fat-1mice prevent high-fat plus high-sugar diet-induced non-alcoholic fatty liver disease

2017 ◽  
Vol 8 (11) ◽  
pp. 4053-4061 ◽  
Author(s):  
Xiao-fei Guo ◽  
Jin-long Gao ◽  
Jiao-mei Li ◽  
Duo Li
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Causal Role ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
High Sugar ◽  
Alcoholic Fatty Liver Disease

High-fat and high-sugar (HFS) diets have been suggested to play a causal role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD).

scholarly journals Hepatoprotective effects ofErythrina abyssinicaLam Ex Dc against Non Alcoholic Fatty Liver Disease in Sprague Dawley Rats

2019 ◽  
Author(s):  
Felix Kanyi Macharia ◽  
Peter Waweru Mwangi ◽  
Abiy Yenesew ◽  
Frederick Bukachi ◽  
Nelly Murugi Nyaga ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Bark Extract ◽  
P Value ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
High Sugar ◽  
Freeze Dried ◽  
Alcoholic Fatty Liver Disease

ABSTRACTBackgroundNon-alcoholic fatty liver disease (NFLD) is the hepatic manifestation of the metabolic syndrome recognized as the most prevalent chronic liver disease across all age groups. NFLD is strongly associated with obesity, insulin resistance, hypertension and dyslipidemia. Extensive research efforts are geared, through pharmacological approach, towards preventing or reversing this.Erythrina abyssinicaLam ex DC is an indigenous tree used widely used in traditional medicine, including for the treatment of liver related diseases, and has been shown to possess hypoglycemic, anti-oxidant, antimicrobial and anti-plasmodia effects. The present study is aimed at establishing the effects ofE. abyssinicaon the development of Non-alcoholic fatty liver disease induced by a high-fat and high-sugar diet in rats,in-vivomodel.MethodsForty rats (40) were randomly divided into five groups: positive control (pioglitazone), Negative control (high fat/high sugar diet), low test dose (200 mg/kg), high test dose (400 mg/kg) and normal group (standard chow pellets and fresh water).The inhibitory effect of the stem bark extract ofE. abyssinicaon the development of NAFLD was evaluated by chronic administration the herb extracts to rats on a high-fat/high-sugar diet. Biochemical indices of hepatic function including serum lipid profile, serum aspartate transaminase and alanine transaminase levels were then determined. Histological analysis of liver samples was carried out to quantify the degree of steato-hepatitis. Liver weights were taken and used to determine the hepatic index. The data was analyzed using one-way ANOVA, and Tukey’s post-hoc tests were done in cases of significance. Histology data was analyzed using Kruskal-Wallis and Dunn’s post-hoc test was done in cases of significance. Significance was set at p<0.05.ResultsThe freeze dried extract ofE. abyssinicahad significant effects onfasting blood glucose[5.43 ± 0.17 (HF/HSD) vs 3.8 ± 0.15 (E 400 mg/kg) vs 4.54 ± 0.09 (E 200 mg/kg) vs. 4.16 ± 0.13 (PIOG) vs. 2.91 ± 0.16 (normal control): P value < 0.0001], andinsulin sensitivity[329.4 ± 13.48 mmol/L · min (HF/HSD) vs. 189.8 ± 12.11 mmol/L · min (E 400 mg/kg) vs. 233.8 ± 6.55 mmol/L· min (E 200 mg/kg) vs. 211.1 ± 7.35 mmol/L · min (PIOG) vs. 142.9 ± 11.94 mmol/L · min: P value < 0.0001],The extract had significant effects on hepatic indices including,hepatic triglycerides(P value < 0.0001),liver weights(P value < 0.0001),liver weight-body weight ratio(P value < 0.0001),serum ALT levels(P value < 0.0001),serum AST(P value < 0.0017),serum total cholesterol(P value < 0.0001),serum triglycerides(P value < 0.0001), andserum LDL-cholesterol(P value < 0.0001). The extracts however showed no significant effects onHDL-cholesterol(P value = 0.4759).Histological analysis showed that the extract appears to possess protective effects against steatosis, inflammation and hepatic ballooning, with the high dose (400mg/kg) being more hepato-protective.ConclusionThe freeze dried stem bark extract ofErythina abyssinicapossesses significant inhibitory effects against the development of NAFLD in Sprague Dawley rats.

