scholarly journals Possible Amelioration of the Severity of Nutritional Steatohepatitis by Guggulsterone in Mice

2019 ◽  
Vol 28 (1) ◽  
pp. 17-23
Author(s):  
Sara Ameen Nafeer ◽  
Munaf Zalzala
Keyword(s):  
Liver Disease ◽  
High Fat Diet ◽  
Control Group ◽  
Free Access ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Commercial Diet ◽  
Group I ◽  
Alcoholic Fatty Liver Disease ◽  
Control Group Group

Non-alcoholic fatty liver disease (NAFLD) has become one of the most common chronic liver diseases worldwide, which characterized by steatosis, inflammation, and fibrosis. The aim of this designed study is to evaluate the ability of guggulsterone to prevent high fat diet induced steatohepatitis in mice. Five groups of male mice were selected and treated as the following: group I, mice had free access to standard commercial diet and considered as control group, group II, mice were fed a specially formulated high-fat diet for 12 weeks to induce non-alcoholic liver disease, while groups III, IV and V the mice were administered high fat diet containing guggulsterone at 500, 1000 and 2000 ppm concentration respectively for 12 weeks. Maintaining mice on fat rich diet only resulted in inducing the metabolic and histological NAFLD associated. While the treatment with guggulsterone significantly improves the evaluated markers. These results demonstrate guggulsterone may be useful in preventing the development of steatohepatitis.

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 Coenzyme Q10 Attenuates High-fat Diet-induced Non-alcoholic Fatty Liver Disease Through Activation of AMPK Pathway (P06-060-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Chen Ke ◽  
Ling Wenhua
Keyword(s):  
Liver Disease ◽  
Weight Gain ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Ampk Pathway ◽  
Alcoholic Fatty Liver Disease

Abstract Objectives To explore whether CoQ10 has an effect on NAFLD and the potential mechanism. Methods 2.1 Animal studies Thirty male C57BL/6 J mice (four weeks) were randomly distributed into three groups (n = 10): control group (10% Kcal from fat), the high-fat group (60% Kcal from fat), the CoQ10 group (CoQ10 1800 mg/kg, 60% Kcal from fat). The intervention time is 24 weeks. 2.2 Biochemical indicator Serum and liver biochemical markers were detected with appropriate test kits. 2.3 Histopathological evaluation H&E staining, immunohistochemistry and immunofluorescence were used to valuate the degree of NAFLD. Results 3.1 CoQ10 ameliorates high-fat diet-induced weight gain and dyslipidaemia. CoQ10 decreased the weight gain (Fig. 1A). In addition, CoQ10 reduced the high-fat diet-induced subcutaneous and visceral fat. Serum levels of TC and TG decreased in mice fed HFD with supplementation of CoQ10 (Fig. 1C). The level of HDL-c showed an unremarkable increase in mice supplemented with CoQ10, while LDL-c in this group decreased (Fig. 1D). 3.2 CoQ10 inhibited NAFLD induced by high-fat diet. The lipid droplet was reduced in the mice fed CoQ10(Fig. 2A). Analysis of Sirius Red staining showed that hepatic fibrosis was ameliorated in the mice fed CoQ10(Fig. 2B). Staining of macrophage marker, F4/80, and the leukocyte marker, CD45 showed that CoQ10 can alleviate inflammation(Fig.2C, D). CoQ10 also induce the injury of liver(Fig. 2E). 3.3 CoQ10 regulates liver lipid metabolism. CoQ10 reversed the increase of ACC and FAS and reversed the decrease of PPAR-α and CPT-1 both in mRNA and protein expression. CoQ10 could activate AMPK. Conclusions Co Q10 may attenuates high-fat diet-induced non-alcoholic fatty liver disease through activation of AMPK pathway. Funding Sources The key Project of National Natural Science Fund (grant number: 81730090). Supporting Tables, Images and/or Graphs

scholarly journals Pengaruh Fraksi Air Buah Lemon terhadap Gambaran Morfologi Jaringan Hati Mencit Tua yang Diberi Pakan Tinggi Lemak

