AIMS: Fucoidan, consisting of L-fucose together with xylose, galactose and mannose, is a sulfated polysaccharide from brown seaweeds, which has been reported to affect the development of adipocytes. However, the role of fucoidan in adipogenesis remains elusive. In the present study, we have investigated the inhibitory effects of fucoidan on adipocyte differentiation via mitogen-activated protein kinase (MAPK) signaling pathway in 3T3-L1 preadipocytes. MAIN METHODS: Differentiation of 3T3-L1 preadipocytes was induced in the presence or absence of fucoidan. The effects of fucoidan on adipogenic gene expression and MAPK activation were investigated. KEY FINDINGS: Fucoidan treatment inhibits adipocyte differentiation, evidenced by decreased lipid accumulation and down regulation of adipocyte markers. Fucoidan then inhibited the expression of both early CCAAT-enhancer-binding proteins alpha (C/EBPalpha) and peroxisome proliferator-activated receptors gamma (PPARgamma) and late activating protein 2 (aP2) adipogenic transcription factors, which is a crucial role for adipocyte development. Moreover, our results revealed that fucoidan inhibited the early activation of p38 MAPKs, extracellular signal-regulated kinases (ERK) and Jun N-terminal kinase (JNK). SIGNIFICANCE: Overall, these findings are a strong indication that fucoidan might inhibit adipogenesis in 3T3-L1 preadipocytes, due to inhibition of the MAPK signaling pathway that involves adipogenic transcription factors.
AIMS: Fucoidan, consisting of L-fucose together with xylose, galactose and mannose, is a sulfated polysaccharide from brown seaweeds, which has been reported to affect the development of adipocytes. However, the role of fucoidan in adipogenesis remains elusive. In the present study, we have investigated the inhibitory effects of fucoidan on adipocyte differentiation via mitogen-activated protein kinase (MAPK) signaling pathway in 3T3-L1 preadipocytes. MAIN METHODS: Differentiation of 3T3-L1 preadipocytes was induced in the presence or absence of fucoidan. The effects of fucoidan on adipogenic gene expression and MAPK activation were investigated. KEY FINDINGS: Fucoidan treatment inhibits adipocyte differentiation, evidenced by decreased lipid accumulation and down regulation of adipocyte markers. Fucoidan then inhibited the expression of both early CCAAT-enhancer-binding proteins alpha (C/EBPalpha) and peroxisome proliferator-activated receptors gamma (PPARgamma) and late activating protein 2 (aP2) adipogenic transcription factors, which is a crucial role for adipocyte development. Moreover, our results revealed that fucoidan inhibited the early activation of p38 MAPKs, extracellular signal-regulated kinases (ERK) and Jun N-terminal kinase (JNK). SIGNIFICANCE: Overall, these findings are a strong indication that fucoidan might inhibit adipogenesis in 3T3-L1 preadipocytes, due to inhibition of the MAPK signaling pathway that involves adipogenic transcription factors.