scholarly journals Reduced Oxidative Stress and Enhanced FGF21 Formation in Livers of Endurance-Exercised Rats with Diet-Induced NASH

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2709 ◽  
Author(s):  
Janin Henkel ◽  
Katja Buchheim-Dieckow ◽  
José P. Castro ◽  
Thomas Laeger ◽  
Kristina Wardelmann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endurance Exercise ◽  
Weight Reduction ◽  
Dietary Intervention ◽  
Exercise Group ◽  
Severe Form ◽  
Alcoholic Fatty Liver ◽  
Male Wistar Rats ◽  
Underlying Mechanisms ◽  
The Impact

Non-alcoholic fatty liver diseases (NAFLD) including the severe form with steatohepatitis (NASH) are highly prevalent ailments to which no approved pharmacological treatment exists. Dietary intervention aiming at 10% weight reduction is efficient but fails due to low compliance. Increase in physical activity is an alternative that improved NAFLD even in the absence of weight reduction. The underlying mechanisms are unclear and cannot be studied in humans. Here, a rat NAFLD model was developed that reproduces many facets of the diet-induced NAFLD in humans. The impact of endurance exercise was studied in this model. Male Wistar rats received control chow or a NASH-inducing diet rich in fat, cholesterol, and fructose. Both diet groups were subdivided into a sedentary and an endurance exercise group. Animals receiving the NASH-inducing diet gained more body weight, got glucose intolerant and developed a liver pathology with steatosis, hepatocyte hypertrophy, inflammation and fibrosis typical of NAFLD or NASH. Contrary to expectations, endurance exercise did not improve the NASH activity score and even enhanced hepatic inflammation. However, endurance exercise attenuated the hepatic cholesterol overload and the ensuing severe oxidative stress. In addition, exercise improved glucose tolerance possibly in part by induction of hepatic FGF21 production.

scholarly journals Overexpression of the Lias gene attenuates hepatic steatosis in Leprdb/db mice

2020 ◽  
Author(s):  
Guangcui Xu ◽  
Tingtian Yan ◽  
Qiang Peng ◽  
Haibin Li ◽  
Weidong Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Antioxidant Capacity ◽  
Liver Steatosis ◽  
The Novel ◽  
Alcoholic Fatty Liver ◽  
New Model ◽  
Underlying Mechanisms ◽  
Endogenous Antioxidant ◽  
The Impact

Oxidative stress is proposed to be involved in non-alcoholic fatty liver disease (NAFLD). However, antioxidant therapy results in controversial outcomes. Therefore, we generated a new antioxidant/NAFLD mouse model, LiasHigh/HighLeprdb/db mice, by crossbreeding Leprdb/dbmice, an obesity mouse model, with LiasHigh/High mice, generated by overexpression of lipoic acid synthase gene (Lias) and having increased endogenous antioxidant capacity, to investigate whether the new model could block the development of NAFLD. We have systemically characterized the novel model based on the main features of human NAFLD, determined the impact of enhanced endogenous antioxidant capacity on the retardation of NAFLD and elucidated the underlying mechanisms using various biological and pathological methods. We found that LiasHigh/HighLeprdb/db mice ameliorated many pathological changes of NAFLD compared with the control. In particular, LiasHigh/HighLeprdb/db mice displayed the improved liver mitochondrial function, reflecting the decline of mitochondrial microvesicular steatosis, and reduced oxidative stress, which mainly contribute to alleviation of pathologic alterations of the NAFLD progression. Our new model shows that mitochondrial dysfunction is a major pathogenesis for liver steatosis. Overexpression of Lias gene effectively reduces oxidative stress and protects mitochondria, and consequently attenuates NAFLD/NASH.

Prevalence, diagnosis and treatment with 3 different statins of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in military personnel. Do genetics play a role?

