The anti-obesity effect of local black pigmented-rice and its molecular mechanism (s) of action in 3T3-L1 adipocytes

• Main Authors: Jhih-Yi Liou, 劉芝驛
• Other Authors: Shu-Jing Wu
• Format: Others
• Language: zh-TW
• Published: 2015
• Online Access: http://ndltd.ncl.edu.tw/handle/28kxnj

碩士 === 嘉南藥理大學 === 保健營養系 === 103 === Obesity is a disease of metabolic disorders. Many studies have displayed that the black pigmented-rice (Oryza sativa L.) possessed anti-cancer, antioxidant, anti-inflammatory and reducing hepatic steatosis activities. The anti-obesity effect of BPR and its molecular mechanism (s) of action remain unclear. In this study, our aims were (i) to examine the total flavonoied and phenol concentrations , as well as anti-proliferative and lipid accumulation effects of Hualien (eastern region) and Changhua (western region) black pigmented-rice of water and ethanol) extracts ( EBPRWE, WBPRWE, EBPREE and WBPREE) were analyzed, and (ii) to investigate the EBPREE-mediated anti-adipogenic effect of the FAS, HSL, ATGL, PPAR-γ, LXRα, Sirt family proteins (1 and 3), PGC-1α, ACC and AMPK molecular pathways in 3T3-L1 adipocytes. Among all the extracts tested, EBPREE demonstrated the highest total flavonoid (368.81±4.81mg/g) and phenol contents (37.15±0.64mg/g). compared effects with other extracts, Results revealed that EBPREE possessed the most potent anti-proliferative effect on 3T3-L1 cells. In the 3T3-L1 adipocytes, WBPRWE displayed the strongest inhibition on lipid accumulation than other extracts (P<0.05). EBPREE significantly up-regulated the phosphorylated ACC and AMPK proteins, and Sirt1 proteins, while down-regulated the activation of ACC and AMPK proteins, as well as FAS proteins. In addition, EBPREE up-regulated the expression of PGC-1α, PPAR-γ, LXRα, HSL and Sirt3 proteins. Taken together, these results suggest that EBPREE has contributed to the potent anti-obesity and anti-adipogenesis effects in 3T3-L1 adipocytes through the modulation of Sirt family proteins (1 and 3), phosphorylation of ACC and AMPK, and PGC-1α signaling pathways.