Abstract
BackgroundMetabolic syndrome may lead to many complications, such as nonalcoholic fatty liver disease (NAFLD). A natural and effective therapeutic agent for patients with NAFLD is urgently needed. In a previous study, we showed that Rhodiola crenulata root extract (RCE) regulated hepatic gluconeogenesis through activation of AMPK signaling. However, the manner in which RCE regulates hepatic lipid and glycogen metabolism remains unclear. The current study was conducted to investigate the effects of RCE on hepatic glycogen and lipid metabolism, as well as the mechanisms underlying such effects.MethodsHuman hepatoma HepG2 cells were treated with RCE for 6 h under high glucose conditions, after which glycogen synthesis, lipogenesis, and relative gene expression were examined. In addition, lipogenesis-related genes were investigated in vivo.ResultsRCE significantly increased glycogen synthesis and inhibited lipogenesis, while regulating genes related to these processes, including glycogen synthase kinase 3β (GSK3β), glycogen synthase (GS), fatty acid synthase (FAS), CCAAT/enhancer-binding protein (C/EBP), and sterol regulatory element-binding protein 1c (SREBP-1c). However, the effects caused by RCE were neutralized by compound C, an AMPK antagonist. Further studies showed that expression levels of lipogenic genes decreased at the protein and mRNA levels in the rat liver.ConclusionsOur results demonstrate that RCE regulates hepatic glycogen and lipid metabolism through the AMPK signaling pathway. These results suggest that RCE is a potential intervention for patients with NAFLD.
Highlights
Metabolic syndrome may lead to many complications, such as nonalcoholic fatty liver disease (NAFLD)
Rhodiola crenulata root extract (RCE) significantly increases AMP-activated protein kinase (AMPK) and acetylCoA carboxylase (ACC) phosphorylation To clarify the regulatory effect of RCE on AMPK signaling in the liver, HepG2 cells were incubated with RCE
ACC phosphorylation following RCE treatment was concentration-dependent (1.31 ± 0.12, 1.76 ± 0.32, 1.65 ± 0.12, and 1.54 ± 0.11-fold over the control sample for 1.5, 3.0, 15.0, and 30.0 μg/mL, respectively; p < 0.05, p < 0.05, p < 0.001, and p < 0.001, respectively; Fig. 1a and c). These results indicate that pretreatment with RCE significantly increased the activity of the AMPK-ACC
Summary
Metabolic syndrome may lead to many complications, such as nonalcoholic fatty liver disease (NAFLD). The manner in which RCE regulates hepatic lipid and glycogen metabolism remains unclear. The current study was conducted to investigate the effects of RCE on hepatic glycogen and lipid metabolism, as well as the mechanisms underlying such effects. Metabolic disorder may subsequently develop into cardiovascular disease and type II diabetes mellitus [2]. It has become a major public health concern in developed nations [3]. Enhanced lipogenesis and decreased glycogen synthesis are hallmarks of hepatic insulin-resistance, which might subsequently lead to the development of type II diabetes mellitus [7].
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