Santamarina Aline B, Oliveira Juliana L, Silva Fernanda P, Carnier June, Mennitti Laís V, Santana Aline A, de Souza Gabriel H I, Ribeiro Eliane B, Oller do Nascimento Cláudia M, Lira Fábio S, Oyama Lila M
Departamento de Fisiologia-Universidade Federal de São Paulo, São Paulo, Brazil.
Programa de Pós-Graduação Interdisciplinar em Ciências da Saúde-Universidade Federal de São Paulo, Santos, Brazil.
PLoS One. 2015 Nov 4;10(11):e0141227. doi: 10.1371/journal.pone.0141227. eCollection 2015.
Supplementation with epigallocatechin-3-gallate has been determined to aid in the prevention of obesity. Decaffeinated green tea extract appears to restore a normal hepatic metabolic profile and attenuate high-fat diet (HFD)-induced effects, thereby preventing non-alcoholic fatty liver disease in mice. Mice were maintained on either a control diet (CD) or HFD for 16 weeks and supplemented with either water or green tea extract (50 mg/kg/day). The body mass increase, serum adiponectin level, and lipid profile were measured over the course of the treatment. Furthermore, the AMPK pathway protein expression in the liver was measured. From the fourth week, the weight gain in the CD + green tea extract (CE) group was lower than that in the CD + water (CW) group. From the eighth week, the weight gain in the HFD + water (HFW) group was found to be higher than that in the CW group. Moreover, the weight gain in the HFD + green tea extract (HFE) group was found to be lower than that in the HFW group. Carcass lipid content was found to be higher in the HFW group than that in the CW and HFE groups. Serum analysis showed reduced non-esterified fatty acid level in the CE and HFE groups as compared with their corresponding placebo groups. Increased adiponectin level was observed in the same groups. Increased VLDL-TG secretion was observed in the HFW group as compared with the CW and HFE groups. Increased protein expression of AdipoR2, SIRT1, pLKB1, and pAMPK was observed in the HFE group, which explained the reduced expression of ACC, FAS, SREBP-1, and ChREBP in this group. These results indicate that the effects of decaffeinated green tea extract may be related to the activation of AMPK via LKB1 in the liver of HFD-fed mice.
已确定补充表没食子儿茶素 -3- 没食子酸酯有助于预防肥胖。脱咖啡因绿茶提取物似乎能恢复正常的肝脏代谢谱,并减轻高脂饮食(HFD)诱导的影响,从而预防小鼠非酒精性脂肪肝病。将小鼠维持在对照饮食(CD)或HFD上16周,并补充水或绿茶提取物(50毫克/千克/天)。在治疗过程中测量体重增加、血清脂联素水平和血脂谱。此外,测量肝脏中AMPK途径蛋白的表达。从第四周起,CD + 绿茶提取物(CE)组的体重增加低于CD + 水(CW)组。从第八周起,发现HFD + 水(HFW)组的体重增加高于CW组。此外,发现HFD + 绿茶提取物(HFE)组的体重增加低于HFW组。发现HFW组的胴体脂质含量高于CW组和HFE组。血清分析显示,与相应的安慰剂组相比,CE组和HFE组的非酯化脂肪酸水平降低。在同一组中观察到脂联素水平升高。与CW组和HFE组相比,HFW组观察到VLDL-TG分泌增加。在HFE组中观察到AdipoR2、SIRT1、pLKB1和pAMPK的蛋白表达增加,这解释了该组中ACC、FAS、SREBP-1和ChREBP表达的降低。这些结果表明,脱咖啡因绿茶提取物的作用可能与高脂饮食喂养小鼠肝脏中通过LKB1激活AMPK有关。