Abresham ameliorates dyslipidemia, hepatic steatosis and hypertension in high-fat diet fed rats by repressing oxidative stress, TNF-α and normalizing NO production

2012 ◽  
Vol 64 (7-8) ◽  
pp. 705-712 ◽  
Author(s):  
Saroj Nepal ◽  
Salma Malik ◽  
Ashok Kumar Sharma ◽  
Saurabh Bharti ◽  
Narender Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
No Production ◽  
High Fat ◽  
Tnf Α

scholarly journals Lipoic Acid Prevents High-Fat Diet-Induced Hepatic Steatosis in Goto Kakizaki Rats by Reducing Oxidative Stress Through Nrf2 Activation

2018 ◽  
Vol 19 (9) ◽  
pp. 2706 ◽  
Author(s):  
Cristina Sena ◽  
Maria Cipriano ◽  
Maria Botelho ◽  
Raquel Seiça
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Liver Function ◽  
Hepatic Steatosis ◽  
Lipoic Acid ◽  
High Fat Diet ◽  
Control Group ◽  
High Fat ◽  
Tnf Α

Prevention of hepatic fat accumulation may be an important approach for liver diseases due to the increased relevance of hepatic steatosis in this field. This study was conducted to investigate the effects of the antioxidant α-lipoic acid (α-LA) on hepatic steatosis, hepatocellular function, and oxidative stress in a model of type 2 diabetes fed with a high fat diet (HFD). Goto-Kakizaki rats were randomly divided into four groups. The first group received only a standard rat diet (control GK) including groups 2 (HFD), 3 (vehicle group), and 4 (α-LA group), which were given HFD, ad libitum during three months. Wistar rats are the non-diabetic control group. Carbohydrate and lipid metabolism, liver function, plasma and liver tissue malondialdehyde (MDA), liver GSH, tumor necrosis factor-α (TNF-α) and nuclear factor E2 (erythroid-derived 2)-related factor-2 (Nrf2) levels were assessed in the different groups. Liver function was assessed using quantitative hepatobiliary scintigraphy, serum aspartate, and alanine aminotransferases (AST, ALT), alkaline phosphatase, gamma-glutamyltranspeptidase, and bilirubin levels. Histopathologically steatosis and fibrosis were evaluated. Type 2 diabetic animals fed with HFD showed a marked hepatic steatosis and a diminished hepatic extraction fraction and both were fully prevented with α-LA. Plasma and liver tissue MDA and hepatic TNF-α levels were significantly higher in the HFD group when compared with the control group and significantly lower in the α-LA group. Systemic and hepatic cholesterol, triglycerides, and serum uric acid levels were higher in hyperlipidemic GK rats and fully prevented with α-LA. In addition, nuclear Nrf2 activity was significantly diminished in GK rats and significantly augmented after α-LA treatment. In conclusion, α-LA strikingly ameliorates steatosis in this animal model of diabetes fed with HFD by decrementing the inflammatory marker TNF-α and reducing oxidative stress. α-LA might be considered a useful therapeutic tool to prevent hepatic steatosis by incrementing antioxidant defense systems through Nrf2 and consequently decreasing oxidative stress and inflammation in type 2 diabetes.

Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

2020 ◽  
Author(s):  
Xiaoling Wu ◽  
Xinyu Zou ◽  
Mi Zhang ◽  
Haiqiang Hu ◽  
Xueliang Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Inflammatory Reaction ◽  
High Fat Diet ◽  
Laying Hens ◽  
Density Lipoprotein ◽  
Inflammatory Factors ◽  
Pathological Changes ◽  
High Fat ◽  
Tnf Α