2019 ◽  
Vol 1 (1) ◽  
pp. 49-53
Author(s):  
Nur Azmiati Mundiri ◽  
Meta Maulida Damayanti ◽  
Maya Tejasari ◽  
Annisa Rahmah Furqaani ◽  
R.A. Retno Ekowati
Keyword(s):  
Liver Disease ◽  
Liver Injury ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
Citrus Limon ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Water Fraction ◽  
Alcoholic Fatty Liver Disease

Dislipidemia merupakan salah satu faktor risiko dari non alcoholic fatty liver disease (NAFLD). NAFLD mempunyai karakteristik steatosis hepatik, hepatocyte ballooning, inflamasi lobular, dan fibrosis.  Kandungan flavonoid pada Citrus limon dipercaya dapat mencegah steatosis hepatik. Tujuan penelitian ini mengetahui pengaruh fraksi air buah lemon terhadap gambaran morfologi jaringan hati mencit tua yang diberi pakan tinggi lemak. Penelitian ini merupakan penelitian eksperimental dengan subjek penelitian adalah mencit (Mus musculus) jantan galur DDY tua yang dibagi menjadi empat kelompok secara acak, terdiri atas kelompok kontrol dan tiga kelompok perlakuan dengan konsentrasi fraksi air buah lemon 20,6; 41,2; 82,4 mg/20 gram BB mencit. Data jumlah hepatosit dengan droplet lemak dan hepatocyte ballooning dianalisis menggunakan uji ANOVA dan Uji Kruskal Willis. Terdapat  perbedaan jumlah hepatosit dengan droplet lemak (p=0,063) dan hepatosit yang mengalami pembengkakan (p=0,109) antara kelompok kontrol dan kelompok perlakuan. Simpulan penelitian ini adalah fraksi air buah lemon dapat mencegah hepatocyte ballooning dan pembentukan droplet lemak pada hepatosit mencit tua yang diberikan pakan tinggi lemak.  PROTECTIVE EFFECT OF WATER FRACTION OF LEMON ON HIGH-FAT DIET-INDUCED LIVER INJURY IN OLD MICEDyslipidemia is one of the risk factors of non alcoholic fatty liver disease (NAFLD). NAFLD is characterized by hepatic steatosis, hepatocyte ballooning, lobular inflammation, and fibrosis. Flavonoid in Citrus limon is believed to prevent hepatic steatosis. The aim of this study is to know the protective effect of lemon’s water fraction on high-fat diet-induced liver injury in old mice. This was an experimental study with old male mice (Mus musculus) DDY strain divided into four groups randomly, consisting of control group and three groups given with water fraction of lemon at concentration 20.6; 41.2; 82.4 mg/20 gram mice body weight. Total count of hepatocytes with fat droplets and hepatocytes ballooning were analyzed using ANOVA and Kruskal Willis tests. There are differences in the amount of hepatocytes with fat droplets (p=0.063) and hepatocytes ballooning (p=0.109) between the control group and the treatment group. The conclusion of this study is lemon’s water fraction can prevent the formation of hepatocyte ballooning and fat droplet in old mice’s hepatocyte fed by high-fat diet.

scholarly journals Inhibition of Neuropilin-1 improves non-alcoholic fatty liver disease via PI3K/AKT/mTOR signaling in high-fat-diet induced obese mouse

2021 ◽  
Author(s):  
Jian Zhou ◽  
Sihuan Xu ◽  
Yue Zhu ◽  
Xin Li ◽  
Ao Wang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Injection Group ◽  
Neuropilin 1 ◽  
Alcoholic Fatty Liver Disease

