Sake lees extract improves hepatic lipid accumulation in high fat diet-fed mice.
Sake lees extract improves hepatic lipid accumulation in high fat diet-fed mice.
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DOI：
10.1186/s12944-017-0501-y
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发表时间：
2017-06-03
影响因子：
4.5
通讯作者：
Saito K
中科院分区：
文献类型：
--
作者：
Kubo H;Hoshi M;Matsumoto T;Irie M;Oura S;Tsutsumi H;Hata Y;Yamamoto Y;Saito K
非酒精性脂肪性肝病（NAFLD）作为慢性肝病的主要原因之一，在全球范围内不断增加。清酒酒糟（SL）是清酒生产的二次产品，被认为对人类健康有有益的影响。为了研究这些作用，我们使用了用或不用SL提取物处理的高脂肪饮食（HFD）喂养的小鼠。小鼠自由进食HFD 8周，并在最后4周每天通过喂食针给予500 μL蒸馏水（含或不含SL浸提液（350 mg/mL））。测量摄食量、体重和肝脏重量。测定肝组织中甘油三酯含量以及各种脂质和葡萄糖代谢相关基因的mRNA和蛋白表达水平。测定血清中甘油三酯、游离脂肪酸、葡萄糖、胰岛素和肝细胞损伤标志物的水平。在存在或不存在SL提取物的情况下评估HepG 2细胞中脂肪酸诱导的脂质蓄积。喂食HFD并接受SL提取物处理的小鼠显示肝脏脂质蓄积以及肝脏中过氧化物酶体增殖物激活受体γ（PPARγ）、PPARα、CD 36和磷酸烯醇式丙酮酸羧激酶1的mRNA和蛋白水平显著降低，而SL提取物不影响体重和摄食量。此外，给予SL提取物后，喂食HFD的小鼠的胰岛素抵抗和肝脏炎症得到改善。在HepG 2细胞中，SL提取物抑制脂肪酸诱导的细胞内脂质积累。这些发现表明，用SL提取物治疗可能会降低NAFLD发展的风险，并且SL提取物可能在临床上用于治疗NAFLD。
Nonalcoholic fatty liver disease (NAFLD) is increasing worldwide as one of the leading causes of chronic liver disease. Sake lees (SL) are secondary products of sake manufacturing and are considered to have beneficial effects on human health. To investigate these effects, we used high fat diet (HFD)-fed mice treated with or without the SL extract. Mice were the HFD ad libitum for 8 weeks and were administered 500 μL of distilled water with or without the SL extract (350 mg/mL) by a feeding needle daily for the last 4 weeks. Food intake, body weight, and liver weight were measured. Triacylglycerol content and the mRNA and protein expression levels of various lipid and glucose metabolism-related genes were determined in liver tissues. The levels of triglyceride, free fatty acids, glucose, insulin, and liver cell damage markers were determined in serum. Fatty acid-induced lipid accumulation in HepG2 cells was assessed in the presence or absence of the SL extract. Mice fed a HFD and treated with the SL extract demonstrated a significant reduction in hepatic lipid accumulation and mRNA and protein levels of peroxidome proliferator-activated receptor γ (PPARγ), PPARα, CD36, and phosphoenolpyruvate carboxykinase 1 in the liver, while the SL extract did not affect body weight and food intake. Moreover, insulin resistance and hepatic inflammation in HFD-fed mice improved after administration of the SL extract. In HepG2 cells, the SL extract suppressed fatty acid-induced intracellular lipid accumulation. These findings suggest that treatment with the SL extract could potentially reduce the risk of NAFLD development, and that the SL extract may be clinically useful for the treatment of NAFLD.