2020 ◽  
Vol 18 ◽  
Author(s):  
Georgios Sfikas ◽  
Michael Psallas ◽  
Charalambos Koumaras ◽  
Konstantinos Imprialos ◽  
Evangelos Perdikakis ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Military Personnel ◽  
Fatty Liver Disease ◽  
Exercise Group ◽  
Severe Form ◽  
Laboratory Evaluation ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Steatohepatitis ◽  
Alcoholic Fatty Liver Disease

Background: Non-alcoholic fatty liver disease (NAFLD) and its severe form, non-alcoholic steatohepatitis (NASH), are major health problems worldwide. Genetics may play a role in the pathogenesis of NAFLD/NASH. Aim: To investigate the prevalence of NAFLD/NASH in 5,400 military personnel and evaluate the effect of treatment with 3 statins on NAFLD/NASH using 2 non-invasive scores [NAFLD Activity Score (NAS); Fibrosis-4 score (FIB-4)]. Methods: During the mandatory annual medical check-up, military personnel underwent a clinical and laboratory evaluation. Participants with NAFLD/NASH were randomised to 4 groups (n=151 each): dietexercise, atorvastatin, rosuvastatin or pitavastatin for 1 year (i.e. until the next routine evaluation). Results: From all the participants, 613 had NAFLD/NASH (prevalence 11.3 vs 39.8% in the general population, p<0.001); 604 consented to participate in the study. After a year of treatment, the diet-exercise group showed no significant changes in both scores (NAS 4.98 baseline vs 5.62, p=0.07; FIB-4 3.42 vs 3.52, p=0.7). For the atorvastatin group, both scores were reduced (NAS 4.97 vs 1.95, p<0.001, FIB-4 3.56 vs 0.83, p<0.001), for rosuvastatin (NAS 5.55 vs 1.81, p<0.001, FIB-4 3.61 vs 0.79, p<0.001), and for pitavastatin (NAS 4.89 vs 1.99, p<0.001, FIB-4 3.78 vs 0.87, p<0.001). Conclusions : Atorvastatin, rosuvastatin and pitavastatin have a beneficial and safe effect in NAFLD/NASH patients as recorded by the improvement in the NAS (representing NAFLD activity) and FIB-4 (representing liver fibrosis) scores. Since both those with and without NAFLD/NASH shared several baseline characteristics, genetics may play a role in the pathogenesis of NAFLD/NASH and its treatment with statins.

scholarly journals Inflammation in Obesity-Related Complications in Children: The Protective Effect of Diet and Its Potential Role as a Therapeutic Agent

Biomolecules ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 1324
Author(s):  
Valeria Calcaterra ◽  
Corrado Regalbuto ◽  
Debora Porri ◽  
Gloria Pelizzo ◽  
Emanuela Mazzon ◽  
...  
Keyword(s):  
Dietary Intervention ◽  
Critical Role ◽  
Overweight And Obesity ◽  
Alcoholic Fatty Liver ◽  
Nutrition And Diet ◽  
Pediatric Overweight ◽  
Healthy Growth ◽  
The Impact

Obesity is a growing health problem in both children and adults, impairing physical and mental state and impacting health care system costs in both developed and developing countries. It is well-known that individuals with excessive weight gain frequently develop obesity-related complications, which are mainly known as Non-Communicable Diseases (NCDs), including cardiovascular disease, type 2 diabetes mellitus, metabolic syndrome, non-alcoholic fatty liver disease, hypertension, hyperlipidemia and many other risk factors proven to be associated with chronic inflammation, causing disability and reduced life expectancy. This review aims to present and discuss complications related to inflammation in pediatric obesity, the critical role of nutrition and diet in obesity-comorbidity prevention and treatment, and the impact of lifestyle. Appropriate early dietary intervention for the management of pediatric overweight and obesity is recommended for overall healthy growth and prevention of comorbidities in adulthood.

scholarly journals Effects of dietary fat modification on oxidative stress and inflammatory markers in the LIPGENE study