Abstract Background Research findings indicate Neuropilin-1 plays a critical role in lipid metabolism and obesity-associated insulin resistance, on such a basis, this study aims to explore the effects and working mechanism of Neuropilin-1 inhibition on the non-alcoholic fatty liver disease in high-fat-diet induced obese mice. Methods Firstly, the pcDNA3.1-NRP-1 recombinant plasmid containing Neuropilin-1 gene and the Neuropilin-1 gene RNA interference plasmid shRNA-NRP1 were successfully constructed. A total of 36 C57BL/6 mice were randomly assigned to 6 groups, blank group, control group, pcDNA3.1 injection group, pcDNA3.1-NRP-1 injection group, pGenesil-1.1 injection group and shRNA-NRP1 injection group. Expression of phospho-PI3K, phospho-AKT, phospho-mTOR and Neuropilin-1 in liver was measured as well as body and liver weight, blood glucose, serum transaminases and lipid levels of the mice. Results The weight and liver mass of high-fat-diet fed mice injected with pcDNA3.1-NRP-1 were significantly higher than those from the control group, but their body weight and liver mass decreased significantly after shRNA-NRP1 injection. The results also showed that Neuropilin-1 expression can significantly influence the severity of hepatic steatosis in high-fat-diet fed mice, decreased serum FPG, LDL, AST, ALT levels and the expression of TNF-α, IL-1β, and IL-6 mRNA. In addition, the Neuropilin-1 expression will also influence the p-PI3K, p-AKT and p-mTOR in mice. Conclusions This study concluded that the inhibition of Neuropilin-1 could improve Non-alcoholic fatty liver disease by decreasing body weight and reduce inflammation in high-fat-diet induced obese mice by modulating the PI3K/AKT/mTOR signaling pathway.

scholarly journals Inhibition of Neuropilin-1 Improves Non-Alcoholic Fatty Liver Disease via PI3K/AKT/Mtor Signaling in High-Fat-Diet induced Obese Mouse

2021 ◽  
Author(s):  
Jian Zhou ◽  
Sihuan Xu ◽  
Yue Zhu ◽  
Xin Li ◽  
Ao Wang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Injection Group ◽  
Neuropilin 1 ◽  
Alcoholic Fatty Liver Disease

Abstract Background: Research findings indicate Neuropilin-1 plays a critical role in lipid metabolism and obesity-associated insulin resistance, on such a basis, this study aims to explore the effects and working mechanism of Neuropilin-1 inhibition on the non-alcoholic fatty liver disease in high-fat-diet induced obese mice. Methods: Firstly, the pcDNA3.1-NRP-1 recombinant plasmid containing Neuropilin-1 gene and the Neuropilin-1 gene RNA interference plasmid shRNA-NRP1 were successfully constructed. A total of 36 C57BL/6 mice were randomly assigned to 6 groups, blank group, control group, pcDNA3.1 injection group, pcDNA3.1-NRP-1 injection group, pGenesil-1.1 injection group and shRNA-NRP1 injection group. Expression of phospho-PI3K, phospho-AKT, phospho-mTOR and Neuropilin-1 in liver was measured as well as body and liver weight, blood glucose, serum transaminases and lipid levels of the mice.Results: The weight and liver mass of high-fat-diet fed mice injected with pcDNA3.1-NRP-1 were significantly higher than those from the control group, but their body weight and liver mass decreased significantly after shRNA-NRP1 injection. The results also showed that Neuropilin-1 expression can significantly influence the severity of hepatic steatosis in high-fat-diet fed mice, decreased serum FPG, LDL, AST, ALT levels and the expression of TNF-α, IL-1β, and IL-6 mRNA. In addition, the Neuropilin-1 expression will also influence the p-PI3K, p-AKT and p-mTOR in mice.Conclusions: This study concluded that the inhibition of Neuropilin-1 could improve Non-alcoholic fatty liver disease by decreasing body weight and reduce inflammation in high-fat-diet induced obese mice by modulating the PI3K/AKT/mTOR signaling pathway.

