Hyeon-Son Choi1, Hui-Jeon Jeon2, Ok-Hwan Lee3, Boo-Yong Lee2. 1. Department of Food Science and Technology, Seoul Women's University, Hwarang, Nowon, Seoul, South Korea. 2. Department of Food Science and Biotechnology, CHA University, Seongnam, Gyeonggi, South Korea. 3. Department of Food Science and Biotechnology, Kangwon National University, Chuncheon, South Korea.
Abstract
SCOPE: Dieckol is a major polyphenol of Ecklonia cava. This study demonstrates a mechanistic role for dieckol in the suppression of lipid accumulation using three models. METHODS AND RESULTS: Mice were split into four experimental groups (n = 10 per group): normal diet, high-fat diet (HFD), and dieckol-supplemented diets. Dieckol-supplemented mice groups showed a significant decrease of body weight gain (38%) as well as fats of organs including epididymal (45%) compared with a HFD-fed group. LDL cholesterol level was reduced by 55% in dieckol-supplemented group. Adipogenic factors and lipid synthetic enzymes were analyzed via real-time PCR or immunoblotting. Dieckol regulated mRNA expressions of early adipogenic genes in 3T3-L1 cells. These results were reflected in downregulation of late adipogenic factors, resulting in a decrease in triacylglycerol content. These data were also verified in zebrafish and mouse models. Dieckol activated AMP-activated protein kinase α (AMPKα) signaling to inhibit lipid synthesis in 3T3-L1 and mouse model. Dieckol was also shown to inhibit mitotic clonal expansion via cell-cycle arrest. CONCLUSION: Our data demonstrate that dieckol inhibits lipid accumulation via activation of AMPKα signaling and cell-cycle arrest.
SCOPE: Dieckol is a major polyphenol of Ecklonia cava. This study demonstrates a mechanistic role for dieckol in the suppression of lipid accumulation using three models. METHODS AND RESULTS:Mice were split into four experimental groups (n = 10 per group): normal diet, high-fat diet (HFD), and dieckol-supplemented diets. Dieckol-supplemented mice groups showed a significant decrease of body weight gain (38%) as well as fats of organs including epididymal (45%) compared with a HFD-fed group. LDL cholesterol level was reduced by 55% in dieckol-supplemented group. Adipogenic factors and lipid synthetic enzymes were analyzed via real-time PCR or immunoblotting. Dieckol regulated mRNA expressions of early adipogenic genes in 3T3-L1 cells. These results were reflected in downregulation of late adipogenic factors, resulting in a decrease in triacylglycerol content. These data were also verified in zebrafish and mouse models. Dieckol activated AMP-activated protein kinase α (AMPKα) signaling to inhibit lipid synthesis in 3T3-L1 and mouse model. Dieckol was also shown to inhibit mitotic clonal expansion via cell-cycle arrest. CONCLUSION: Our data demonstrate that dieckol inhibits lipid accumulation via activation of AMPKα signaling and cell-cycle arrest.