Coconut oil has gained in popularity over recent years as a healthy oil due to its potential cardiovascular benefits. Coconut oil contains medium chain triglycerides (MCT) including lauric acid and capric acid that display beneficial properties in human health. Licorice (Glycyrrhiza uralensis) is used as a sweetener and in traditional Chinese medicine with anti-inflammatory, antimicrobial, and antioxidant activities. This study investigated the in vivo effects of medium chain-triglycerides (MCT)-coconut oil (MCO) and its combination with licorice extract (LE-MCO) on serum lipid profile, hepatic steatosis, and local fat pad proteins in diet-induced obese mice. No liver toxicity was observed in 45% fat diet (HFD)-fed mice orally treated with LE, MCO, and LE-MCO for 12 weeks. Their supplementation reduced HFD-enhanced body weight, blood glucose, and insulin in mice. Plasma levels of both PLTP and LCAT were boosted in LE-MCO-administered mice. Supplementation of LE-MCO diminished plasma levels of TG and TC with concomitant reduction of the LDL-C level and tended to raise blood HDL-C level compared to that of HFD alone-mice. Treatment of LE-MCO encumbered the hepatic induction of hepatosteatosis-related proteins of SREBP2, SREBP1c, FAS, ACC, and CD36 in HFD-fed mice. Substantial suppression of this induction was also observed in the liver of mice treated with MCO. Oral administration of LE-MCO to HFD mice boosted hepatic activation of AMPK and the induction of UCP-1 and FATP1 in brown fat. Conversely, LE-MCO disturbed hepatic PPAR-LXR-RXR signaling in HFD-fed animals and reversed HFD-elevated epididymal PPARγ. Collectively, oral administration of LE-MCO may impede hyperlipidemia and hepatosteatosis through curtailing hepatic lipid synthesis.

中文翻译：

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富含中链甘油三酸酯的椰子油与甘草提取物组合对实验性高脂血症小鼠的降脂作用

椰子油由于其潜在的心血管益处，近年来作为一种健康油而广受欢迎。椰子油含有中链甘油三酸酯（MCT），其中包括月桂酸和癸酸，它们对人体健康具有有益的作用。甘草（甘草））用作甜味剂，并在中药中具有抗炎，抗微生物和抗氧化作用。这项研究调查了中链甘油三酸酯（MCT）-椰子油（MCO）及其与甘草提取物（LE-MCO）的组合对饮食诱导肥胖的血清脂质谱，肝脂肪变性和局部脂肪垫蛋白的体内作用老鼠。在口服LE，MCO和LE-MCO治疗12周的45％脂肪饮食（HFD）喂养的小鼠中，未观察到肝毒性。他们的补充减少了小鼠的HFD增强的体重，血糖和胰岛素。在LE-MCO给予的小鼠中，PLTP和LCAT的血浆水平均升高。与单独使用HFD的小鼠相比，补充LE-MCO可降低血浆TG和TC水平，同时降低LDL-C水平，并倾向于升高血液HDL-C水平。LE-MCO的治疗妨碍了在喂食HFD的小鼠中肝脂肪变性相关蛋白SREBP2，SREBP1c，FAS，ACC和CD36的肝诱导作用。在用MCO治疗的小鼠的肝脏中也观察到了这种诱导的显着抑制。对HFD小鼠口服LE-MCO可以增强AMPK的肝激活以及棕色脂肪中UCP-1和FATP1的诱导。相反，LE-MCO干扰了饲喂HFD的动物的肝PPAR-LXR-RXR信号，并逆转了HFD升高的附睾PPARγ。总之，口服LE-MCO可能会通过减少肝脏脂质的合成来阻止高脂血症和肝脂肪变性。对HFD小鼠口服LE-MCO可以增强AMPK的肝激活以及棕色脂肪中UCP-1和FATP1的诱导。相反，LE-MCO干扰了饲喂HFD的动物的肝PPAR-LXR-RXR信号，并逆转了HFD升高的附睾PPARγ。总之，口服LE-MCO可能会通过减少肝脏脂质的合成来阻止高脂血症和肝脂肪变性。对HFD小鼠口服LE-MCO可以促进AMPK的肝激活以及棕色脂肪中UCP-1和FATP1的诱导。相反，LE-MCO干扰了饲喂HFD的动物的肝PPAR-LXR-RXR信号，并逆转了HFD升高的附睾PPARγ。总之，口服LE-MCO可能会通过减少肝脏脂质的合成来阻止高脂血症和肝脂肪变性。