Coral calcium hydride prevents hepatic steatosis in high fat diet-induced obese rats: A potent mitochondrial nutrient and phase II enzyme inducer
Coral calcium hydride prevents hepatic steatosis in high fat diet-induced obese rats: A potent mitochondrial nutrient and phase II enzyme inducer
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DOI：
10.1016/j.bcp.2015.12.020
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发表时间：
2016-03-01
影响因子：
5.8
通讯作者：
Long, Jiangang
中科院分区：
文献类型：
--
作者：
Hou, Chen;Wang, Yongyao;Long, Jiangang
饮食诱导的非酒精性脂肪性肝病（NAFLD）的特征是严重的脂质蓄积，并与炎症反应、氧化应激和肝线粒体功能障碍相关。我们以前证明，一些线粒体营养素有效地改善高脂饮食（HFD）诱导的肝脂肪变性和代谢紊乱。富氢液体或吸入气体中的分子氢，已被证实在清除活性氧和防止线粒体衰变，改善患者和动物模型的代谢综合征。珊瑚氢化钙（CCH）是一种以珊瑚钙为原料的新型固体分子氢载体。然而，CCH是否以及如何影响HFD诱导的肝脂肪变性仍然没有研究。在本研究中，我们将CCH应用于HFD诱导的NAFLD大鼠模型13周。我们发现，CCH持久地产生氢在体内和体外。CCH治疗显着减少体重增加，改善葡萄糖和脂质代谢，并减弱HFD诱导的肥胖大鼠的肝脏脂肪变性，对食物和水的摄入量没有影响。此外，CCH有效地改善HFD诱导的肝线粒体功能障碍，降低氧化应激，并激活II相酶。我们的研究结果表明，CCH是一种有效的富氢剂，它可以通过激活II相酶和改善线粒体功能来预防HFD诱导的NAFLD。(C)2016 Elsevier Inc. All rights reserved.
Diet-induced nonalcoholic fatty liver disease (NAFLD) is characterized by profound lipid accumulation and associated with an inflammatory response, oxidative stress and hepatic mitochondrial dysfunction. We previously demonstrated that some mitochondrial nutrients effectively ameliorated high fat diet (HFD)-induced hepatic steatosis and metabolic disorders. Molecular hydrogen in hydrogen-rich liquid or inhaling gas, which has been confirmed in scavenging reactive oxygen species and preventing mitochondrial decay, improved metabolic syndrome in patients and animal models. Coral calcium hydride (CCH) is a new solid molecular hydrogen carrier made of coral calcium. However, whether and how CCH impacts HFD-induced hepatic steatosis remains uninvestigated. In the present study, we applied CCH to a HFD-induced NAFLD rat model for 13 weeks. We found that CCH durably generated hydrogen in vivo and in vitro. CCH treatment significantly reduced body weight gain, improved glucose and lipid metabolism and attenuated hepatic steatosis in HFD-induced obese rats with no influence on food and water intake. Moreover, CCH effectively improved HFD-induced hepatic mitochondrial dysfunction, reduced oxidative stress, and activated phase II enzymes. Our results suggest that CCH is an efficient hydrogen-rich agent, which could prevent HFD-induced NAFLD via activating phase II enzymes and improving mitochondrial function. (C) 2016 Elsevier Inc. All rights reserved.