Dieckol, a phlorotannin isolated from a brown seaweed, Ecklonia cava, inhibits adipogenesis through AMP-activated protein kinase (AMPK) activation in 3T3-L1 preadipocytes

Ko, Seok‐Chun; Lee, Myoungsook; Lee, Ji-Hyeok; Lee, Seung‐Hong; Lim, Yunsook; Jeon, You‐Jin

doi:10.1016/j.etap.2013.10.011

Cited by 82 publications

(55 citation statements)

References 32 publications

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“…Metformin administration enhanced the expression of UCP1 and Cidea in WT BAT but not in KO BAT. Our findings are consistent with accumulating evidences showing the promotional effects of AMPK activation on brown and beige adipogenesis [17, 31–34]. On the other side, the expression of fibrogenic markers was higher in transplanted BAT with AMPK deficiency.…”

Section: Discussionsupporting

confidence: 92%

AMPKα1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development

Zhao

Yang

Zhang

et al. 2017

Biochemical and Biophysical Research Communications

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Brown adipose tissue (BAT) dissipates energy for thermogenesis which reduces or prevents obesity and metabolic dysfunction. AMP-activated protein kinase (AMPK) is a master regulator of energy metabolism and its activity is inhibited in the developing BAT due to obesity. We previously found that AMPK is required for brown fat development and thermogenic function, but the non-brown adipogenic differentiation of progenitor cells due to AMPKα1 deficiency has not been defined. We found that, in vivo, the thermogenic capacity and morphology of BAT were compromised due to AMPK deficiency, which was correlated with decreased progenitor density in BAT. In addition, the expression of fibrogenic markers was higher in AMPK deficient compared to wild-type mice. Furthermore, we transplanted AMPKα1 wild-type (WT) and floxed BAT into the same recipient mice; following tamoxifen induced AMPKα1 knockout in floxed BAT, the fibrogenesis was enhanced compared to WT mice. Taken together, our data demonstrated that AMPKα1 deficiency suppressed brown adipogenesis in favor of fibrogenesis during BAT development.

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Section: Discussionsupporting

confidence: 92%

AMPKα1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development

Zhao

Yang

Zhang

et al. 2017

Biochemical and Biophysical Research Communications

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“…Dieckol is a natural and non-toxic polyphenol compound and its antioxidant properties have previously been examined (23,24). A previous study revealed the anti-inflammatory and anticancer activities of dieckol are based on the induction of apoptosis and inhibition of aberrant proliferation by oxidative stress (14).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of dieckol on hypoxia-induced epithelial-mesenchymal transition of HT29 human colorectal cancer cells

Jeong

Jeon

Park

2016

Molecular Medicine Reports

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Hypoxia-induced epithelial-mesenchymal transition (EMT) has been identified as essential for tumor progression and metastasis. The present study examined the effects of an antioxidant, dieckol, on hypoxia-induced EMT in HT29 human colorectal cancer cells. HT29 cells were treated with a hypoxia-inducing agent, CoCl2, and an increase in the levels of intracellular reactive oxygen species (ROS) and various morphological changes, such as loss of cell-cell contact and aggressive cell migration were observed. CoCl2 also induced an increase in the expression of hypoxia-inducible factor 1α (HIF1α) and various mesenchymal-specific markers, including vimentin and snail family transcriptional repressor 1 (Snail1), and a decrease in the expression of E-cadherin, thus suggesting that CoCl2 induced EMT in HT29 cells. Conversely, the CoCl2-induced EMT of HT29 cells was suppressed following treatment with dieckol. In addition, ROS generation, EMT marker protein expression and intracellular localization, cell migration and cell invasion were attenuated following dieckol treatment. The findings of the present study suggested that dieckol may inhibit hypoxia-induced EMT in HT29 cells by regulating the levels of cellular ROS and protein expression levels downstream of the HIF1α signaling pathway. Therefore, dieckol has the potential to become an attractive therapeutic agent for the treatment of colorectal cancer.

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“…Yeo et al (2012) reported that both polyphenols and dieckols isolated from EC inhibited 3T3-L1 adipocyte differentiation, Kong et al (2010) showed that a compound isolated from EC inhibited lipid accumulation and adipocyte differentiation by the down-regulation of the genes involved in lipogenesis and adipogenesis and Ko et al (2013) showed that dieckol, a phlorotannin isolated from EC, inhibited adipogenesis through AMP-activated protein kinase (AMPK) activation in 3T3-L1 cells.…”

Section: Discussionmentioning

confidence: 99%

Clinical Trial of the Hypolipidemic Effects of a Brown Alga Ecklonia cava Extract in Patients with Hypercholesterolemia

Choi¹,

Park²,

Ha³

et al. 2015

International J. of Pharmacology

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A B S T R A C TEcklonia cava, an edible brown alga, is recognized as a rich source of polyphenols and the lipid-lowering effects of which have not yet been studied well. We investigated the efficacy and safety of Ecklonia cava extract (ECE) on blood lipid profiles in subjects with hypercholesterolemia. Eighty healthy subjects with more than 200 mg dLG 1 of total cholesterol or more than 110 mg dLG 1 of LDL-cholesterol level were randomly assigned to receive ECE (n = 40) or placebo (n = 40) for 12 weeks. Changes in serum total cholesterol, LDL-cholesterol, HDL-cholesterol, triglyceride and waist-hip ratio levels were measured after the 12-week intervention. The ECE significantly lowered total cholesterol level by 2.8% and LDL-cholesterol level by 11.1% after 12 week supplementation as compared to the placebo (p = 0.039, 0.030, respectively). The HDL-cholesterol level did not change in the ECE group, whereas an increase of 5.6% was observed in the placebo group with a significant difference between groups (p = 0.021). No corresponding changes were seen for triglyceride and waist-hip ratio levels between the two groups. There was no causal relationship between the ingestion of ECE and adverse drug reactions. We found that ECE supplementation improved blood lipid profiles through decreasing total cholesterol and LDL-cholesterol levels which are known as major cardiovascular risk factors. This result suggests that ECE supplementation may be effective in the prevention and treatment of atherosclerotic cardiovascular diseases but more studies are needed to establish the long-term safety and effectiveness.

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Dieckol, a phlorotannin isolated from a brown seaweed, Ecklonia cava, inhibits adipogenesis through AMP-activated protein kinase (AMPK) activation in 3T3-L1 preadipocytes

Cited by 82 publications

References 32 publications

AMPKα1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development

AMPKα1 deficiency suppresses brown adipogenesis in favor of fibrogenesis during brown adipose tissue development

Inhibitory effects of dieckol on hypoxia-induced epithelial-mesenchymal transition of HT29 human colorectal cancer cells

Clinical Trial of the Hypolipidemic Effects of a Brown Alga Ecklonia cava Extract in Patients with Hypercholesterolemia

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