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Chalcones suppress fatty acid-induced lipid accumulation through a LKB1/AMPK signaling pathway in HepG2 cells.
Food Funct. 2014 Jun; 5(6):1134-41.FF

Abstract

Excessive lipid accumulation in the liver has been proposed to cause hyperlipidemia, diabetes and fatty liver disease. 4-Hydroxyderricin (4HD), xanthoangelol (XAG), cardamonin (CAR) and flavokawain B (FKB) are chalcones that have exhibited various biological effects against obesity, inflammation, and diabetes; however, little is known about the inhibitory effects of these chalcones on fatty liver disease. In the present study, we investigated the ability of 4HD, XAG, CAR, and FKB to reduce lipid accumulation in hepatocytes. When HepG2 cells were treated with a mixture of fatty acids (FAs; palmitic acid : oleic acid = 1 : 2 ratio), significant lipid accumulation was observed. Under the same experimental conditions, addition of chalcones at 5 μM significantly suppressed the FA-induced lipid accumulation. We found that the expression of sterol regulatory element-binding protein-1 (SREBP-1), a key molecule involved in lipogenesis, was decreased in these chalcone-treated cells. We also found that these chalcones increased the expression of peroxisome proliferator-activated receptor α (PPARα), which is involved in FA oxidation. Moreover, these chalcones increased phosphorylation of AMP-activated protein kinase (AMPK) and liver kinase B1 (LKB1), upstream regulators of SREBP-1 and PPARα. We confirmed that an AMPK inhibitor, compound C, reversed chalcone-induced changes in SREBP-1 and PPARα expression in the HepG2 cells. Collectively, we found that 4HD, XAG, CAR, and XAG attenuated lipid accumulation through activation of the LKB1/AMPK signaling pathway in HepG2 cells.

Authors+Show Affiliations

Department of Agrobioscience, Graduate School of Agricultural Science, Kobe University, Kobe 657-8501, Japan. ashida@kobe-u.ac.jp.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24722377

Citation

Zhang, Tianshun, et al. "Chalcones Suppress Fatty Acid-induced Lipid Accumulation Through a LKB1/AMPK Signaling Pathway in HepG2 Cells." Food & Function, vol. 5, no. 6, 2014, pp. 1134-41.
Zhang T, Yamamoto N, Ashida H. Chalcones suppress fatty acid-induced lipid accumulation through a LKB1/AMPK signaling pathway in HepG2 cells. Food Funct. 2014;5(6):1134-41.
Zhang, T., Yamamoto, N., & Ashida, H. (2014). Chalcones suppress fatty acid-induced lipid accumulation through a LKB1/AMPK signaling pathway in HepG2 cells. Food & Function, 5(6), 1134-41. https://doi.org/10.1039/c3fo60694e
Zhang T, Yamamoto N, Ashida H. Chalcones Suppress Fatty Acid-induced Lipid Accumulation Through a LKB1/AMPK Signaling Pathway in HepG2 Cells. Food Funct. 2014;5(6):1134-41. PubMed PMID: 24722377.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chalcones suppress fatty acid-induced lipid accumulation through a LKB1/AMPK signaling pathway in HepG2 cells. AU - Zhang,Tianshun, AU - Yamamoto,Norio, AU - Ashida,Hitoshi, Y1 - 2014/04/11/ PY - 2014/4/12/entrez PY - 2014/4/12/pubmed PY - 2015/1/30/medline SP - 1134 EP - 41 JF - Food & function JO - Food Funct VL - 5 IS - 6 N2 - Excessive lipid accumulation in the liver has been proposed to cause hyperlipidemia, diabetes and fatty liver disease. 4-Hydroxyderricin (4HD), xanthoangelol (XAG), cardamonin (CAR) and flavokawain B (FKB) are chalcones that have exhibited various biological effects against obesity, inflammation, and diabetes; however, little is known about the inhibitory effects of these chalcones on fatty liver disease. In the present study, we investigated the ability of 4HD, XAG, CAR, and FKB to reduce lipid accumulation in hepatocytes. When HepG2 cells were treated with a mixture of fatty acids (FAs; palmitic acid : oleic acid = 1 : 2 ratio), significant lipid accumulation was observed. Under the same experimental conditions, addition of chalcones at 5 μM significantly suppressed the FA-induced lipid accumulation. We found that the expression of sterol regulatory element-binding protein-1 (SREBP-1), a key molecule involved in lipogenesis, was decreased in these chalcone-treated cells. We also found that these chalcones increased the expression of peroxisome proliferator-activated receptor α (PPARα), which is involved in FA oxidation. Moreover, these chalcones increased phosphorylation of AMP-activated protein kinase (AMPK) and liver kinase B1 (LKB1), upstream regulators of SREBP-1 and PPARα. We confirmed that an AMPK inhibitor, compound C, reversed chalcone-induced changes in SREBP-1 and PPARα expression in the HepG2 cells. Collectively, we found that 4HD, XAG, CAR, and XAG attenuated lipid accumulation through activation of the LKB1/AMPK signaling pathway in HepG2 cells. SN - 2042-650X UR - https://www.unboundmedicine.com/medline/citation/24722377/Chalcones_suppress_fatty_acid_induced_lipid_accumulation_through_a_LKB1/AMPK_signaling_pathway_in_HepG2_cells_ L2 - https://doi.org/10.1039/c3fo60694e DB - PRIME DP - Unbound Medicine ER -