Send to

Choose Destination
Food Sci Biotechnol. 2017 Dec 20;26(6):1715-1723. doi: 10.1007/s10068-017-0230-z. eCollection 2017.

The suppressive effect of Gelidium amansi-EtOH extracts on the adipogenesis with MAPK signals in adipocytes with or without macrophages.

Author information

1Research Institute of Obesity Sciences, Sungshin Women's University, Seoul, 01133 Republic of Korea.
Seojin Biotech Co. Ltd., Dongbaekjunang-ro, Giheung-Gu, Yongin-si, Gyeonggi-do 17015 Republic of Korea.
3Department of Food and Nutrition and Research Institute of Obesity Science, Sungshin Women's University, Seoul, 01133 Republic of Korea.


To elucidate the anti-inflammatory and anti-adipogenetic effects of Gelidium amansii (GA) ethanol extracts and their mechanisms, we performed two culture systems, adipocytes cultured with or without macrophages. Purified GA-3 fraction (GAE) contains high flavonoids and phenolics, reduced the mRNA levels of PPARγ and C/EBPα with GLUT4 expression in adipocyte with or without macrophages. GAE also increased the protein expression of HSL and ATGL enzymes, lipolysis biomarkers in fat cells. In co-culture system, GAE suppressed not only the transcription factors for adipogenesis, but also the production of pro-inflammatory cytokines, TNF-α. Compared to MAPK pathways such as JNK and p-38, the phosphorylation of both ERK1/2 (Thr202/Tyr204) was strongly suppressed by GAE with dose-dependent manner in both culture system. Otherwise, an increased JNK expression caused by GAE treatments blocked an insulin-induced GLUT4 translocation in adipocytes culture. In conclusion, GAE depressed the expression of adipogenetic genes, corresponding to a reduction in fat accumulation while preadipocytes developed into adipocytes with the modulation of MAPK pathways and inflammatory cytokines.


Adipocytes; ERK1/2; Gelidium amansii; MAPK; Macrophages; TNF-α

Conflict of interest statement

Compliance with ethical standardsThe authors declare no conflict of interest.

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center