Chang Ya-Yuan, Su Hui-Min, Chen Szu-Han, Hsieh Wen-Tsong, Chyuan Jong-Ho, Chao Pei-Min
Department of Nutrition, China Medical University, Taichung 404, Taiwan.
Graduate Institute of Physiology, National Taiwan University, Taipei 100, Taiwan.
Nutrients. 2016 Dec 12;8(12):805. doi: 10.3390/nu8120805.
We previously reported that bitter melon seed oil (BMSO) was an effective anti-steatosis and antiobesity agent. Since the major fatty acid α-eleostearic acid (α-ESA) in BMSO is a peroxisome proliferator-activated receptor α (PPARα) activator, the objective was to investigate the role of PPARα in BMSO-modulated lipid disorders and α-ESA metabolism. C57BL/6J wild (WD) and PPARα knockout (KO) mice were fed a high-fat diet containing BMSO (15% soybean oil + 15% BMSO, HB) or not (30% soybean oil, HS) for 5 weeks. The HB diet significantly reduced hepatic triglyceride concentrations and increased acyl-CoA oxidase activity in WD, but not in KO mice. However, regardless of genotype, body fat percentage was lowered along with upregulated protein levels of uncoupling protein 1 (UCP1) and tyrosine hydroxylase, as well as signaling pathway of cAMP-dependent protein kinase and AMP-activated protein kinase in the white adipose tissue of HB-treated groups compared to HS cohorts. In WD-HB and KO-HB groups, white adipose tissue had autophagy, apoptosis, inflammation, and browning characteristics. Without PPARα, in vivo reduction of α-ESA into rumenic acid was slightly but significantly lowered, along with remarkable reduction of hepatic retinol saturase () expression. We concluded that BMSO-mediated anti-steatosis depended on PPARα, whereas the anti-adiposity effect was PPARα-independent. In addition, PPARα-dependent enzymes may participate in α-ESA conversion, but only have a minor role.
我们之前报道过苦瓜籽油（BMSO）是一种有效的抗脂肪变性和抗肥胖剂。由于BMSO中的主要脂肪酸α-桐酸（α-ESA）是一种过氧化物酶体增殖物激活受体α（PPARα）激活剂，目的是研究PPARα在BMSO调节的脂质紊乱和α-ESA代谢中的作用。给C57BL/6J野生型（WD）和PPARα基因敲除（KO）小鼠喂食含BMSO的高脂饮食（15%大豆油+15%BMSO，HB）或不含BMSO的高脂饮食（30%大豆油，HS）5周。HB饮食显著降低了WD小鼠的肝脏甘油三酯浓度并增加了酰基辅酶A氧化酶活性，但在KO小鼠中未出现此现象。然而，无论基因型如何，与HS组相比，HB处理组白色脂肪组织中的体脂百分比降低，同时解偶联蛋白1（UCP1）和酪氨酸羟化酶的蛋白水平上调，以及环磷酸腺苷依赖性蛋白激酶和AMP激活的蛋白激酶的信号通路也上调。在WD-HB和KO-HB组中，白色脂肪组织具有自噬、凋亡、炎症和褐色化特征。没有PPARα时，体内α-ESA向瘤胃酸的转化略有但显著降低，同时肝脏视黄醇饱和酶（）的表达也显著降低。我们得出结论，BMSO介导的抗脂肪变性依赖于PPARα，而抗肥胖作用则不依赖于PPARα。此外，PPARα依赖性酶可能参与α-ESA的转化，但作用较小。