scholarly journals Maternal tadalafil therapy for fetal growth restriction prevents non-alcoholic fatty liver disease and adipocyte hypertrophy in the offspring

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takuya Kawamura ◽  
Hiroaki Tanaka ◽  
Ryota Tachibana ◽  
Kento Yoshikawa ◽  
Shintaro Maki ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fetal Growth ◽  
Fetal Programming ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

AbstractWe aimed to investigate the effects of maternal tadalafil therapy on fetal programming of metabolic function in a mouse model of fetal growth restriction (FGR). Pregnant C57BL6 mice were divided into the control, L-NG-nitroarginine methyl ester (L-NAME), and tadalafil + L-NAME groups. Six weeks after birth, the male pups in each group were given a high-fat diet. A glucose tolerance test (GTT) was performed at 15 weeks and the pups were euthanized at 20 weeks. We then assessed the histological changes in the liver and adipose tissue, and the adipocytokine production. We found that the non-alcoholic fatty liver disease activity score was higher in the L-NAME group than in the control group (p < 0.05). Although the M1 macrophage numbers were significantly higher in the L-NAME/high-fat diet group (p < 0.001), maternal tadalafil administration prevented this change. Moreover, the epididymal adipocyte size was significantly larger in the L-NAME group than in the control group. This was also improved by maternal tadalafil administration (p < 0.05). Further, we found that resistin levels were significantly lower in the L-NAME group compared to the control group (p < 0.05). The combination of exposure to maternal L-NAME and a high-fat diet induced glucose impairment and non-alcoholic fatty liver disease. However, maternal tadalafil administration prevented these complications. Thus, deleterious fetal programming caused by FGR might be modified by in utero intervention with tadalafil.

scholarly journals Ezetimibe prevents the development of non-alcoholic fatty liver disease induced by high-fat diet in C57BL/6J mice

2014 ◽  
Vol 10 (6) ◽  
pp. 2917-2923 ◽  
Author(s):  
XIANG WANG ◽  
QIAOHUA REN ◽  
TAO WU ◽  
YONG GUO ◽  
YONG LIANG ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals Alleviating effect of Ficus racemosa in high-fat-high-fructose diet-induced non-alcoholic fatty liver disease

2021 ◽  
Vol 65 ◽  
pp. 12-20
Author(s):  
Nilay D. Solanki ◽  
Kirti Vadi ◽  
Sandip Patel
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Lipid Profile ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Serum Leptin ◽  
High Fructose ◽  
Ficus Racemosa ◽  
Alcoholic Fatty Liver Disease

Objectives: Non-alcoholic fatty liver disease (NAFLD) is one of the chronic liver diseases. Ficus racemosa has been used for many years in the Ayurvedic medicine system and is closely related with the management of metabolic conditions. The study investigated alleviating effects of methanolic extract of F. racemosa (FRM) bark on high-fat-high-fructose (HFHF) diet -induced NAFLD. Materials and Methods: HFHF-based model was developed for a period of 10 weeks. In treatment groups, FRM (100 mg/kg, 200 mg/kg, and 400 mg/kg) and atorvastatin (20 mg/kg) were administered for 6 weeks after initiating HFHF diet and continued for another 4 weeks. Liver functions test, lipid profile, serum leptin, and antioxidant parameters and histopathology were evaluated. Results: Elevated liver enzymes, lipid markers, and leptin were observed, with significant reduction in antioxidants in disease control rats. FRM treatment significantly improved serum aminotransferase activities, lipid profile, and oxidative changes and brought back to normal. Liver histopathology showed the fatty modifications induced by the HFHF diet, and reduction in fatty changes was observed due to FRM. Significant decline in serum leptin was observed with high-dose FRM. Conclusion: FRM showed positive effects in the reversal of NAFLD and different polyphenolic compounds in the plant were responsible for the proven action.

