scholarly journals Effect of Kelussia odoratissima Mozaff extract on PNPLA3 gene expression in non-alcoholic fatty liver and control rats

2021 ◽  
pp. 335-345
Keyword(s):  
Gene Expression ◽  
Treatment Group ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Blood Lipids ◽  
Control Group ◽  
Protective Effects ◽  
High Fat ◽  
Biochemical Tests ◽  
Alcoholic Fatty Liver

Background and Aims: Non-alcoholic fatty liver disease (NAFLD) is associated with such symptoms as steatosis, fibrosis, and liver cirrhosis. Kelussia has attracted assiduous attention due to its protective effects on the liver. The PNPLA3 gene is mainly expressed in the liver and plays a major role in the degradation rate of hepatic triglycerides. Therefore, the present study aimed to assess the effect of Kelussia extract on PNPLA3 gene expression in rats with fatty liver and healthy rats. Materials and Methods: This experimental study was conducted on 24 male Wistar rats in the control group (no treatment), obese group (which received a high-fat diet), treatment group 1 (which received a high-fat diet with Kelussia extract 400 mg/kg) and treatment group 2 (a high-fat diet with Kelussia extract 800 mg/kg) for six weeks. Blood samples were taken from rats and the factors of (LDL, HDL, Cholesterol, Triglyceride, and fasting sugar) were measured. After sampling the rat liver, the effect of Kelussia on PNPLA3 gene expression was investigated using the Real-time reverse transcription-polymerase chain reaction (RT-PCR) technique and analyzed in SPSS software (version 22). Results: Based on the results, Kelussia extract at a dose of 800 mg/kg resulted in a more dramatic decrease in PNPLA3 gene expression in rats with fatty liver, compared to a dose of 400 mg /kg, and this reduction was statistically significant, compared to the fatty liver group (P<0.05). The results of biochemical tests confirmed liver improvement in the rats treated with Kelussia extract at a dose of 800 mg/kg. Conclusion: It can be said that Kelussia had a beneficial effect on the reduction of blood lipids; moreover, it reduces the accumulation of triglycerides in the liver and improves the tissue structure of the liver by reducing the expression of PNPLA3 gene; therefore, with more studies, it can be considered a supplement to reduce blood lipids.

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 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 Modulation of Gut Microbiota by Lonicera caerulea L. Berry Polyphenols in a Mouse Model of Fatty Liver Induced by High Fat Diet

Molecules ◽  
2018 ◽  
Vol 23 (12) ◽  
pp. 3213 ◽  
Author(s):  
Shusong Wu ◽  
Ruizhi Hu ◽  
Hironobu Nakano ◽  
Keyu Chen ◽  
Ming Liu ◽  
...  
Keyword(s):  
Mouse Model ◽  
Gut Microbiota ◽  
Fatty Liver ◽  
Relative Abundance ◽  
High Fat Diet ◽  
Rrna Gene ◽  
Protective Effects ◽  
High Fat ◽  
Lonicera Caerulea ◽  
Alcoholic Fatty Liver

Polyphenols from the Lonicera caerulea L. berry have shown protective effects on experimental non-alcoholic fatty liver disease (NAFLD) in our previous studies. As endotoxins from gut bacteria are considered to be the major trigger of inflammation in NAFLD, this study aims to clarify the regulatory effects of L. caerulea L. berry polyphenols (LCBP) on gut microbiota in a high fat diet (HFD)-induced mouse model. C57BL/6N mice were fed with a normal diet, HFD, or HFD containing 0.5–1% of LCBP for 45 days. The results revealed that supplementation with LCBP decreased significantly the levels of IL-2, IL-6, MCP-1, and TNF-α in serum, as well as endotoxin levels in both serum and liver in HFD-fed mice. Fecal microbiota characterization by high throughput 16S rRNA gene sequencing revealed that a HFD increased the Firmicutes/Bacteroidetes ratio, and LCBP reduced this ratio by increasing the relative abundance of Bacteroides, Parabacteroides, and another two undefined bacterial genera belonging to the order of Bacteroidales and family of Rikenellaceae, and also by decreasing the relative abundance of six bacterial genera belonging to the phylum Firmicutes, including Staphylococcus, Lactobacillus, Ruminococcus, and Oscillospira. These data demonstrated that LCBP potentially attenuated inflammation in NAFLD through modulation of gut microbiota, especially the ratio of Firmicutes to Bacteroidetes.

scholarly journals Effect of grapefruit juice on CYP2E1 gene expression in obese and control rats