2010 ◽  
Vol 104 (9) ◽  
pp. 1357-1362 ◽  
Author(s):  
Helena Petersson ◽  
Ulf Risérus ◽  
Jolene McMonagle ◽  
Hanne L. Gulseth ◽  
Audrey C. Tierney ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dietary Fat ◽  
Dietary Intervention ◽  
Stress Indicator ◽  
Reactive Protein ◽  
The Metabolic Syndrome ◽  
Markers Of Oxidative Stress ◽  
Fat Diets ◽  
The Impact ◽  
And Oxidative Stress

Subjects with the metabolic syndrome (MetS) have enhanced oxidative stress and inflammation. Dietary fat quality has been proposed to be implicated in these conditions. We investigated the impact of four diets distinct in fat quantity and quality on 8-iso-PGF2α (a major F2-isoprostane and oxidative stress indicator), 15-keto-13,14-dihydro-PGF2α (15-keto-dihydro-PGF2α, a major PGF2α metabolite and marker of cyclooxygenase-mediated inflammation) and C-reactive protein (CRP). In a 12-week parallel multicentre dietary intervention study (LIPGENE), 417 volunteers with the MetS were randomly assigned to one of the four diets: two high-fat diets (38 % energy (%E)) rich in SFA or MUFA and two low-fat high-complex carbohydrate diets (28 %E) with (LFHCC n-3) or without (LFHCC) 1·24 g/d of very long chain n-3 fatty acid supplementation. Urinary levels of 8-iso-PGF2α and 15-keto-dihydro-PGF2α were determined by RIA and adjusted for urinary creatinine levels. Serum concentration of CRP was measured by ELISA. Neither concentrations of 8-iso-PGF2α and 15-keto-dihydro-PGF2α nor those of CRP differed between diet groups at baseline (P>0·07) or at the end of the study (P>0·44). Also, no differences in changes of the markers were observed between the diet groups (8-iso-PGF2α, P = 0·83; 15-keto-dihydro-PGF2α, P = 0·45; and CRP, P = 0·97). In conclusion, a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study.

scholarly journals Inhibition of Oxidative Stress in Brain During Rat Adjuvant Arthritis by Carnosine, Trolox and Novel Trolox-Carnosine

2015 ◽  
pp. S489-S496
Author(s):  
S. PONIŠT ◽  
L. SLOVÁK ◽  
V. KUNCÍROVÁ ◽  
T. FEDOROVA ◽  
A. LOGVINENKO ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Weight Reduction ◽  
Adjuvant Arthritis ◽  
The Body ◽  
Protein Carbonyls ◽  
Therapeutic Effects ◽  
Arthritic Score ◽  
Markers Of Inflammation ◽  
Rat Adjuvant Arthritis ◽  
The Impact

Carnosine (CARN) is an anti-glycating agent able to quench superoxide, and to neutralize 4-hydroxynonenal. Trolox-carnosine (CARN-T) was synthesized because of its resistance against degradation and to improve CARN antioxidant capacity. We evaluated the impact of trolox (TRO), CARN and its derivative CARN-T on oxidative stress (OS) in brain during rat adjuvant arthritis (AA). The experiments were done on healthy, control arthritic and arthritic animals with administration of CARN 150 mg/kg b.w., TRO 41 mg/kg b.w. and CARN-T 75 mg/kg b.w. in a daily dose during 28 days. Antioxidants did not affect the body weight on day 14, but on day 28 TRO enhanced the weight reduction. On day 14 and 28 CARN-T and TRO reduced arthritic score. IL-1beta, MCP-1 and MMP-9 were measured in plasma on day 14. MCP-1 was decreased by CARN-T and TRO. All antioxidants reduced IL-1beta and MMP-9 levels. Malondialdehyde, 4-hydroxynonenal and protein carbonyls were increased in brain. CARN, CARN-T and TRO prevented higher lipid and protein oxidation in brain. CARN and CARN-T caused no weight reduction like TRO that has an advantage in inflammatory arthritis. Moreover the antioxidants administered had a similar therapeutic effects on arthritic score, markers of inflammation in plasma and OS in brain.

