(E)-3-(4-(tert-Butyl)Phenyl)-N-Isobutyl-2-Methylacrylamide Suppresses Adipogenesis in High-Fat-Fed Mice

J. Hur, Sanghee Kim, Bo-ra Yoon, Guijae Yoo, In-Hae Choi, Ho-Young Park, Sang Yoon Choi
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Abstract

Obesity is caused by excessive adipogenesis and leads to metabolic diseases such as diabetes, hypertension, and degenerative arthritis. Therefore, there is an ever-increasing need to identify new anti-obesity compounds. In this study, the anti-obesity effects of (E)-3-(4-(tert-butyl)phenyl)-N-isobutyl-2-methylacrylamide (BPIMA) were evaluated using pre-adipocytes and a high-fat-fed C57BL/6J mouse model. As the results, BPIMA effectively inhibited adipocyte differentiation (64.3% at 40 μM) without exhibiting any cytotoxicity. Additionally, BPIMA decreased the protein levels of PPARγ, FAS, C/EBP, and SREBP in 3T3-L1 cells in a concentration-dependent manner. In C57BL/6J mice, a significant decrease in body weight, adipose tissue, and fatty liver was observed in the BPIMA-treated high-fat group compared to that observed in the vehicle-treated high-fat group; the serum levels of total cholesterol and glucose also significantly decreased in the BPIMA-treated high-fat group. Moreover, the weight and fat level of liver and serum AST, ALT activity in the BPIMA-treated high-fat group were similar to low fat diet-control group. These findings show that BPIMA may be a potential anti-obesity compound.
(E)-3-(4-(叔丁基)苯基)-N-异丁基-2-甲基丙烯酰胺能抑制高脂喂养小鼠的脂肪生成
肥胖症是由过度的脂肪生成引起的,并导致糖尿病、高血压和退行性关节炎等代谢性疾病。因此,人们越来越需要找到新的抗肥胖化合物。本研究利用前脂肪细胞和高脂肪喂养的 C57BL/6J 小鼠模型,评估了 (E)-3-(4-(tert-butyl)phenyl)-N-isobutyl-2-methylacrylamide (BPIMA) 的抗肥胖作用。结果表明,BPIMA 能有效抑制脂肪细胞的分化(40 μM 时抑制率为 64.3%),且无任何细胞毒性。此外,BPIMA 还能以浓度依赖的方式降低 3T3-L1 细胞中 PPARγ、FAS、C/EBP 和 SREBP 的蛋白水平。在 C57BL/6J 小鼠中,观察到 BPIMA 处理的高脂肪组小鼠的体重、脂肪组织和脂肪肝水平比车辆处理的高脂肪组小鼠显著下降;BPIMA 处理的高脂肪组小鼠的血清总胆固醇和葡萄糖水平也显著下降。此外,BPIMA处理的高脂组肝重量和脂肪水平以及血清AST、ALT活性与低脂饮食对照组相似。这些研究结果表明,BPIMA可能是一种潜在的抗肥胖化合物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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