scholarly journals Activation of AMP-Activated Protein Kinase Inhibits Oxidized LDL-Triggered Endoplasmic Reticulum Stress In Vivo

Diabetes ◽  
2010 ◽  
Vol 59 (6) ◽  
pp. 1386-1396 ◽  
Author(s):  
Y. Dong ◽  
M. Zhang ◽  
S. Wang ◽  
B. Liang ◽  
Z. Zhao ◽  
...  
Circulation ◽  
2010 ◽  
Vol 121 (6) ◽  
pp. 792-803 ◽  
Author(s):  
Yunzhou Dong ◽  
Miao Zhang ◽  
Bin Liang ◽  
Zhonglin Xie ◽  
Zhengxing Zhao ◽  
...  

2017 ◽  
Vol 8 (4) ◽  
pp. 1481-1493 ◽  
Author(s):  
Wenqi Yang ◽  
Xu Chen ◽  
Ming Chen ◽  
Yanping Li ◽  
Qing Li ◽  
...  

ER stress inhibition through AMPK activation may explain the protective effects of fish oil against HFD-induced insulin resistance.


2021 ◽  
Author(s):  
Xiaocheng Huang ◽  
Jian Sun ◽  
Chenchen Bian ◽  
Shanghong Ji ◽  
Hong ji

Abstract Background: The liver is the primary organ for frontline immune defense and lipid metabolism. Excessive lipid accumulation in the liver severely affects its metabolic homeostasis and causes metabolic diseases. Docosahexaenoic acid (DHA) is known for its beneficial effects on lipid metabolism and anti-inflammation, but its molecular mechanism remains unknown, especially in fish. In this study, we evaluated the protective effects of DHA on hepatic steatosis of grass carp (Ctenopharyngodon idella) in vivo and in vitro and mainly focused on lipogenesis and inflammation. Grass carp were fed with purified diets supplemented with 0%, 0.5% and 1% DHA for 8 weeks in vivo. Hepatocytes were treated with palmitic acid (PA) (200 μM) with or without DHA (50 or 100 μM) for 24 h in vitro. In addition, Compound C (CC, the inhibitor of AMP-activated protein kinase) was used to examine the mechanism of DHA on hepatic steatosis in vitro.Results: In this study, 1% DHA significantly decreased the liver triglyceride (TG), malondialdehyde (MDA), serum tumor necrosis factor α (TNFα) and nuclear factor kappa B (NFκB) contents. DHA (100 μM) effectively attenuated PA-induced lipid accumulation (P<0.05). Furthermore, DHA significantly inhibited endoplasmic reticulum (ER) stress and stimulated the expression of AMP-activated protein kinase (AMPK) and its downstream factors related to hepatic inflammation and lipogenesis in vivo and in vitro. However, the effects of DHA could be abrogated by CC in vitro.Conclusions: DHA exerted a protective effect on hepatic steatosis by inhibiting ER stress, improving antioxidant ability, relieving hepatic inflammation and inhibiting hepatic lipogenesis in an AMPK-dependent manner. Our findings give a theoretical foundation for further elucidation of the beneficial role of DHA in vertebrates.


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