scholarly journals Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma

2021 ◽  
Vol 12 ◽  
Author(s):  
Chioma Enweasor ◽  
Cameron H. Flayer ◽  
Angela Haczku
Keyword(s):  
Oxidative Stress ◽  
Airway Inflammation ◽  
Γδ T Cells ◽  
Air Pollutant ◽  
Glucocorticoid Resistance ◽  
Primary Data ◽  
Alveolar Type ◽  
Underlying Mechanisms ◽  
The Impact

Despite recent advances in using biologicals that target Th2 pathways, glucocorticoids form the mainstay of asthma treatment. Asthma morbidity and mortality remain high due to the wide variability of treatment responsiveness and complex clinical phenotypes driven by distinct underlying mechanisms. Emerging evidence suggests that inhalation of the toxic air pollutant, ozone, worsens asthma by impairing glucocorticoid responsiveness. This review discusses the role of oxidative stress in glucocorticoid resistance in asthma. The underlying mechanisms point to a central role of oxidative stress pathways. The primary data source for this review consisted of peer-reviewed publications on the impact of ozone on airway inflammation and glucocorticoid responsiveness indexed in PubMed. Our main search strategy focused on cross-referencing “asthma and glucocorticoid resistance” against “ozone, oxidative stress, alarmins, innate lymphoid, NK and γδ T cells, dendritic cells and alveolar type II epithelial cells, glucocorticoid receptor and transcription factors”. Recent work was placed in the context from articles in the last 10 years and older seminal research papers and comprehensive reviews. We excluded papers that did not focus on respiratory injury in the setting of oxidative stress. The pathways discussed here have however wide clinical implications to pathologies associated with inflammation and oxidative stress and in which glucocorticoid treatment is essential.

scholarly journals Paraoxonase-1 as a Regulator of Glucose and Lipid Homeostasis: Impact on the Onset and Progression of Metabolic Disorders

2019 ◽  
Vol 20 (16) ◽  
pp. 4049 ◽  
Author(s):  
Meneses ◽  
Silvestre ◽  
Sousa-Lima ◽  
Macedo
Keyword(s):  
Oxidative Stress ◽  
Metabolic Disorders ◽  
Physiological Role ◽  
Normal Activity ◽  
Protective Role ◽  
Paraoxonase 1 ◽  
Alcoholic Fatty Liver ◽  
Glucose And Lipid Homeostasis ◽  
The Impact ◽  
And Oxidative Stress

Metabolic disorders are characterized by an overall state of inflammation and oxidative stress, which highlight the importance of a functional antioxidant system and normal activity of some endogenous enzymes, namely paraoxonase-1 (PON1). PON1 is an antioxidant and anti-inflammatory glycoprotein from the paraoxonases family. It is mainly expressed in the liver and secreted to the bloodstream, where it binds to HDL. Although it was first discovered due to its ability to hydrolyze paraoxon, it is now known to have an antiatherogenic role. Recent studies have shown that PON1 plays a protective role in other diseases that are associated with inflammation and oxidative stress, such as Type 1 and Type 2 Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease. The aim of this review is to elucidate the physiological role of PON1, as well as the impact of altered PON1 levels in metabolic disorders.

scholarly journals Impact of dietary fat on the development of non-alcoholic fatty liver disease in Ldlr−/− mice

2015 ◽  
Vol 75 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Donald B. Jump ◽  
Christopher M. Depner ◽  
Sasmita Tripathy ◽  
Kelli A. Lytle
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Hepatic Injury ◽  
Liver Steatosis ◽  
Primary Hepatocellular Carcinoma ◽  
Alcoholic Fatty Liver ◽  
The Impact ◽  
Alcoholic Fatty Liver Disease

