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 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

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 lupine (Lupinus angustifolious L.) peptide prevents non-alcoholic fatty liver disease in high-fat-diet-induced obese mice

2020 ◽  
Vol 11 (4) ◽  
pp. 2943-2952 ◽  
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 ◽  
Obese Mice ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

A lupine (Lupinus angustifolious L.) peptide prevents non-alcoholic fatty liver disease in high-fat-diet-induced obese mice.

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