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Polyacetylene From Dendropanax morbifera Alleviates Diet-Induced Obesity and Hepatic Steatosis by Activating AMPK Signaling Pathway.

ABSTRACT: The extract tea of Dendropanax morbifera is popular beverages in Korea, and their preventive and therapeutic roles in metabolic disorders have been reported. However, the molecular mechanism has not been studied despite the known efficacy of D. morbifera. Eleven fractions (fr.1-fr.11) were divided by MPLC to find the active compound. Among them, Fr.5 was superior to others in that the inhibitory efficacy of de novo triglyceride (TG) biosynthesis. NMR analysis revealed that Fr.5 is composed 98% or more (9Z,16S)-16-hydroxy-9,17-octadecadiene-12,14-diynoic acid (HOD). Treatment of HOD diminished oleic acid (OA)-induced TG accumulation in HepG2 hepatocytes and differentiation of 3T3-L1 preadipocytes by activating LKB1/AMPK. In addition, we determined the effect of the oral administration of the extract of D. morbifera on obesity and hepatic steatosis in high-fat diet (HFD)-induced obese mice. This study proved that D. morbifera containing HOD, the active substance, can show preventive or therapeutic efficacy on obesity and hepatic steatosis through the targeting LKB1/AMPK axis.

SUBMITTER: Kang MJ

PROVIDER: S-EPMC5975361 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Polyacetylene From Dendropanax morbifera Alleviates Diet-Induced Obesity and Hepatic Steatosis by Activating AMPK Signaling Pathway.

Kang Myung-Ji MJ Kwon Eun-Bin EB Ryu Hyung Won HW Lee Seoghyun S Lee Jae-Won JW Kim Doo-Young DY Lee Mi Kyeong MK Oh Sei-Ryang SR Lee Hyun-Sun HS Lee Su Ui SU Kim Mun-Ock MO

Frontiers in pharmacology 20180523

The extract tea of Dendropanax morbifera is popular beverages in Korea, and their preventive and therapeutic roles in metabolic disorders have been reported. However, the molecular mechanism has not been studied despite the known efficacy of D. morbifera. Eleven fractions (fr.1-fr.11) were divided by MPLC to find the active compound. Among them, Fr.5 was superior to others in that the inhibitory efficacy of de novo triglyceride (TG) biosynthesis. NMR analysis revealed that F ...[more]

PMID: 29875667

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Project description:Liraglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), has been demonstrated to alleviate non-alcoholic fatty liver disease (NAFLD). However, the underlying mechanism has not been fully elucidated. Increasing evidence suggests that autophagy is involved in the pathogenesis of hepatic steatosis. In this study, we examined whether liraglutide could alleviate hepatic steatosis through autophagy-dependent lipid degradation and investigated the underlying mechanisms. Herein, the effects of liraglutide on NAFLD were evaluated in a high-fat diet (HFD)-induced mouse model of NAFLD as well as in mouse primary and HepG2 hepatocytes exposed to palmitic acid (PA). The expression of the GLP-1 receptor (GLP-1R) was measured in vivo and in vitro. Oil red O staining was performed to detect lipid accumulation in hepatocytes. Electron microscopy was used to observe the morphology of autophagic vesicles and autolysosomes. Autophagic flux activity was measured by infecting HepG2 cells with mRFP-GFP-LC3 adenovirus. The roles of GLP-1R and transcription factor EB (TFEB) in autophagy-lysosomal activation were explored using small interfering RNA. Liraglutide treatment alleviated hepatic steatosis in vivo and in vitro. In models of hepatic steatosis, microtubule-associated protein 1B light chain-3-II (LC3-II) and SQSTM1/P62 levels were elevated in parallel to blockade of autophagic flux. Liraglutide treatment restored autophagic activity by improving lysosomal function. Furthermore, treatment with autophagy inhibitor chloroquine weakened liraglutide-induced autophagy activation and lipid degradation. TFEB has been identified as a key regulator of lysosome biogenesis and autophagy. The protein levels of nuclear TFEB and its downstream targets CTSB and LAMP1 were decreased in hepatocytes treated with PA, and these decreases were reversed by liraglutide treatment. Knockdown of TFEB expression compromised the effects of liraglutide on lysosome biogenesis and hepatic lipid accumulation. Mechanistically, GLP-1R expression was decreased in HFD mouse livers as well as PA-stimulated hepatocytes, and liraglutide treatment reversed the downregulation of GLP-1R expression in vivo and in vitro. Moreover, GLP-1R inhibition could mimic the effect of the TFEB downregulation-mediated decrease in lysosome biogenesis. Thus, our findings suggest that liraglutide attenuated hepatic steatosis via restoring autophagic flux, specifically the GLP-1R-TFEB-mediated autophagy-lysosomal pathway.

Dataset Information

Polyacetylene From Dendropanax morbifera Alleviates Diet-Induced Obesity and Hepatic Steatosis by Activating AMPK Signaling Pathway.

Publications

Polyacetylene From <i>Dendropanax morbifera</i> Alleviates Diet-Induced Obesity and Hepatic Steatosis by Activating AMPK Signaling Pathway.

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