scholarly journals Peer Review #1 of "Polyphenol-rich Trapa quadrispinosa pericarp extract ameliorates high-fat diet induced non-alcoholic fatty liver disease by regulating lipid metabolism and insulin resistance in mice (v0.3)"

Author(s):  
P Fernandes
2019 ◽  
Vol 10 (2) ◽  
pp. 814-823 ◽  
Author(s):  
Ke Chen ◽  
Xu Chen ◽  
Hongliang Xue ◽  
Peiwen Zhang ◽  
Wanjun Fang ◽  
...  

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


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e8165 ◽  
Author(s):  
Tunyu Jian ◽  
Han Lü ◽  
Xiaoqin Ding ◽  
Yuexian Wu ◽  
Yuanyuan Zuo ◽  
...  

In China, Trapa quadrispinosa (also called water caltrop) has long been used as a function food and folk medicine to treat diabetes mellitus for years. In the present study, the extract of T. quadrispinosa pericarp (TQPE) which mainly contains hydrolysable tannins was prepared to investigate the potential therapeutic action in non-alcoholic fatty liver disease (NAFLD) mice induced by high fat-diet (HFD). After the administration of TQPE (15, 30 mg/kg/day) for 8 weeks, the increased weight of body and liver were significantly suppressed. TQPE also ameliorated liver lipid deposition and reduced lipids parameters of blood in mice. Moreover, TQPE attenuated oxidative stress and showed a hepatoprotective effect in mice. TQPE was also found to decrease the value of homeostatic model assessment for insulin resistance. In addition, TQPE administration increased the phosphorylation of AMP-activated protein kinase (AMPK) and Acetyl-CoA carboxylase (ACC) and inhibited sterol regulatory element-binding protein (SREBP) in the liver tissue. Meanwhile, TQPE elevated insulin receptor substrate-1 (IRs-1) and protein kinase B (Akt) phosphorylation. These results reflected that, as a nature product, TQPE is a potential agent for suppressing the process of NAFLD via regulation of the AMPK/SREBP/ACC and IRs-1/Akt pathways.


2018 ◽  
Vol 45 (6) ◽  
pp. 2187-2198 ◽  
Author(s):  
Dongxia Fu ◽  
Haibin Cui ◽  
Yunna Zhang

Background/Aims: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease. This study aims to investigate whether chloride channel 2 (ClC-2) is involved in high fat diet (HFD)-induced NAFLD and possible molecular mechanisms. Methods: ClC-2 expression was liver-specifically downregulated using adeno-associated virus in C57BL/6 mice treated with a chow diet or HFD for 12 weeks. Peripheral blood and liver tissues were collected for biochemical and pathological estimation respectively. Western blotting was applied to detect the protein expressions of lipid synthesis-related enzymes and the phosphorylated level of IRS-1, Akt and mTOR. Results: ClC-2 mRNA level was significantly increased in patients with non-alcoholic steatohepatitis, which positively correlated with the plasma levels of alanine transaminase (ALT), aspartate transaminase (AST) and insulin. Knockdown of ClC-2 in liver attenuated HFD-induced weight gain, obesity, hepatocellular ballooning, and liver lipid accumulation and fibrosis, accompanied by reduced plasma free fatty acid (FFA), triglyceride (TG), total cholesterol (TC), ALT, AST, glucose and insulin levels and homeostasis model of insulin resistance (HOMA-IR) value. Moreover, HFD-treated mice lacking ClC-2 showed inhibited hepatic lipid accumulation via regulating lipid metabolism through decreasing sterol regulatory element binding protein (SREBP)-1c expression and its downstream targeting enzymes such as fatty acid synthase (FAS), HMG-CoA reductase (HMGCR) and acetyl-Coenzyme A carboxylase (ACCα). In addition, in vivo and in vitro results demonstrated that ClC-2 downregulation in HFD-treated mice or HepG2 cells increased the sensitivity to insulin via activation of IRS-1/Akt/mTOR signaling pathway. Conclusion: Our present study reveals a critical role of ClC-2 in regulating metabolic diseases. Mice lacking ClC-2 are associated with a remarkably beneficial metabolic phenotype, suggesting that decreasing ClC-2 may be an attractive therapeutic strategy for the treatment of NAFLD.


Nutrition ◽  
2009 ◽  
Vol 25 (11-12) ◽  
pp. 1157-1168 ◽  
Author(s):  
Ghada M. Safwat ◽  
Stefania Pisanò ◽  
Emanuela D'Amore ◽  
Giorgio Borioni ◽  
Mariarosaria Napolitano ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Shimaa A. Sadek ◽  
Asmaa E. Farouk ◽  
Sohair R. Fahmy ◽  
Amel M. Soliman

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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