2021 ◽  
pp. 260-269
Keyword(s):  
Gene Expression ◽  
Treatment Group ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Grapefruit Juice ◽  
Diet Group ◽  
The Body ◽  
High Fat ◽  
Cyp2e1 Gene ◽  
And Control

Background and Aims: The CYP2E1 gene encodes cytochrome P450 enzymes that play an essential role in liver fat metabolism. Additionally, grapefruit reduces plasma lipids in the body. Therefore, herbal medicines can be considered as an important treatment strategy. The present study aimed to evaluate the effect of grapefruit juice on CYP2E1 gene expression in obese and control rats. Materials and Methods: This experimental study was performed on 24 male Wistar rats weighing 180±20 g. Rats were divided into four groups: control (no treatment), high-fat diet group, treatment group 1 (high cholesterol diet with grapefruit juice 4 ml/kg), and treatment group 2 (high-fat diet with grapefruit juice) (8 ml/kg). They also gavaged for 6 weeks and CYP2E1 gene expression was finally determined. Statistical analyzes were performed using SPSS software (version 22). Results: The results of CYP2E1 gene expression indicated that grapefruit juice at a dose of 8 ml/kg can further reduce the expression of CYP2E1 gene in rats with fatty liver (1.09 ±0.038) than the dose of 4 ml/kg (1.27 ±0.24). This reduction in expression was statistically significant compared to that of the high-fat diet group (3.61 ±0.25) (P=0.003). Conclusion: The results of this study demonstrated that grapefruit juice reduces the expression of the CYP2E1 gene in obese rats due to naringin and recovers the disease by reducing the accumulation of triglycerides in the liver. Therefore, grapefruit juice can be considered as a therapeutic target in fatty liver disease and obesity.

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.

Withdrawn: Hepatoprotective effects of Tribulus terrestris L. (Zygophyllales: Zygophyllaceae) hydro-alcholic extract on non-alcoholic fatty liver-induced rats

2016 ◽  
Vol 3 (5) ◽  
pp. 143
Author(s):  
Fatemeh Almasi ◽  
Mozafar Khazaei ◽  
Shima Chehrei ◽  
Ali Ghanbari
Keyword(s):  
Fatty Liver ◽  
Liver Tissue ◽  
Serum Lipid ◽  
Histopathological Examination ◽  
Serum Levels ◽  
Lipid Profiles ◽  
Control Group ◽  
Tribulus Terrestris ◽  
Protective Effects ◽  
Alcoholic Fatty Liver

Non-alcoholic fatty liver induces many complications to the liver tissue and also serum related parameters. Medicinal plants are the safe therapeutic strategy for the treatment of diseases. In this regards, the present study was conducted to evaluate the effect of Tribulus terrestris L. (Zygophyllales: Zygophyllaceae) extract on non-alcoholic fatty liver in rats. In this experimental study, thirty male Wistar rats were divided into five groups (n = 6). Animals in experimental groups were received high fructose diet (70%) (HDF) daily alone or in combined with daily intraperitoneal injection of 500, 700 and 1,000 mg/kg extract of T. terrestris. Control group of rats was feed with standard chow. The serum levels of biomarkers of liver and serum lipid profiles were assessed, also histopathological examination of liver tissue done. Data were analyzed using One-way ANOVA method followed by Tukey’s post-hoc multiple comparison test and P < 0.05 was considered statistically significant. There were significant improvements for biomarkers of liver tissue (P < 0.05) and serum lipid profiles (P < 0.01) in the HFD-fed rats that were treated with T. terrestris extract compare to HFD-fed group. In addition, accumulation of lipids in hepatocytes was significantly reduced in the HFD-fed + extract administrated groups in comparison to HFD-fed rats (P < 0.01). T. terrestris extract has protective effects against non-alcoholic fatty liver by changing biomarkers of liver tissue, serum lipid profiles and histopathological anomalies of liver tissue, to normal range.

scholarly journals Protective effects of a unique combination of nutritionally active ingredients on risk factors and gene expression associated with atherosclerosis in C57BL/6J mice fed a high fat diet

2021 ◽  
Author(s):  
Joe W. E. Moss ◽  
Jessica O Williams ◽  
Wijdan Al-Ahmadi ◽  
Victoria O'Morain ◽  
Yee-Hung Chan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
High Fat Diet ◽  
Inflammatory Disorder ◽  
Protective Effects ◽  
Unique Combination ◽  
Omega 3 ◽  
High Fat ◽  
Food Ingredients

Atherosclerosis, an inflammatory disorder of the vasculature and the underlying cause of cardiovascular disease, is responsible for one in three global deaths. Consumption of active food ingredients such as omega-3...

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