Program

OR33-2

Marine Drug Discovery: Anti-obesity Mechanism of Palmaria Mollis in Zebrafish and Mice

[Speaker] Yasuhito Shimada:1,2,3
[Co-author] Hiroko Nakayama:4, Liqing Zang:4, Masahiro Terasawa:5, Kaoru Nishiura:5, Koichi Matsuda:5, Charles Toombs:6, Chris Langdon:7, Norihiro Nishimura:3,4
1:Department of Integrative Pharmacology, Graduate School of Medicine, Mie Univeristy, Japan, 2:Department of Bioinformatics, Mie University Advanced Science Research Promotion Center, Japan, 3:Mie University Zebrafish Anticancer Drug Screening Center, Japan, 4:Graduate School of Regional Innovation Studies, Mie University, Japan, 5:Konan Chemical Manufacturing Co., Ltd., Japan, 6:College of Business, Oregon State University, USA, 7:Department of Fisheries and Wildlife, College of Agricultural Sciences, Oregon State University, USA

Background: The red seaweed Palmaria mollis (PM) has recently become popular as foodstuffs due to their relatively high proteins, in addition to their potential as a source of biofunctional molecules and antioxidant ingredients. We previously performed small-scale screening with diet-induced obese (DIO) zebrafish, and found that PM is one of strong candidates for the treatment of obesity and its-related diseases.
Methods: We fed PM-containing feed to DIO-zebrafish and mice and evaluated the effects on obese phenotypes, including body weight gain, dyslipidaemia, hepatic steatosis and visceral adiposity. To clarify the anti-obesity mechanisms of PM, we performed gene expression analyses of the liver and visceral adipose tissues in these model animals.
Results: PM suppressed hepatic steatosis, dyslipidaemia and visceral adiposity both in DIO-zebrafish and mice, especially in the early stage of obese development. In liver tissues of DIO-zebrafish and mice, PM upregulated peroxisome proliferator-activated receptor alpha (PPARA) pathways and downregulated PPARG pathways, suggesting that the lipid-lowering effect of PM might be caused by activation of beta-oxidation and inhibition of lipogenesis. In visceral adipose tissues, while PM showed the similar effects in zebrafish and mice, their gene expression changes were different between these DIO-animals. PM downregulated genes involved in early and late adipocyte differentiation in zebrafish, but not in mice. Instead, PM suppressed the elevation of sterol regulatory element binding transcription factor 1 in obese mice.
Conclusion: We demonstrated that PM has a powerful lipid-lowering effect and prevention of hepatic steatosis and visceral adiposity for the first time. Intake of PM as a functional food may be suitable for obesity prevention and reduction of the prevalence of obesity-related diseases. Phenotype-driven zebrafish screening would facilitate the drug discovery from marine bioresources. We further continue zebrafish screening to find the bioactive compounds in PM.

Advanced Search