scholarly journals AP39 ameliorates high fat diet-induced liver injury in young rats via alleviation of oxidative stress and mitochondrial impairment

2021 ◽  
Author(s):  
Yue YU ◽  
Shu-Ming YE ◽  
De-Yun LIU ◽  
Li-Qi YANG
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
High Fat Diet ◽  
High Fat ◽  
Young Rats ◽  
Mitochondrial Impairment

An experimental MODEL study to investigate the pathogenesis of oxaliplatin-induced liver injury.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 184-184
Author(s):  
Stuart M. Robinson ◽  
Jelena Mann ◽  
Derek M. Manas ◽  
Derek A. Mann ◽  
Steve A. White
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
High Fat Diet ◽  
Therapeutic Potential ◽  
Negative Impact ◽  
Acid Synthesis ◽  
Sinusoidal Obstruction Syndrome ◽  
High Fat ◽  
Expression Of Genes ◽  
Folfox Chemotherapy

184 Background: Oxaliplatin based chemotherapy is widely utilized pre-operatively in patients with colorectal liver metastases. Its use is associated with injury to the liver in the form of sinusoidal obstruction syndrome (SOS) the presence of which can have a negative impact on surgical outcomes. The pathogenesis of this condition is poorly understood. Methods: C57Bl/6 mice (n=10 per group) were treated with 5-FU/oxaliplatin/folinic acid chemotherapy (FOLFOX) weekly for 5 weeks or their respective vehicle controls. Animals were culled one week following the final treatment and liver tissue harvested for histological and biochemical analysis. mRNA was extracted from snap frozen liver and subject to genome wide expression analysis the results of which were confirmed using qRT-PCR. To determine the effect of background steatosis on the development of liver injury the experiment was repeated using mice maintained on a high fat diet. To assess the ability of antioxidants to prevent SOS development diet was supplemented with 3% butylated hydroxyanisole (BHA). Results: H&E stained tissue sections confirmed the presence of SOS in all FOLFOX treated animals. Microarray identified changes in expression of over 604 genes in the liver of animals with FOLFOX induced SOS. In particular there was increased expression of genes implicated in oxidative stress (e.g. Metallothionein 1; 22 fold; p<0.001), cell cycle arrest (e.g. p21; 21 fold; p<0.001) and angiogenesis (VEGF-A; 2 fold; p<0.001). Administration of the antioxidant BHA alongside chemotherapy prevented the development of SOS confirming the role of oxidative stress in the pathogenesis of this condition. There was down regulation of a number of genes implicated in fatty acid synthesis (e.g. FASN; 8 fold; p<0.001). In support of this mice maintained on a high fat diet treated with FOLFOX do not develop steatosis unlike those treated with vehicle alone. Conclusions: FOLFOX chemotherapy is specifically associated with SOS and not hepatic steatosis. We have identified some of the molecular pathways involved in the pathogenesis of this condition. Manipulation of these pathways may be of therapeutic potential in preventing the development of chemotherapy-associated liver injury.

Dietary d-limonene alleviates insulin resistance and oxidative stress–induced liver injury in high-fat diet and L-NAME-treated rats

2011 ◽  
Vol 51 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Jesudoss Victor Antony Santiago ◽  
Jayaraman Jayachitra ◽  
Madhavan Shenbagam ◽  
Namasivayam Nalini
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Injury ◽  
High Fat Diet ◽  
High Fat ◽  
And Oxidative Stress

Folic acid supplementation attenuates high fat diet induced hepatic oxidative stress via regulation of NADPH oxidase

2012 ◽  
Vol 90 (2) ◽  
pp. 155-165 ◽  
Author(s):  
Lindsei K. Sarna ◽  
Nan Wu ◽  
Pengqi Wang ◽  
Sun-Young Hwang ◽  
Yaw L. Siow ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Liver Injury ◽  
Nadph Oxidase ◽  
High Fat Diet ◽  
Folic Acid Supplementation ◽  
High Fat ◽  
Acid Supplementation ◽  
Hepatic Oxidative Stress ◽  
Enhanced Expression

Diets high in saturated fat and cholesterol facilitate weight gain, a predisposing factor that contributes to the onset of obesity and metabolic disorders. Hepatic oxidative stress is commonly reported in various animal models of obesity and has been associated with enhanced expression of NADPH oxidase. We have previously reported several antioxidant mechanisms through which folic acid confers protection during hyperhomocysteinemia-induced oxidative stress. The objective of the present study was to investigate whether folic acid supplementation ameliorates high-fat diet induced oxidative stress in the liver, and to identify the underlying mechanisms. Male C57BL/6J mice were fed a control diet, a high-fat diet, or a high-fat diet supplemented with folic acid for 12 weeks. A high-fat diet led to increased body mass, hepatic lipid peroxidation, and liver injury. There was a significant increase in hepatic NADPH oxidase activity, which was associated with enhanced expression of several NADPH-oxidase subunits. Folic acid supplementation had a protective effect against high-fat diet induced hepatic oxidative stress and liver injury. Further analysis revealed that the antioxidant effect of folic acid was attributed, in part, to transcriptional regulation of NADPH oxidase. These results suggested that folic acid supplementation may be hepatoprotective from liver injury associated with a high-fat diet.

Hesperetin ameliorates hepatic oxidative stress and inflammation via the PI3K/AKT-Nrf2-ARE pathway in oleic acid-induced HepG2 cells and a rat model of high-fat diet-induced NAFLD

2021 ◽  
Author(s):  
Jingda Li ◽  
Tianqi Wang ◽  
Panpan Liu ◽  
Fuyuan Yang ◽  
Xudong Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oleic Acid ◽  
Rat Model ◽  
High Fat Diet ◽  
Hepg2 Cells ◽  
Citrus Fruits ◽  
High Fat ◽  
Hepatic Oxidative Stress

Hesperetin as a major bioflavonoid in citrus fruits improves NAFLD by suppressing hepatic oxidative stress and inflammation.

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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