scholarly journals A high-fat diet as a model of fatty liver disease in rats

2011 ◽  
Vol 26 (suppl 2) ◽  
pp. 25-30 ◽  
Author(s):  
Monike Garlipp Picchi ◽  
Andresa Marques de Mattos ◽  
Marina Rodrigues Barbosa ◽  
Camila Passos Duarte ◽  
Maria de Azevedo Gandini ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Weight Gain ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Control Group ◽  
High Fat ◽  
The Metabolic Syndrome ◽  
Hepatic Fat ◽  
Induce Weight Gain

PURPOSE: The objective of the present study was to analyze the physiological and metabolic changes occurring in rats subjected to high-fat diet for one month. METHODS: The animals received a modified AIN-93 diet with increased lipid content and decreased carbohydrate content, while the control group received the normal AIN-93 diet. RESULTS: It was observed that the high-fat diet did not induce weight gain but led to greater gain of hepatic fat compared to control. Biochemcal parameters, glycemia, total cholesterol and serum protein did not differ between groups. In parallel, rats receiving the high-fat diet consumed less feed. CONCLUSION: The development of obesity through high-fat diet is associated with increased energy intake and time of exposure to the diet, while the metabolic syndrome is more associated with the combination of a diet rich in fat and carbohydrates.

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 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.

Activated TNF-α/RIPK3 signaling is involved in prolonged high fat diet-stimulated hepatic inflammation and lipid accumulation: inhibition by dietary fisetin intervention

2019 ◽  
Vol 10 (3) ◽  
pp. 1302-1316 ◽  
Author(s):  
Minxuan Xu ◽  
Chenxu Ge ◽  
Yuting Qin ◽  
Tingting Gu ◽  
Jinxiao Lv ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Hepatic Inflammation ◽  
High Fat ◽  
Predisposing Factor ◽  
Nonalcoholic Fatty Liver ◽  
Tnf Α

Increasing evidence indicates that high-fat diet (HFD) is a predisposing factor for metabolic syndrome-associated systemic inflammation and nonalcoholic fatty liver disease (NAFLD).

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 Jiangzhi Ligan Decoction Alleviated Nonalcoholic Fatty Liver Disease Induced by High-Fat-Diet in Rats via GSDMD-mediated Canonical/Non-canonical Pyroptosis Pathway

2021 ◽  
Author(s):  
XIAO ZHOU ◽  
Kangkang Yin ◽  
Wei Jiang ◽  
Ziwei Dai ◽  
Biao Tang
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Liver Lipid ◽  
Normal Control Group ◽  
Control Group ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Hepatoprotective Effects

Abstract Background Hepatoprotective effects of Chinese herbal formula Jiangzhi Ligan Decoction (JZLGD) against nonalcoholic fatty liver disease (NAFLD) have been demonstrated, but its mechanism is not clear. The aim of this study was to evaluate the protective effects of against high-fat diet (HFD) induced NAFLD in rat, and to further explore the potential molecular mechanism. Methods SD rats were assigned to five different groups: normal control group, NAFLD model group and JZLGD-treated NAFLD group (3 doses of JZLGD: 2.3, 4.6, 9.2 g/kg of body weight, respectively). All the rats were fed a HFD for 18 weeks except the normal control group(a normal diet). After 12 weeks, rats in JZLGD-treated NAFLD group were administered different doses of JZLGD by oral gavage once daily for another period of 6 weeks, and the rest were given the same dosage of normal saline. After the intervention, blood and liver from each sample were carefully removed and analyzed accordingly. Results We found that JZLGD significantly reduced the liver index, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum. Furthermore, pathological examinations showed that JZLGD markedly reduced liver lipid droplets and improved liver lipid accumulation, NAFLD activity score and ballooning pathology scoring were also decreased. The detection of cytokines showed that JZLGD could significantly reduced the levels of serum inflammatory factors IL-1β, IL-18, tumor necrosis factor α (TNF-α) and IL-6, protected HFD rats from inflammation. In addition, NAFLD treatment, exhibited significant reduction in serum triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL) and free fatty acid (FFA) when compared to NAFLD control rats. JZLGD intervention also reduced the level of serum lipopolysaccharide (LPS) and the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), caspase-1, caspase-11, GSDMD, GSDMD N-terminus (GSDMD-N), IL-1β, IL-18 in the liver. Conclusion These results demonstrate the hepatoprotective effects of JZLGD in NAFLD mice, the effects may be mediated via downregulation of NLRP3 /caspase-1/GSDMD mediated canonical pyroptosis pathway and LPS /caspase-11/GSDMD mediated non-canonical pyroptosis 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 Perinatal exposure to bisphenol A exacerbates nonalcoholic steatohepatitis-like phenotype in male rat offspring fed on a high-fat diet

