Coenzyme Q10 attenuates high-fat diet-induced non-alcoholic fatty liver disease through activation of the AMPK pathway

2019 ◽  
Vol 10 (2) ◽  
pp. 814-823 ◽  
Author(s):  
Ke Chen ◽  
Xu Chen ◽  
Hongliang Xue ◽  
Peiwen Zhang ◽  
Wanjun Fang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Coenzyme Q10 ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Ampk Pathway ◽  
Alcoholic Fatty Liver Disease

Coenzyme Q10 regulates lipid metabolism to ameliorate the progression of NAFLD by activating the AMPK pathway.

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

Holothuria arenicola extract attenuated hepatic steatosis in splenectomized rat fed high fat diet

2021 ◽  
Vol 11 ◽  
Author(s):  
Shimaa A. Sadek ◽  
Asmaa E. Farouk ◽  
Sohair R. Fahmy ◽  
Amel M. Soliman
Keyword(s):  
Lipid Metabolism ◽  
Liver Disease ◽  
Fatty Liver ◽  
Enzyme Activities ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Holothuria Arenicola ◽  
Alcoholic Fatty Liver Disease

Background: Non-alcoholic fatty liver disease (NAFLD) is a considerable public health concern due to the excessive dietary consumption of high caloric diet and subsequent obesity. Additionally, splenectomy is considered as one of major common risk factor for NAFLD. Objective: Regardless of non-alcoholic fatty liver disease (NAFLD) being the most common chronic disorder, there are no effective cure for it. Therefore, the current study aimed to investigate Holothuria arenicola extract (HaE) efficacy on hepatic steatosis in splenectomized (SPX) rats fed High fat diet (HFD). Methods: Male Wistar rats (n=28) were randomly assigned to four groups: sham rats fed a standard diet, sham rats+ HFD, SPX+HFD and SPX+HFD+HaE. The estimation of hematological and some biochemical parameters as well as oxidative status were analyzed. Results: Oral administration of HaE caused a significant amelioration in all hematological parameters relative to untreated splenectomized rats. Concerning lipid metabolism, HaE treatment caused a pronounced amelioration in lipid metabolism, as indicated by the decreased total cholesterol, triglycerides and LDL-cholesterol contents as well as the increased HDL- cholesterol level. HaE treatment significantly enhanced hepatic function, as exhibited by the reduction in liver enzyme activities as well as the increase of protein and albumin content. Moreover, HaE could retard the hepatic oxidative stress via a pronounced increase in hepatic GSH content and antioxidant enzyme activities besides decreasing in MDA, NO and H2O2 formation. Conclusion: HaE could be utilized as a potential alternative hepatoprotective remedy via lipid metabolism and oxidative damage attenuation.

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