, we performed a therapeutic study, which is more relevant to clinical situations in humans, to investigate antiobesity effects of empagliflozin and illustrate the mechanism underlying empagliflozin-mediated enhanced fat browning in obese mice.Research design and methodsAfter 8 weeks on a high-fat diet (HFD), C57BL/6J mice exhibited obesity, accompanied by insulin resistance and low-grade chronic inflammation. Cohorts of obese mice were continued on the HFD for an additional 8-week treatment period with or without empagliflozin.ResultsTreatment with empagliflozin for 8 weeks markedly increased glucose excretion in urine, and suppressed HFD-induced weight gain, insulin resistance and hepatic steatosis. Notably, empagliflozin enhanced oxygen consumption and carbon dioxide production, leading to increased energy expenditure. Consistently, the level of uncoupling protein 1 expression was increased in both brown and white (WAT) adipose tissues of empagliflozin-treated mice. Furthermore, empagliflozin decreased plasma levels of interleukin (IL)-6 and monocyte chemoattractant protein-1, but increased plasma levels of IL-33 and adiponectin in obese mice. Finally, we found that empagliflozin reduced M1-polarized macrophage accumulation, while inducing the anti-inflammatory M2 phenotype of macrophages in the WAT and liver, thereby attenuating obesity-related chronic inflammation.ConclusionsTreatment with empagliflozin attenuated weight gain by increasing energy expenditure and adipose tissue browning, and alleviated obesity-associated inflammation and insulin resistance by alternative macrophage activation in the WAT and liver of obese mice.

scholarly journals Effect of febuxostat on biochemical parameters of hyperlipidemia induced by a high-fat diet in rabbits

2019 ◽  
Vol 97 (7) ◽  
pp. 611-622 ◽  
Author(s):  
Mohammed M. Heikal ◽  
Ahmed A. Shaaban ◽  
Wagdi F. Elkashef ◽  
Tarek M. Ibrahim
Keyword(s):  
Xanthine Oxidase ◽  
High Fat Diet ◽  
Biochemical Parameters ◽  
Density Lipoprotein ◽  
Oxidase Inhibitor ◽  
Diet Group ◽  
Control Group ◽  
High Fat ◽  
Xanthine Oxidase Inhibitor ◽  
Anti Inflammatory

Febuxostat, a highly potent xanthine oxidase inhibitor with an antioxidant effect, inhibits elevated xanthine oxidase, leading to reduction of reactive oxygen species and oxidative stress, the main causes of vascular inflammation in hyperlipidemia. The aim of this study was to test the potential antioxidant and anti-inflammatory effects of febuxostat and (or) stopping a high-fat diet on the biochemical parameters in rabbits with hyperlipidemia induced by a high-fat diet. Male New Zealand rabbits were distributed into 3 groups: a normal control group fed standard chow for 12 weeks and 2 other groups fed a high-fat diet with 1% cholesterol for 8 weeks, and then shifted to standard chow for 4 weeks. During the last 4 weeks, one high-fat diet group received 0.5% carboxymethyl cellulose, whereas the other group was treated with febuxostat (2 mg/kg per day p.o.). Febuxostat significantly lowered low-density lipoprotein cholesterol (“bad” cholesterol) compared to the untreated group (high-fat diet group). Febuxostat also displayed a potent anti-inflammatory and antioxidant activity by decreasing serum levels of lipid peroxidation index, proinflammatory cytokines, and enhancing antioxidant enzyme activity. Stopping the hyperlipidemic diet in the high-fat diet group did not show improvement. These findings indicate the antioxidant and anti-inflammatory effects of febuxostat that may be common mechanisms of the anti-hyperlipidemic effect of this drug. Stopping a hyperlipidemic diet without treatment is not sufficient once injury has occurred.

scholarly journals Ameliorative Effects of Oral Glucosamine on Insulin Resistance and Pancreatic Tissue Damage in Experimental Wistar rats on a High-fat Diet

