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  • Title: Lipid-Lowering Effects of Medium-Chain Triglyceride-Enriched Coconut Oil in Combination with Licorice Extracts in Experimental Hyperlipidemic Mice.
    Author: Lee EJ, Oh H, Kang BG, Kang MK, Kim DY, Kim YH, Lee JY, Ji JG, Lim SS, Kang YH.
    Journal: J Agric Food Chem; 2018 Oct 10; 66(40):10447-10457. PubMed ID: 30244576.
    Abstract:
    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.
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