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Updated: Jun 13, 2026
Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Anti-adipogenic effect of dioxinodehydroeckol via AMPK activation in 3T3-L1 adipocytes
1Marine Bioprocess Research Center, Pukyong National University, Busan, Republic of Korea. sknkim@pknu.ac.kr
Abstract:
Dioxinodehydroeckol (DHE) isolated from Ecklonia cava, has previously been investigated for its inhibition of the differentiation of 3T3-L1 preadipocytes into adipocytes. Levels of lipid accumulation were measured, along with changes in the expression of genes and proteins associated with adipogenesis and lipolysis. Confluent 3T3-L1 preadipocytes in medium with or without different concentrations of DHE for 7 days were differentiated into adipocytes. Lipid accumulation was quantified by measuring direct triglyceride contents and Oil-Red O staining. The expression of genes and proteins associated with adipogenesis and lipolysis was measured using RT-PCR, quantitative real-time RT-PCR and Western blotting analysis. It was found that the presence of DHE significantly reduced lipid accumulation and down-regulated the expression of peroxisome proliferator-activated receptor-gamma (PPARgamma), sterol regulatory element-binding protein 1 (SREBP1) and CCAAT/enhancer-binding proteins (C/EBPalpha) in a dose-dependent manner. Moreover, DHE suppressed regulation of the adipocyte-specific gene promoters such as fatty acid binding protein (FABP4), fatty acid transport protein (FATP1), fatty acid synthase (FAS), lipoprotein lipase (LPL), acyl-CoA synthetase 1 (ACS1), leptin, perilipin and HSL compared to control adipocytes. The specific mechanism mediating the effects of DHE was confirmed by activation of phosphorylated AMP-activated protein kinase (pAMPK). Therefore, these results suggest that DHE exerts anti-adipogenic effect on adipocyte differentiation through the activation and modulation of the AMPK signaling pathway.
Insights
Dioxinodehydroeckol (DHE) from Ecklonia cava inhibits fat cell formation by reducing lipid accumulation and key gene expression. This anti-adipogenic effect is mediated by activating the AMP-activated protein kinase (AMPK) pathway.
Area of Science:
- Biochemistry
- Molecular Biology
- Cell Biology
Background:
- Ecklonia cava contains Dioxinodehydroeckol (DHE), a compound previously studied for its effects on adipogenesis.
- Adipogenesis, the process of fat cell formation, is a complex pathway involving specific genes and proteins.
- Understanding inhibitors of adipogenesis is crucial for metabolic disease research.
Purpose of the Study:
- To investigate the anti-adipogenic effects of Dioxinodehydroeckol (DHE) on 3T3-L1 preadipocytes.
- To elucidate the molecular mechanisms underlying DHE's action on adipogenesis and lipolysis.
- To determine if DHE modulates the AMP-activated protein kinase (AMPK) signaling pathway.
Main Methods:
- 3T3-L1 preadipocytes were differentiated into adipocytes in the presence of varying DHE concentrations.
- Lipid accumulation was quantified using triglyceride content measurement and Oil-Red O staining.
- Gene and protein expression related to adipogenesis and lipolysis were analyzed via RT-PCR and Western blotting; AMPK pathway activation was assessed.
Main Results:
- DHE significantly reduced lipid accumulation in a dose-dependent manner.
- DHE down-regulated the expression of key adipogenic factors, including PPARγ, SREBP1, and C/EBPα.
- DHE suppressed the expression of adipocyte-specific genes and activated phosphorylated AMP-activated protein kinase (pAMPK).
Conclusions:
- Dioxinodehydroeckol (DHE) exhibits significant anti-adipogenic properties.
- DHE inhibits adipocyte differentiation by modulating the expression of critical adipogenic genes and proteins.
- The anti-adipogenic effects of DHE are mediated through the activation of the AMPK signaling pathway.
