Raspberry Ketone Reduced Lipid Accumulation in 3T3-L1 Cells and Ovariectomy-Induced Obesity in Wistar Rats by Regulating Autophagy Mechanisms.
J Agric Food Chem. 2017 Dec 20 ;65(50):10907-10914. Epub 2017 Dec 11. PMID: 29164883
This study aimed to determine the antiobesity effects of raspberry ketone (RK), one of the major aromatic compounds contained in raspberry, and its underlying mechanisms. During adipogenesis of 3T3-L1 cells, RK (300μM) significantly reduced lipid accumulation and downregulated the expression of CCAAT/enhancer-binding protein α (C/EBPα), peroxisome proliferation-activated receptor γ (PPARγ), fatty acid-binding protein 4 (FABP4), and fatty acid synthase (FAS). RK also reduced the expression of light chain 3B (LC3B), autophagy-related protein 12 (Atg12), sirtuin 1 (SIRT1), and phosphorylated-tuberous sclerosis complex 2 (TSC2), whereas it increased the level of p62 and phosphorylated-mammalian target of rapamycin (mTOR). Daily administration of RK decreased the body weight (ovariectomy [Ovx] + RK, 352.6 ± 5 vs Ovx, 386 ± 5.8 g; P<0.05), fat mass (Ovx + RK, 3.2± 0.05 vs Ovx, 5.0 ± 0.4 g; P<0.05), and fat cell size (Ovx + RK, 6.4± 0.6 vs Ovx, 11.1 ± 0.7 × 10μm; P<0.05) in Ovx-induced obesity in rats. The expression of PPARγ, C/EBPα, FAS, and FABP4 was significantly reduced in the Ovx + RK group compared with that in the Ovx group. Similar patterns were observed in autophagy-related proteins and endoplasmic reticulum stress proteins. These results suggest that RK inhibited lipid accumulation by regulating autophagyin 3T3-L1 cells and Ovx-induced obese rats.