2014 ◽  
Vol 222 (3) ◽  
pp. 313-325 ◽  
Author(s):  
Jie Wei ◽  
Xia Sun ◽  
Yajie Chen ◽  
Yuanyuan Li ◽  
Liqiong Song ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Liver Function ◽  
Bisphenol A ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Perinatal Exposure ◽  
High Fat ◽  
Rat Offspring

Bisphenol A (BPA) is one of the environmental endocrine disrupting chemicals, which is present ubiquitously in daily life. Accumulating evidence indicates that exposure to BPA contributes to metabolic syndrome. In this study, we examined whether perinatal exposure to BPA predisposed offspring to fatty liver disease: the hepatic manifestation of metabolic syndrome. Wistar rats were exposed to 50 μg/kg per day BPA or corn oil throughout gestation and lactation by oral gavage. Offspring were fed a standard chow diet (SD) or a high-fat diet (HFD) after weaning. Effects of BPA were assessed by examination of hepatic morphology, biochemical analysis, and the hepatic expression of genes and/or proteins involved in lipogenesis, fatty acid oxidation, gluconeogenesis, insulin signaling, inflammation, and fibrosis. On a SD, the offspring of rats exposed to BPA exhibited moderate hepatic steatosis and altered expression of insulin signaling elements in the liver, but with normal liver function. On a HFD, the offspring of rats exposed to BPA showed a nonalcoholic steatohepatitis-like phenotype, characterized by extensive accumulation of lipids, large lipid droplets, profound ballooning degeneration, impaired liver function, increased inflammation, and even mild fibrosis in the liver. Perinatal exposure to BPA worsened the hepatic damage caused by the HFD in the rat offspring. The additive effects of BPA correlated with higher levels of hepatic oxidative stress. Collectively, exposure to BPA may be a new risk factor for the development of fatty liver disease and further studies should assess whether this finding is also relevant to the human population.

scholarly journals Managing the Combination of Nonalcoholic Fatty Liver Disease and Metabolic Syndrome with Chinese Herbal Extracts in High-Fat-Diet Fed Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Tan ◽  
Weiguo Lao ◽  
Linda Xiao ◽  
Zhenzhong Wang ◽  
Wei Xiao ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Herbal Extracts ◽  
Hepatic Enzymes ◽  
High Fat ◽  
Nonalcoholic Fatty Liver ◽  
Chinese Herbal

Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome (MetS). The aim of the study was to evaluate the effects of Chinese herbal extracts fromSalvia miltiorrhizaandGardenia jasminoides(SGE) on the combination of NAFLD and MetS induced by a high-fat diet (HFD) in rats. After 6 weeks of HFD feeding, rats (n=10each group) were treated with saline, rosiglitazone (RSG), and SGE for 4 weeks. HFD rats were obese, hyperinsulinemic, hyperlipidemic and increased hepatic enzymes with the histological images of NAFLD. Treatment with SGE significantly reduced serum triglycerides (TG), nonesterified fatty acids and enhanced insulin sensitivity, and ameliorated the elevated serum hepatic enzymes compared with HFD-saline group. SGE treatment also attenuated hepatic TG by 18.5% (P<0.05). Histological stains showed SGE decreased lipids droplets in hepatocytes (P<0.05) and normalized macrovesicular steatosis in HFD rats. Significant reduction of TNF-αand IL6 in adipose tissue was detected in SGE treated rats. The anti-inflammatory action may be, at least in part, the mechanism of SGE on MetS associated with NAFLD. This study discovered that SGE is capable of managing metabolic and histological abnormalities of NAFLD and MetS. SGE may be an optimal treatment for the combination of NAFLD and MetS.

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