Journal
MOLECULAR NUTRITION & FOOD RESEARCH
Volume 59, Issue 8, Pages 1458-1471Publisher
WILEY-BLACKWELL
DOI: 10.1002/mnfr.201500021
Keywords
3T3-L1; Adipogenesis; Dieckol; Mice; Zebrafish
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Funding
- Ministry of Education and Science Technology, Korea
- National Research Foundation of Korea [2013 RIA1A2064024]
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ScopeDieckol 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 resultsMice 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 (AMPK) signaling to inhibit lipid synthesis in 3T3-L1 and mouse model. Dieckol was also shown to inhibit mitotic clonal expansion via cell-cycle arrest. ConclusionOur data demonstrate that dieckol inhibits lipid accumulation via activation of AMPK signaling and cell-cycle arrest.
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