scholarly journals Effect of diosmetin on young rats with high-fat diet-induced non-alcoholic fatty liver disease

2022 ◽  
Vol 20 (2) ◽  
pp. 315-320
Author(s):  
Guoying Zhang ◽  
Yuewu Yan ◽  
Xujiao Feng
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Diet Group ◽  
Control Group ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Tnf Α ◽  
Alcoholic Fatty Liver Disease

Purpose: To determine the effect of diosmetin on young, non-alcoholic fatty liver disease (NAFLD) rats. Methods: Five groups of SD rats were used: control group, high-fat diet group, low-dose diosmetin group, medium-dose diosmetin group, and high-dose diosmetin group, each with 10 rats. After 3 months, interleukin 6 (IL-6), IL-1β) and TNF-α) were assayed. Protein expressions of p-AMPKα, CPT-1 and PPAR-α, AMPKα, SREBP-1c and FAS were assayed. Results: In the high-fat diet group, the levels of p-AMPKα, CPT-1 and PPAR-α were lower than the corresponding control values, while p-AMPKα, CPT-1 and PPAR-α levels were dose-dependently higher in all diosmetin groups than in NAFLD group (p < 0.05). There were higher levels of SREBP-1c and FAS in the high-fat diet group than in control group, while SREBP-1c and FAS levels in all diosmetin groups were dose-dependently lower than the corresponding levels in NAFLD group. Serum IL-6, IL-1β and TNF-α levels in NAFLD group were raised, relative to control values (p < 0.05). Conclusion: Diosmetin alleviates NAFLD lesions induced by high-fat diet, slows down liver cell apoptosis, and inhibits inflammation via activation of AMPK pathway. Thus, diosmetin has potentials for use in the repair of hepatic damage induced by high-fat diet.

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

Triterpenoid-Rich Fraction from Ilex hainanensis Merr. Attenuates Non-Alcoholic Fatty Liver Disease Induced by High Fat Diet in Rats

2013 ◽  
Vol 41 (03) ◽  
pp. 487-502 ◽  
Author(s):  
Wei-Xi Cui ◽  
Jie Yang ◽  
Xiao-Qing Chen ◽  
Qian Mao ◽  
Xiang-Lan Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Density Lipoprotein ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Cyp2e1 Expression ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) has become a major challenge to the healthcare system. This study was designed to evaluate the effect of the triterpenoid-rich fraction (TF) from Ilex hainanensis Merr. on NAFLD. Male Sprague-Dawley (SD) rats were fed a normal diet (control) or high fat diet (NAFLD model). After four weeks, the high fat diet group was orally administrated TF (250 mg/kg) for another two weeks. High fat diet fed rats displayed hyperlipidemia and a decline in liver function compared with control. However, administration with TF could effectively improve these symptoms, as demonstrated by decreasing the plasma levels of triglyceride (p <0.05), total cholesterol (p < 0.01), low-density lipoprotein cholesterol (p < 0.05), alanine transaminase (p < 0.05), aspartate aminotransferase (p < 0.01), liver index (p < 0.05) and insulin resistance index (p < 0.05) while increasing the high-density lipoprotein cholesterol (p < 0.05). Meanwhile, histopathological examination of livers also showed that TF could reduce the incidence of liver lesions induced by high fat diet. Furthermore, TF could alleviate oxidative stress and inflammation status indicated by the decline malondialdehyde and superoxide dismutase levels (p < 0.01, both) and levels of interleukin 6 and tumor necrosis factor-α (p < 0.05). In addition, immunohistochemistry showed TF evidently elevated the peroxisome proliferator-activated receptor (PPARα) expression (p < 0.01), while it diminished the Cytochrome P450 2E1 (CYP2E1) expression (p < 0.01) in liver. These results demonstrate that TF has potential ability to protect liver against NAFLD by regulating lipids metabolism and alleviating insulin resistance, inflammation and oxidative stress. This effect might be associated with regulating PPARα and CYP2E1 expression.

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