Abstract
The primary aim of this study was to investigate whether mulberry leaf extract (MLE) attenuates obesity-induced hepatic lipogenesis and fibrosis in high fat diet (HFD)-induced obese mice and to elucidate its underlying mechanism in which MLE regulates lipogenesis and fibrosis. HFD-induced obese mice treated with 133 mg/kg and 666 mg/kg MLE showed significantly improved plasma lipid profiles and atherogenic index. MLE treatment significantly reversed up-regulation of genes associated with LXRa-mediated lipogenesis (LPL, SREBP1c, FAS, C/EBPa, and aP2), and genes related to hepatic fibrosis (a-SMA and Type1 collagen) whereas MLE significantly stimulated expressions of lipolysis related genes (UCP2 and PPARa) in the HFD-fed obese mice. Moreover, MLE protected the anti-oxidant defense system from obesity-induced oxidative stress through Nrf2 activation in the HFD-induced obese mice. In conclusion, MLE might inhibit hepatic lipogenesis and fibrosis, and stimulate lipolysis by regulation of Nrf2 activation. Therefore, the present study suggests MLE might be a potential therapeutic substance for obesity-induced non-alcoholic fatty liver disease (NAFLD).
Highlights
The editorial board announced this article has been retracted on March 15, 2015
Volume and Number: Vol 7, No 3, 2015
Summary
The editorial board announced this article has been retracted on March 15, 2015.
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