Abstract Background: Osteocalcin (OCN), as an energy-regulating hormone, involves in preventing nonalcoholic steatohepatitis. Laying hens have been used as an animal model for investigating liver function and related metabolic disordersas that the synthesis of fat in laying hens is much faster than in mammals with limited adipose tissue. The aim of this study was to investigate the effects of OCN on fatty liver hemorrhagic syndrome (FLHS) in aged laying hens. Methods: Thirty 68-week-old White Plymouth laying hens were randomly assigned into conventional single-bird cages, and the cages were randomly allocated into one of three treatments: normal diet (ND + vehicle , ND+V), high-fat diet (HFD + vehicle, HFD+V), and HFD + OCN (3 μg/bird, 1 time/2 days, i.m.) for 40 days. At experimental day 30, oral glucose tolerance tests (OGTT) and insulin tolerance tests (ITT) were performed. At the end of experiment, the hens were euthanized followed blood collection. The plasma aspartate transaminase (AST), alkaline phosphatase (ALP), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using an automatic biochemistry analyzer. Pathological changes in the liver were examined under both light and transmission electron microscopes. The plasma inflammatory factors including interleukin-1 (IL-1), IL-6, and tumor Necrosis Factor-alpha (TNF-α) were analyzed by ELISA, and the gene expressions of these inflammatory factors in the liver were analyzed by Real-time PCR. And oxidative stress was evaluated using Malondialdehyde (MDA) and Glutathione peroxidase (GSH-Px) assay kits. Results: The results showed HFD hens had more severe liver haemorrhage and fibrosis than ND hens. The ultra-microstructural examination showed that hepatocytes of HFD hens appeared necrotic pyknosis associated with great intracellular electron, mitochondrial swelling, shrunk nucleus and absence of autolysosomes. OCN mitigated these pathological changes by improved HFD hens’ insulin resistance via alleviating the glucose intolerence and improving insulin sensitivity; inhibited HFD-induced oxidative stress as evidenced by decreased liver concentrations of MDA but increased GSH-Px; and reduced the inflammatory reaction with reducing blood IL-6 and TNF-α concentrations and mRNA expressions. Conclusion: These results suggest a high-fat diet promotes the FLHS development in aged hens, while OCN prevents the FLHS process through inhibiting insulin resistance, inflammatory reaction, oxidative stress and fibrosis, and acting autophagy.

scholarly journals Açaí (Euterpe oleracea Mart.) seed extract protects against hepatic steatosis and fibrosis in high-fat diet-fed mice: Role of local renin-angiotensin system, oxidative stress and inflammation

2020 ◽  
Vol 65 ◽  
pp. 103726 ◽  
Author(s):  
Matheus Henrique Romão ◽  
Graziele Freitas de Bem ◽  
Izabelle Barcellos Santos ◽  
Ricardo de Andrade Soares ◽  
Dayane Teixeira Ognibene ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Renin Angiotensin System ◽  
Seed Extract ◽  
Euterpe Oleracea ◽  
High Fat ◽  
Angiotensin System ◽  
Euterpe Oleracea Mart

Amla (Emblica officinalis) improves hepatic and renal oxidative stress and the inflammatory response in hypothyroid female wistar rats fed with a high-fat diet

2018 ◽  
Vol 29 (2) ◽  
pp. 175-184 ◽  
Author(s):  
P. Rajaa Muthu ◽  
Zachariah Bobby ◽  
P. Sankar ◽  
V. Vickneshwaran ◽  
Sajini Elizabeth Jacob
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
High Fat Diet ◽  
Wistar Rats ◽  
Molecular Techniques ◽  
Emblica Officinalis ◽  
High Fat ◽  
Tnf Α ◽  
Female Wistar Rats ◽  
Liver And Kidney