scholarly journals Lupine (Lupinus angustifolius L.) Peptide Prevents Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice

2019 ◽  
Author(s):  
Ana Lemus-Conejo ◽  
Elena Grao-Cruces ◽  
Rocio Toscano ◽  
Lourdes M Varela ◽  
Carmen Claro ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Lupinus Angustifolius ◽  
Standard Diet ◽  
Obese Mice ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

Bioactive peptides are related to the prevention and treatment of many diseases. GPETAFLR is an octapeptide which was isolated from lupine (Lupinus angustifolius L.) and showed anti-inflammatory properties. The aim of this study was to evaluate the potential activity of GPETAFLR to prevent non-alcoholic fatty liver disease (NAFLD) in high-fat diet (HFD)-induced obese mice. C57BL/6J mice were fed a standard diet or an HFD. Two of the groups fed the HFD diet were treated with GPETAFLR in their drinking water at 0,5 mg/kg/d or 1 mg/kg/d. To determine the ability of GPETAFLR to improve the onset and progression of NAFLD, histological studies, hepatic enzyme profile, inflammatory cytokine and lipid metabolism-related genes and proteins were analyzed. Our results suggest that HFD-induced inflammatory metabolic disorders were alleviated by treatment with GPETAFLR. In conclusion, dietary lupine consumption could repair HFD-induced hepatic damage, possibly via modifications in the liver&rsquo;s lipid signalling pathways.

scholarly journals A Slow-Digesting Carbohydrate Diet during Rat Pregnancy Protects Offspring from Non-Alcoholic Fatty Liver Disease Risk through the Modulation of the Carbohydrate-Response Element and Sterol Regulatory Element Binding Proteins

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 844 ◽  
Author(s):  
Rafael Salto ◽  
Manuel Manzano ◽  
María Dolores Girón ◽  
Ainara Cano ◽  
Azucena Castro ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Regulatory Element ◽  
Liver Lipid ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Sterol Regulatory Element ◽  
Carbohydrate Digestion ◽  
Alcoholic Fatty Liver Disease

High-fat (HF) and rapid digestive (RD) carbohydrate diets during pregnancy promote excessive adipogenesis in offspring. This effect can be corrected by diets with similar glycemic loads, but low rates of carbohydrate digestion. However, the effects of these diets on metabolic programming in the livers of offspring, and the liver metabolism contributions to adipogenesis, remain to be addressed. In this study, pregnant insulin-resistant rats were fed high-fat diets with similar glycemic loads but different rates of carbohydrate digestion, High Fat-Rapid Digestive (HF–RD) diet or High Fat-Slow Digestive (HF–SD) diet. Offspring were fed a standard diet for 10 weeks, and the impact of these diets on the metabolic and signaling pathways involved in liver fat synthesis and storage of offspring were analyzed, including liver lipidomics, glycogen and carbohydrate and lipid metabolism key enzymes and signaling pathways. Livers from animals whose mothers were fed an HF–RD diet showed higher saturated triacylglycerol deposits with lower carbon numbers and double bond contents compared with the HF–SD group. Moreover, the HF–RD group exhibited enhanced glucose transporter 2, pyruvate kinase (PK), acetyl coenzyme A carboxylase (ACC) and fatty acid (FA) synthase expression, and a decrease in pyruvate carboxylase (PyC) expression leading to an altered liver lipid profile. These parameters were normalized in the HF–SD group. The changes in lipogenic enzyme expression were parallel to changes in AktPKB phosphorylation status and nuclear expression in carbohydrate-response element and sterol regulatory element binding proteins. In conclusion, an HF–RD diet during pregnancy translates to changes in liver signaling and metabolic pathways in offspring, enhancing liver lipid storage and synthesis, and therefore non-alcoholic fatty liver disease (NAFLD) risk. These changes can be corrected by feeding an HF–SD diet during pregnancy.

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