Zhang Zhiguo, Chen Jing, Jiang Xin, Wang Jian, Yan Xiaoqing, Zheng Yang, Conklin Daniel J, Kim Ki-Soo, Kim Ki Ho, Tan Yi, Kim Young Heui, Cai Lu
Department of Cardiology & Radiation Oncology, First Hospital of Jilin University, Changchun 130021, China ; The Chinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Wenzhou 325035, China ; Department of Pediatrics, Kosair Children Hospital Research Institute, University of Louisville, Louisville, KY 40202, USA.
Department of Pediatrics, Kosair Children Hospital Research Institute, University of Louisville, Louisville, KY 40202, USA.
Oxid Med Cell Longev. 2014;2014:965954. doi: 10.1155/2014/965954. Epub 2014 May 29.
Obesity is caused by a combination of both genetic and environmental risks. Disruption in energy balance is one of these risk factors. In the present study, the preventive effect on high-fat diet- (HFD-) induced obesity and insulin resistance in mice by Magnolia bioactive constituent 4-O-methylhonokiol (MH) was compared with Magnolia officinalis extract BL153. C57BL/6J mice were fed by normal diet or by HFD with gavage-administered vehicle, BL153, low-dose MH, and high-dose MH simultaneously for 24 weeks, respectively. Either MH or BL153 slightly inhibited body-weight gain of mice by HFD feeding although the food intake had no obvious difference. Body fat mass and the epididymal white adipose tissue weight were also mildly decreased by MH or BL153. Moreover, MH significantly lowered HFD-induced plasma triglyceride, cholesterol levels and activity of alanine transaminase (ALT), liver weight and hepatic triglyceride level, and ameliorated hepatic steatosis. BL153 only significantly reduced ALT and liver triglyceride level. Concurrently, low-dose MH improved HFD-induced hyperinsulinemia and insulin resistance. Furthermore, the infiltration of mast cells in adipose tissue was decreased in MH or in BL153 treatment. These results suggested that Magnolia bioactive constituent MH might exhibit potential benefits for HFD-induced obesity by improvement of lipid metabolism and insulin resistance.
肥胖是由遗传和环境风险共同导致的。能量平衡失调是这些风险因素之一。在本研究中,将木兰生物活性成分4-O-甲基和厚朴酚(MH)与厚朴提取物BL153对高脂饮食(HFD)诱导的小鼠肥胖和胰岛素抵抗的预防作用进行了比较。C57BL/6J小鼠分别同时接受正常饮食或高脂饮食,并通过灌胃给予溶媒、BL153、低剂量MH和高剂量MH,持续24周。尽管食物摄入量没有明显差异,但MH或BL153均略微抑制了高脂饮食喂养小鼠的体重增加。MH或BL153也使体脂量和附睾白色脂肪组织重量略有下降。此外,MH显著降低了高脂饮食诱导的血浆甘油三酯、胆固醇水平以及丙氨酸转氨酶(ALT)活性、肝脏重量和肝脏甘油三酯水平,并改善了肝脂肪变性。BL153仅显著降低了ALT和肝脏甘油三酯水平。同时,低剂量MH改善了高脂饮食诱导的高胰岛素血症和胰岛素抵抗。此外,MH或BL153处理可减少脂肪组织中肥大细胞的浸润。这些结果表明,木兰生物活性成分MH可能通过改善脂质代谢和胰岛素抵抗对高脂饮食诱导的肥胖具有潜在益处。