Kamio Naoya, Suzuki Takuma, Watanabe Yuto, Suhara Yoshitomo, Osakabe Naomi
Department of Bio-science and Engineering, Shibaura Institute of Technology, 307 Fukasaku, Munumaku, Saitama 337-8570, Japan.
Department of Bio-science and Engineering, Shibaura Institute of Technology, 307 Fukasaku, Munumaku, Saitama 337-8570, Japan.
Free Radic Biol Med. 2016 Feb;91:256-63. doi: 10.1016/j.freeradbiomed.2015.12.030. Epub 2015 Dec 29.
Numerous clinical studies have found that ingestion of chocolate reduces the risk of metabolic syndrome, however, the mechanisms were remain unclear. We have reported that a single dose of a flavan-3-ol fraction derived from cocoa (FL) enhanced energy expenditure (EE) and increased the mRNA expression levels of uncoupling proteins (UCPs) and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), and the protein level of phosphorylated AMP-activated protein kinase (AMPK)α in tissues, along with plasma adrenaline level. In the present study, we examined whether the EE enhancing activity of FL is mediated by adrenergic effect using several adrenalin receptor (AR) blockers. In the first study, mice were butoxamine, as β2AR blocker, with vehicle or 10mg/kg FL orally. We found that pretreatment with butoxamine prevented the increases of EE, the mRNA expression of UCP-3, and phosphorylated AMPKα that were induced in the gastrocnemius muscle of mice by 10mg/kg FL. Secondly, mice were given SR52930, as β3AR blocker. Pretreatment with SR52930 prevented the increases of EE, the mRNA expression of UCP-3, and phosphorylated AMPKα that were induced in the gastrocnemius muscle of mice by 10mg/kg FL. Pretreatment with a combination of both blockers also reduced the increments in mRNA expression levels of UCPs and PGC-1α, however, phosphorylated AMPKα in skeletal muscle was rather increased. These results suggest that the ability of a single oral dose of FL to enhance metabolic activity is mediated by sympathetic nerve system (SNS).
众多临床研究发现，摄入巧克力可降低代谢综合征的风险，然而，其机制仍不清楚。我们曾报道，单剂量源自可可的黄烷-3-醇组分（FL）可增强能量消耗（EE），并增加组织中解偶联蛋白（UCPs）和过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）的mRNA表达水平，以及磷酸化的AMP激活蛋白激酶（AMPK）α的蛋白水平，同时还会使血浆肾上腺素水平升高。在本研究中，我们使用几种肾上腺素受体（AR）阻滞剂来检测FL增强EE的活性是否由肾上腺素能效应介导。在第一项研究中，给小鼠口服β2肾上腺素能受体阻滞剂布托沙明、溶剂或10mg/kg FL。我们发现，用布托沙明预处理可防止10mg/kg FL诱导的小鼠腓肠肌EE增加、UCP-3的mRNA表达增加以及磷酸化AMPKα增加。其次，给小鼠给予β3肾上腺素能受体阻滞剂SR52930。用SR52930预处理可防止10mg/kg FL诱导的小鼠腓肠肌EE增加、UCP-3的mRNA表达增加以及磷酸化AMPKα增加。用两种阻滞剂联合预处理也降低了UCPs和PGC-1α的mRNA表达水平的增加，然而，骨骼肌中磷酸化的AMPKα反而增加。这些结果表明，单次口服FL增强代谢活性的能力是由交感神经系统（SNS）介导的。
