scholarly journals An albino mouse model of nonalcoholic fatty liver disease induced using high-fat liquid “Lieber-DeCarli” diet: a preliminary investigation

2020 ◽  
Vol 5 (4) ◽  
pp. e071
Author(s):  
Ayokanmi Ore ◽  
Regina Ngozi Ugbaja ◽  
Abideen Idowu Adeogun ◽  
Oluseyi Adeboye Akinloye
Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2433
Author(s):  
Hwi-Jin Im ◽  
Seung-Ju Hwang ◽  
Jin-Seok Lee ◽  
Sung-Bae Lee ◽  
Ji-Yun Kang ◽  
...  

The global prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated to be 25% and has continued to increase; however, no drugs have yet been approved for NAFLD treatments. The ethyl acetate fraction of Amomum xanthioides (EFAX) was previously reported to have an anti-hepatic fibrosis effect, but its effects on steatosis or steatohepatitis remain unclear. This study investigated the anti-fatty liver of EFAX using a high-fat diet mouse model. High-fat diet intake for 8 weeks induced hepatic steatosis with mild inflammation and oxidative damage and increased the adipose tissue weight along with the development of dyslipidemia. EFAX treatment significantly ameliorated the steatohepatic changes, the increased weight of adipose tissues, and the altered serum lipid profiles. These observed effects were possibly due to the lipolysis-dominant activity of EFAX on multiple hepatic proteins including sterol regulatory element-binding protein (mSREBP)-1c, peroxisome proliferator-activated receptor (PPAR)-α, AMP-activated protein kinase, and diglyceride acyltransferases (DGATs). Taken together, these results show that EFAX might be a potential therapeutic agent for regulating a wide spectrum of NAFLDs from steatosis to fibrosis via multiple actions on lipid metabolism-related proteins. Further studies investigating clear mechanisms and their active compounds are needed.


2018 ◽  
Vol 24 (45) ◽  
pp. 5095-5108 ◽  
Author(s):  
Karen Jackson ◽  
Noa Dressler ◽  
Rotem S Ben-Shushan ◽  
Ari Meerson ◽  
Tyler W LeBaron ◽  
...  

2014 ◽  
Vol 306 (6) ◽  
pp. G496-G504 ◽  
Author(s):  
Akihiro Asai ◽  
Pauline M. Chou ◽  
Heng-Fu Bu ◽  
Xiao Wang ◽  
M. Sambasiva Rao ◽  
...  

Liver steatosis in nonalcoholic fatty liver disease is affected by genetics and diet. It is associated with insulin resistance (IR) in hepatic and peripheral tissues. Here, we aimed to characterize the severity of diet-induced steatosis, obesity, and IR in two phylogenetically distant mouse strains, C57BL/6J and DBA/2J. To this end, mice (male, 8 wk old) were fed a high-fat and high-carbohydrate (HFHC) or control diet for 16 wk followed by the application of a combination of classic physiological, biochemical, and pathological studies to determine obesity and hepatic steatosis. Peripheral IR was characterized by measuring blood glucose level, serum insulin level, homeostasis model assessment of IR, glucose intolerance, insulin intolerance, and AKT phosphorylation in adipose tissues, whereas the level of hepatic IR was determined by measuring insulin-triggered hepatic AKT phosphorylation. We discovered that both C57BL/6J and DBA/2J mice developed obesity to a similar degree without the feature of liver inflammation after being fed an HFHC diet for 16 wk. C57BL/6J mice in the HFHC diet group exhibited severe pan-lobular steatosis, a marked increase in hepatic triglyceride levels, and profound peripheral IR. In contrast, DBA/2J mice in the HFHC diet group developed only a mild degree of pericentrilobular hepatic steatosis that was associated with moderate changes in peripheral IR. Interestingly, both C57BL/6J and DBA/2J developed severe hepatic IR after HFHC diet treatment. Collectively, these data suggest that the severity of diet-induced hepatic steatosis is correlated to the level of peripheral IR, not with the severity of obesity and hepatic IR. Peripheral rather than hepatic IR is a dominant factor of pathophysiology in nonalcoholic fatty liver disease.


2022 ◽  
Author(s):  
Wermerson Assunção Barroso ◽  
Mariana Barreto Serra ◽  
Iracelle Carvalho Abreu ◽  
Hermes Vieira Barbeiro ◽  
Jarlei Fiamoncini ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document