2021 ◽  
Author(s):  
Cornelio Barrientos ◽  
Angélica Pérez ◽  
Jorge Vázquez
Keyword(s):  
Insulin Resistance ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Fatty Infiltration ◽  
Pancreatic Tissue ◽  
Protein Glycosylation ◽  
Control Group ◽  
Chow Diet ◽  
High Fat ◽  
Nuclear Pyknosis

Hyperlipidemia due to a high-fat diet (HFD) is a risk factor for inducing insulin resistance (IR) and adverse effects onpancreatic β-cells in obesity and type 2 diabetes mellitus. This relationship may be due to activation of the hexosaminebiosynthesis pathway. Administration of exogenous glucosamine (GlcN) can increase the end product of this pathway(uridine-5′-diphosphate-N-acetyl-glucosamine), which can mediate IR and protein glycosylation. The objective of this study was to evaluate the effects of oral GlcN and HFD on IR and pancreatic histologic damage in a 22 wk study of 4 groups of male Wistar rats: control group with normal chow diet, HFD group (24%. g/g lard), GlcN group (500 mg/kg−1 per day of glucosamine hydrochloride in drinking water) and HFD plus oral GlcN. Metabolic variables related to IR that were measured included triglycerides (TG), free fatty acids (FFAs) and malondialdehyde (MDA). Histopathologic evaluation of the pancreas was also performed. The results showed IR in the HFD group, which had increased pancreatic nuclear pyknosis and vacuolization, with fatty infiltration and structural alteration of the islets of Langerhans. TG, FFAs and MDA were higher in serum and pancreatic tissue as compared with the control group. The GlcN group did not develop IR and had only mild nuclear pyknosis with no significant change in the pancreatic content of TG, FFAs and MDA. However, the combined administration of GlcN and HFD attenuated IR and improved TG, FFAs and MDA levels in serum and pancreatic tissue and the pancreatic histopathologic changes, with no significant differences as compared with the control group. These findings suggest that the oral GlcN at a dose of 500 mg/kg−1 is protective against IR and the pancreatic histologic damage caused by HFD.

scholarly journals The Efficacy of Seluang Fish Oil (Rasbora agrotynea) Related Body Weight, Lipid Profile, Adiponectin and Leptin in Wistar Rats-Induced High Fat Diet

2018 ◽  
Vol 2 (2) ◽  
pp. 25-30
Author(s):  
Fatmawati Karim ◽  
Rachmat Hidayat ◽  
Erizka Rivani ◽  
Husnul Khotimah ◽  
Ester G Pansserga
Keyword(s):  
Body Weight ◽  
Fish Oil ◽  
Lipid Profile ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Adiponectin Level ◽  
Male Rats ◽  
Control Group ◽  
High Fat ◽  
Reduce Body Weight

Background Rasbora agrotynea (local name : Seluang ) is a fish native to Sumatera, Malaya and Borneo. This fish has a potential as a local wisdom for supplementation of omega 3 and omega 6. In Sumatera, Seluang fish was used as traditional food.   Aim of Study Aim of this study to explore the efficacy of seluang fish oil in body weight, lipid profile, adiponectin and leptin level in Wistar Rats-Induced High Fat Diet   Methods This study was an experimental study , pre-post test with control group design. The sample in this study was  30 male rats, 8 weeks old, weight 150-200 gram. Rats were given high fat diet and seluang fish oil  at dose of 0,1 , 0,2  and 0,4 mL/200 gr BW/day for 2 weeks. Seluang fish oil was extracted by distilation methods. The results of this study were assayed by SPSS 18.   Results Seluang fish oil 0,4 mL/200 gr BW  was more potent to reduce body weight gain, triglyseride level,  leptin and increase adiponectin level than seluang fish oil 0,1 mL/200 gr BW, 0,2 mL/200 gr BW, negative control and positive control.   Conclusion Seluang fish oil had a potention to reduce body weight, triglyceride, leptin and increase adiponectin level.   Keywords: Seluang fish Oil – body weight- triglyserida – leptin - adiponectin  

scholarly journals Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0260546
Author(s):  
Mary J. Obayemi ◽  
Christopher O. Akintayo ◽  
Adesola A. Oniyide ◽  
Ayodeji Aturamu ◽  
Olabimpe C. Badejogbin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Food Intake ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Liver Lipid ◽  
Control Group ◽  
Metabolic Dysfunction ◽  
High Fat ◽  
Male Wistar Rats

