Metformin treatment reverses high fat diet- induced non-alcoholic fatty liver diseases and dyslipidemia by stimulating multiple antioxidant and anti-inflammatory pathways

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.

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

Molecular Medicine Reports ◽

10.3892/mmr.2014.2623 ◽

2014 ◽

Vol 10 (6) ◽

pp. 2917-2923 ◽

Cited By ~ 9

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

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Sleeve gastrectomy attenuates high fat diet-induced non-alcoholic fatty liver disease

Lipids in Health and Disease ◽

10.1186/s12944-018-0875-5 ◽

2018 ◽

Vol 17 (1) ◽

Cited By ~ 2

Author(s):

Erli Pei ◽

Yang Liu ◽

Weiqing Jiang ◽

Songruo Lin ◽

Lei Huang ◽

...

Keyword(s):

Sleeve Gastrectomy ◽

Liver Disease ◽

Fatty Liver ◽

High Fat Diet ◽

Fatty Liver Disease ◽

High Fat ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

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

10.20944/preprints201907.0180.v1 ◽

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’s lipid signalling pathways.

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Sodium Butyrate Ameliorates High-Fat-Diet-Induced Non-alcoholic Fatty Liver Disease through Peroxisome Proliferator-Activated Receptor α-Mediated Activation of β Oxidation and Suppression of Inflammation

Journal of Agricultural and Food Chemistry ◽

10.1021/acs.jafc.8b01189 ◽

2018 ◽

Vol 66 (29) ◽

pp. 7633-7642 ◽

Cited By ~ 22

Author(s):

Bo Sun ◽

Yimin Jia ◽

Jian Hong ◽

Qinwei Sun ◽

Shixing Gao ◽

...

Keyword(s):

Liver Disease ◽

Fatty Liver ◽

Sodium Butyrate ◽

High Fat Diet ◽

Fatty Liver Disease ◽

Peroxisome Proliferator ◽

High Fat ◽

Peroxisome Proliferator Activated Receptor ◽

Alcoholic Fatty Liver ◽

Alcoholic Fatty Liver Disease

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Ethanol Extract of Crataegus Oxyacantha L. Ameliorate Dietary Non-Alcoholic Fatty Liver Disease in Rat

Drug Research ◽

10.1055/a-0579-7532 ◽

2018 ◽

Vol 68 (10) ◽

pp. 553-559

Author(s):

Golbahar Saeedi ◽

Fereshteh Jeivad ◽

Mohammadhadi Goharbari ◽

Gholamreza Gheshlaghi ◽

Omid Sabzevari

Keyword(s):

Fatty Liver ◽

Protective Effect ◽

High Fat Diet ◽

Normal Diet ◽

Oxidative Stress Marker ◽

Histopathological Study ◽

Potential Candidate ◽

Diet Change ◽

High Fat ◽

Alcoholic Fatty Liver

Abstract Background Non-alcoholic fatty liver (NAFLD) is one the most prevalent disease worldwide which characterized by fat accumulation in liver with no established efficient therapy. We designed this study to investigate protective and therapeutic effect of Crataegus oxyacantha L. (C. oxyacantha) on NAFLD induced by high fat diet in rat models. Methods NAFLD was induced by High Fat Diet+fructose (HFD), 45 Wistar rats were divided to 8 groups including control, HFD, HFD+diet change, HFD+diet change+C. oxyacantha 20 mg/kg, co treatment of HFD+C. oxyacantha 10, 20 and 40 mg/kg, and normal diet+C. oxyacantha 40 mg. C. oxyacantha was administered orally. Effectiveness of the C. oxyacantha was assessed through measuring the biochemical factors, and oxidative stress marker (FRAP, GSH, and MDA). Histopathological study was performed using H & E staining. Results The diet change from high fat to low fat ameliorated liver damage. However, consumption of C. oxyacantha (10 & 20 mg/kg) caused significant reduction in the level of all examined liver biomarkers specially LDH, that showed C. oxyacantha can restore the hepatocyte damage due to HFD. The C. oxyacantha showed a protective effect which was more prominent in the animals treated with the 20 mg/kg C. oxyacantha. The administration of C. oxyacantha caused increased antioxidant status (GSH and FRAP levels) and decreased lipid peroxidation in treated animals. Major Conclusion Accordingly, C. oxyacantha have both therapeutic and protective effect for NAFLD and may be a potential candidate for further assessments in clinical studies.

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