AbstractBackground:We investigated the protective effects of amla (Emblica officinalis) on the pathogenesis of oxidative stress (OS) and inflammatory response in hypothyroid rats fed with a high-fat diet (HFD) as an experimental model of hypothyroidism (HT) with obesity.Methods:A total of 80 female wistar rats (5-months-old) were divided into eight different groups. Propylthiouracil (PTU) and HFD were used to induce the experimental HT and obesity, respectively. The euthyroid and hypothyroid rats were fed either normal chow or HFD with and without amla extract (AE, 100 mg/kg bw/day) for 6 weeks. The blood and tissues, liver and kidney OS and inflammatory parameters were studied using appropriate biochemical and molecular techniques.Results:PTU and HFD per se caused OS and inflammatory response as evidenced by increased plasma MDA, TNF-α, CRP and GPx in association with decreased levels of TAS and reduced glutathione (GSH). The proteomic analysis revealed that the expressions of pERK, pP38, TNF-α, IL6, COX2 and NOX-4 were up-regulated in the liver and kidney of these rats. In addition, all these metabolic derangements were further augmented when HT was followed by the addition of HFD. This suggested that there was a synergism between HT and the intake of HFD on the development of OS and inflammatory response.Conclusions:The treatment with amla fruit extract significantly restored the redox imbalance and inflammatory signaling and ameliorated OS and inflammatory response, suggesting the use of this natural compound as an alternative remedy or adjuvant for the management of metabolic complications concomitant with HT.

scholarly journals Variable penetrance of metabolic phenotypes and development of high-fat diet-induced adiposity in NEIL1-deficient mice

2011 ◽  
Vol 300 (4) ◽  
pp. E724-E734 ◽  
Author(s):  
Harini Sampath ◽  
Ayesha K. Batra ◽  
Vladimir Vartanian ◽  
J. Russ Carmical ◽  
Deborah Prusak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Oxygen Consumption ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Late Onset ◽  
Excision Repair ◽  
High Fat ◽  
Hepatic Expression ◽  
Base Excision

Exposure to chronic and acute oxidative stress is correlated with many human diseases, including, but not limited to, cancer, heart disease, diabetes, and obesity. In addition to cellular lipids and proteins, cellular oxidative stress can result in damage to DNA bases, especially in mitochondrial DNA. We previously described the development of spontaneous late-onset obesity, hepatic steatosis, hyperinsulinemia, and hyperleptinemia in mice that are deficient in the DNA glycosylase nei-like 1 (NEIL1), which initiates base excision repair of several oxidatively damaged bases. In the current study, we report that exposure to a chronic oxidative stress in the form of a high-fat diet greatly accelerates the development of obesity in neil1−/− mice. Following a 5-wk high-fat diet challenge, neil1−/− mice gained significantly more body weight than neil1+/+ littermates and had increased body fat accumulation and moderate to severe hepatic steatosis. Analysis of oxygen consumption by indirect calorimetry indicated a modest reduction in total oxygen consumption in neil1−/− mice that was abolished upon correction for lean body mass. Additionally, hepatic expression of several inflammatory genes was significantly upregulated in neil1−/− mice following high-fat diet challenge compared with chow-fed or neil1+/+ counterparts. A long-term high-fat diet also induced glucose intolerance as well as a significant reduction in mitochondrial DNA and protein content in neil1−/− mice. Collectively, these data indicate that NEIL1 deficiency results in an increased susceptibility to obesity and related complications potentially by lowering the threshold for tolerance of cellular oxidative stress in neil1−/− mice.

Chicoric acid prevents obesity by attenuating hepatic steatosis, inflammation and oxidative stress in high-fat diet-fed mice

2013 ◽  
Vol 54 (1) ◽  
pp. 345-353 ◽  
Author(s):  
Haifang Xiao ◽  
Guo Xie ◽  
Jiawei Wang ◽  
Xiaofan Hou ◽  
Xiao Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
High Fat ◽  
Chicoric Acid ◽  
And Oxidative Stress

Silybum marianum oil attenuates hepatic steatosis and oxidative stress in high fat diet-fed mice

2018 ◽  
Vol 100 ◽  
pp. 191-197 ◽  
Author(s):  
Shu Yun Zhu ◽  
Ning Jiang ◽  
Jing Yang ◽  
Jie Tu ◽  
Yue Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
High Fat ◽  
Silybum Marianum ◽  
And Oxidative Stress
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