Journal
NUTRIENTS
Volume 10, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/nu10111802
Keywords
Ishige okamurae; obesity; hepatic steatosis; 3T3-L1 cells; high fat diet; mice
Categories
Funding
- project titled 'Development of functional food products with natural materials derived from marine resources' - Ministry of Oceans and Fisheries, Korea
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [2016R1D1A1A09917209]
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Obesity is caused by the expansion of white adipose tissue (WAT), which stores excess triacylglycerol (TG), this can lead to disorders including type 2 diabetes, atherosclerosis, metabolic diseases. Ishige okamurae extract (IOE) is prepared from a brown alga and has anti-oxidative properties. We investigated the detailed mechanisms of the anti-obesity activity of IOE. Treatment with IOE blocked lipid accumulation by reducing expression of key adipogenic transcription factors, such as CCAAT/enhancer-binding protein alpha (C/EBP alpha) and peroxisome proliferator-activated receptor gamma (PPAR gamma), in 3T3-L1 cells. Administration of IOE to high fat diet (HFD)-fed mice inhibited body andWAT mass gain, attenuated fasting hyperglycemia and dyslipidemia. The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBP alpha and PPAR gamma, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), inWAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of beta-oxidation genes, suggested by increases in AMPK alpha and CPT1 expression in WAT and liver. In summary, IOE ameliorates HFD-induced obesity and its related metabolic disease, hepatic steatosis, by regulating multiple pathways.
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