The prevalence of non-alcoholic fatty liver disease (NAFLD) has increased in parallel with central obesity and is now the most common chronic liver disease in developed countries. NAFLD is defined as excessive accumulation of lipid in the liver, i.e. hepatosteatosis. The severity of NAFLD ranges from simple fatty liver (steatosis) to non-alcoholic steatohepatitis (NASH). Simple steatosis is relatively benign until it progresses to NASH, which is characterised by hepatic injury, inflammation, oxidative stress and fibrosis. Hepatic fibrosis is a risk factor for cirrhosis and primary hepatocellular carcinoma. Our studies have focused on the impact of diet on the onset and progression of NASH. We developed a mouse model of NASH by feeding Ldlr−/− mice a western diet (WD), a diet moderately high in saturated and trans-fat, sucrose and cholesterol. The WD induced a NASH phenotype in Ldlr−/− mice that recapitulates many of the clinical features of human NASH. We also assessed the capacity of the dietary n-3 PUFA, i.e. EPA (20 : 5,n-3) and DHA (22 : 6,n-3), to prevent WD-induced NASH in Ldlr−/− mice. Histologic, transcriptomic, lipidomic and metabolomic analyses established that DHA was equal or superior to EPA at attenuating WD-induced dyslipidemia and hepatic injury, inflammation, oxidative stress and fibrosis. Dietary n-3 PUFA, however, had no significant effect on WD-induced changes in body weight, body fat or blood glucose. These studies provide a molecular and metabolic basis for understanding the strengths and weaknesses of using dietary n-3 PUFA to prevent NASH in human subjects.

Fluazifop-p-butyl, an aryloxyphenoxypropionate herbicide, diminishes renal and hepatic functions and triggers testicular oxidative stress in orally exposed rats

2016 ◽  
Vol 33 (5) ◽  
pp. 406-415 ◽  
Author(s):  
Ayokanmi Ore ◽  
Ebenezer Tunde Olayinka
Keyword(s):  
Oxidative Stress ◽  
Hepatic Function ◽  
Dependent Manner ◽  
Lactate Dehydrogenase Activity ◽  
Group I ◽  
Male Wistar Rats ◽  
Glutamyl Transferase ◽  
The Impact ◽  
Dose Dependent ◽  
And Oxidative Stress

Fluazifop- p-butyl (FPB) is a selective aryloxyphenoxypropionate herbicide. Its phytotoxicity mechanism involves inhibition of lipid biosynthesis, free-radical generation, and oxidative stress in vulnerable plants. This study evaluates the impact of orally administered FPB on selected tissues in non-target animal model. Twenty-four male wistar rats (160–180g) were randomized into groups (I–IV). Group-I served as control, while animals in groups II, III, and IV received FPB at 18.75, 37.5, and 75 mg/kg body weight/day p.o., respectively, for 21 days. FPB caused significant ( p < 0.05) increase in plasma biomarkers of renal and hepatic function (urea, creatinine, bilirubin, alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase) when compared to control. Significant reductions in testicular ascorbic acid, glutathione, and activities of glutathione-S transferase, superoxide dismutase, and catalase were observed in FPB-treated animals when compared to control, in a dose-dependent manner. This was accompanied by increased testicular lipid peroxidation in the treated groups. Furthermore, a significant decrease in testicular acid phosphatase and γ-glutamyl transferase activities was also observed in the FPB-treated groups in a dose-dependent manner compared to control. However, testicular lactate dehydrogenase activity was significantly increased in the FPB-treated rats when compared to control. Additionally, histopathological studies revealed severe interstitial oedema and congestion of testicular blood vessels in the FPB-treated groups. Overall, data from this study suggest that FPB induced hepatotoxicity, nephrotoxicity, and oxidative stress-mediated alteration of testicular functions in rat.

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