Abstract
Lycium barbarum polysaccharide (LBP) is well known in traditional Chinese herbal medicine that, has beneficial effects. Previous study reported that LBP reduced blood glucose and serum lipids. However, the underlying LBP-regulating mechanisms remain largely unknown. The main purpose of this study was to investigate whether LBP prevented fatty liver through activation of adenosine monophosphate-activated protein kinase (AMPK) and suppression of sterol regulatory element-binding protein-1c (SREBP-1c). Male C57BL/6J mice were fed a low-fat diet, high-fat diet, or 100 mg/kg LBP-treatment diet for 24 weeks. HepG2 cells were treated with LBP in the presence of palmitic acid. In our study, LBP can improve body compositions and lipid metabolic profiles in high-fat diet-fed mice. Oil Red O staining in vivo and in vitro showed that LBP significantly reduced hepatic intracellular triacylglycerol accumulation. H&E staining also showed that LBP can attenuate liver steatosis. Hepatic genes expression profiles demonstrated that LBP can activate the phosphorylation of AMPK, suppress nuclear expression of SREBP-1c, and decrease protein and mRNA expression of lipogenic genes in vivo or in vitro. Moreover, LBP significantly elevated uncoupling protein-1 (UCP1) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) expression of brown adipose tissue. In summary, LBP possesses a potential novel treatment in preventing diet-induced fatty liver.
Highlights
An imbalance between energy intake and expenditure can cause the excessive accumulation of triacylglycerol in tissues of eukaryotic organisms [1, 2]
The accumulation of triacylglycerol in adipose tissue can result in obesity and in nonadipose tissues, especially liver tissue, which are associated with type 2 diabetes and nonalcoholic fatty liver disease (NAFLD) [3, 4]
Body weight, water intake, and food intake, which play a central role in high-fat diet (HFD) feeding mice, were monitored during the experiment
Summary
An imbalance between energy intake and expenditure can cause the excessive accumulation of triacylglycerol in tissues of eukaryotic organisms [1, 2]. High-fat diet-induced fatty liver is characterized by excessive accumulation of triacylglycerol in the liver, impairs fatty acid oxidation, and increases hepatic de novo lipogenesis [4,5,6]. Long-term high-fat dietinduced dysregulation of hepatic lipid metabolism increases lipolysis, causing an increase in free fatty acid levels [7]. These metabolic changes trigger fatty liver and lead to systemic aggravation of lipid metabolic dysfunction [8]. Activation of adenosine monophosphateactivated protein kinase (AMPK) has been shown to reduce lipogenesis in the liver by inhibiting SREBP-1c expression and further prevent the development of fatty liver [10]. Some pharmacologic agents that inhibit SREBP-1c expression via stimulating AMPK activity in hepatocytes may provide more effective treatment options for fatty liver disease
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