scholarly journals meso-Dihydroguaiaretic Acid Inhibits Hepatic Lipid Accumulation by Activating AMP-Activated Protein Kinase in Human HepG2 Cells

2011 ◽  
Vol 34 (10) ◽  
pp. 1628-1630 ◽  
Author(s):  
Myoung-Su Lee ◽  
Kyung Jin Kim ◽  
Daeyoung Kim ◽  
Kyung-Eun Lee ◽  
Jae-Kwan Hwang
Keyword(s):  
Protein Kinase ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Amp Activated Protein Kinase

Electroacupuncture Attenuates Hepatic Lipid Accumulation via Amp-Activated Protein Kinase (Ampk) Activation in Obese Rats

2016 ◽  
Vol 34 (3) ◽  
pp. 209-214 ◽  
Author(s):  
Meirong Gong ◽  
Chen Cao ◽  
Fengli Chen ◽  
Qian Li ◽  
Xiaolin Bi ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Total Cholesterol ◽  
Lipid Accumulation ◽  
Control Group ◽  
Sprague Dawley ◽  
Fat Pad ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Underlying Mechanisms ◽  
Amp Activated Protein Kinase

Background Electroacupuncture (EA) may offer an effective alternative approach for the treatment of obesity. EA mobilizes energy stores, but its effect on hepatic lipid metabolism is unknown, and the underlying mechanisms remain unclear. Objective To examine the effect of EA on hepatic lipid accumulation in diet-induced obese (DIO) rats, and to explore potential underlying mechanisms. Methods Male Sprague-Dawley rats were fed a normal diet (control group, n=10) or a high-fat diet (HFD) for 12 weeks to induce obesity. Those exhibiting diet-induced obesity were subdivided into two groups, one receiving EA (DIO+EA group, n=10) and one left untreated (DIO group, n=10) and observed for a further 4 weeks. Body, liver and fat pad weight were measured, and liver injury was assessed histologically as well as by measuring serum values of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Hepatic triglyceride (TG) and total cholesterol were quantified by enzymatic colorimetric methods. Expression of liver AMP-activated protein kinase (AMPK), acetyl-coenzyme A carboxylase (ACC), and carnitine palmitoyltransferase (CPT-1) was measured by Western blotting. Results EA treatment led to a reduction in body, liver and fat pad weight in DIO rats. This was accompanied by decreases in hepatic TG and total cholesterol values, fatty droplet accumulation, and serum concentrations of ALT and AST. Furthermore, EA treatment restored phosphorylation levels of AMPK (Thr172) and ACC (Ser79) inhibited by HFD, and increased CPT-1 expression. Conclusions EA reduces HFD-induced hepatic lipid accumulation, an effect that appears to be mediated through AMPK signalling pathways. Our results shed new light on the mechanisms by which EA may reduce obesity.

scholarly journals Nobiletin Inhibits Hepatic Lipogenesis via Activation of AMP-Activated Protein Kinase

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Taewon Yuk ◽  
Younghwa Kim ◽  
Jinwoo Yang ◽  
Jeehye Sung ◽  
Heon Sang Jeong ◽  
...  
Keyword(s):  
Protein Kinase ◽  
High Glucose ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Hepatic Lipogenesis ◽  
Nonalcoholic Fatty Liver ◽  
Compound C ◽  
Amp Activated Protein Kinase

We aimed to investigate the effects of nobiletin on hepatic lipogenesis in high glucose-induced lipid accumulation in HepG2 cells. Nobiletin, a citrus polymethoxyflavonoid with six methoxy groups, is present abundantly in the peels of citrus fruits. HepG2 cells were incubated in Dulbecco’s modified Eagle’s medium containing high glucose (25 mM) and subsequently treated with nobiletin at different concentrations (5, 25, and 50 μM). Results showed that nobiletin markedly inhibited high glucose-induced hepatic lipid accumulation in HepG2 cells. In addition, it reduced the protein expression of lipogenic factors, including sterol regulatory element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS). Nobiletin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. Pretreatment with compound C, an AMPK inhibitor, abolished the inhibitory effects of nobiletin on SREBP-1c and FAS expression. These results suggested that nobiletin might attenuate high glucose-induced lipid accumulation in HepG2 hepatocytes via modulation of AMPK signaling pathway. Therefore, nobiletin might be useful for the prevention and treatment of nonalcoholic fatty liver diseases.

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