Background Adipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. Materials and methods Twenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks. Results HFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin. Conclusion Taken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.

scholarly journals Ampicillin-Improved Glucose Tolerance in Diet-Induced Obese C57BL/6NTac Mice Is Age Dependent

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
I. Rune ◽  
C. H. F. Hansen ◽  
M. Ellekilde ◽  
D. S. Nielsen ◽  
K. Skovgaard ◽  
...  
Keyword(s):  
Dendritic Cell ◽  
Tumor Necrosis Factor ◽  
Glucose Tolerance ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Tumor Necrosis ◽  
Control Group ◽  
High Fat ◽  
Amyloid A ◽  
Necrosis Factor

Ampicillin has been shown to improve glucose tolerance in mice. We hypothesized that this effect is present only if treatment is initiated prior to weaning and that it disappears when treatment is terminated. High-fat fed C57BL/6NTac mice were divided into groups that received Ampicillin at different ages or not at all. We found that both diet and Ampicillin significantly changed the gut microbiota composition in the animals. Furthermore, there was a significant improvement in glucose tolerance in Ampicillin-treated, five-week-old mice compared to nontreated mice in the control group. At study termination, expressions of mRNA coding for tumor necrosis factor, serum amyloid A, and lactase were upregulated, while the expression of tumor necrosis factor (ligand) superfamily member 15 was downregulated in the ileum of Ampicillin-treated mice. Higher dendritic cell percentages were found systemically in high-fat diet mice, and a lower tolerogenic dendritic cell percentage was found both in relation to high-fat diet and late Ampicillin treatment. The results support our hypothesis that a “window” exists early in life in which an alteration of the gut microbiota affects glucose tolerance as well as development of gut immunity and that this window may disappear after weaning.

Serum amyloid A1 levels and amyloid deposition following a high-fat diet challenge in transgenic mice overexpressing hepatic serum amyloid A1

2016 ◽  
Vol 41 (6) ◽  
pp. 640-648 ◽  
Author(s):  
Woo Young Jang ◽  
Jain Jeong ◽  
Seonggon Kim ◽  
Min-cheol Kang ◽  
Yong Hun Sung ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Amyloid Deposition ◽  
Serum Amyloid ◽  
Low Grade ◽  
High Fat ◽  
Metabolic Disturbances ◽  
Amyloid A ◽  
Inflammatory Conditions ◽  
Short Period ◽  
Serum Amyloid A1

Serum amyloid A (SAA) is an acute-phase response protein in the liver, and SAA1 is the major precursor protein involved in amyloid A amyloidosis. This amyloidosis has been reported as a complication in chronic inflammatory conditions such as arthritis, lupus, and Crohn’s disease. Obesity is also associated with chronic, low-grade inflammation and sustained, elevated levels of SAA1. However, the contribution of elevated circulating SAA1 to metabolic disturbances and their complications is unclear. Furthermore, in several recent studies of transgenic (TG) mice overexpressing SAA1 that were fed a high-fat diet (HFD) for a relatively short period, no relationship was found between SAA1 up-regulation and metabolic disturbances. Therefore, we generated TG mice overexpressing SAA1 in the liver, challenged these mice with an HFD, and investigated the influence of elevated SAA1 levels. Sustained, elevated levels of SAA1 were correlated with metabolic parameters and local cytokine expression in the liver following 16 weeks on the HFD. Moreover, prolonged consumption (52 weeks) of the HFD was associated with impaired glucose tolerance and elevated SAA1 levels and resulted in systemic SAA1-derived amyloid deposition in the kidney, liver, and spleen of TG mice. Thus, we concluded that elevated SAA1 levels under long-term HFD exposure result in extensive SAA1-derived amyloid deposits, which may contribute to the complications associated with HFD-induced obesity and metabolic disorders.

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