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Dietary sea cucumber cerebroside alleviates orotic acid-induced excess hepatic adipopexis in rats

机译:食用海参脑苷脂可减轻乳清酸诱导的大鼠肝脏脂肪过多

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Background Nonalcoholic fatty liver disease (NAFLD) is a prevalent chronic liver disease in industrialized countries. The present study was undertaken to explore the preventive effect of dietary sea cucumber cerebroside (SCC) extracted from Acaudina molpadioides in fatty liver rats. Methods Male Wistar rats were randomly divided into four groups including normal control group, NAFLD model group, and two SCC-treated groups with SCC at 0.006% and 0.03% respectively. The fatty liver model was established by administration of 1% orotic acid (OA) to the rats. After 10d, serum and hepatic lipid levels were detected. And the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were also determined. Besides, to gain the potential mechanism, the changes of key enzymes and gene expressions related to the hepatic lipid metabolism were measured. Results Dietary SCC at the level of 0.006% and 0.03% ameliorated the hepatic lipid accumulation in fatty liver rats. SCC administration elevated the serum triglyceride (TG) level and the ALT, AST activities in OA-fed rats. The activities of hepatic lipogenic enzymes including fatty acid synthase (FAS), malic enzyme (ME) and glucose-6-phosphatedehydrogenase (G6PDH) were inhibited by SCC treatment. And the gene expressions of FAS, ME, G6PDH and sterol-regulatory element binding protein (SREBP-1c) were also reduced in rats fed SCC. However, dietary SCC didn't affect the activity and mRNA expression of carnitine palmitoyltransferase (CPT) in liver. Besides, suppression of microsomal triglyceride transfer protein (MTP) activity was observed in SCC-feeding rats. Conclusions These results suggested that dietary SCC could attenuate hepatic steatosis due to its inhibition of hepatic lipogenic gene expression and enzyme activity and the enhancement of TG secretion from liver.
机译:背景技术非酒精性脂肪肝病(NAFLD)是工业化国家中流行的慢性肝病。进行本研究以探讨从甜菜豆中提取的饮食海参脑苷脂(SCC)对脂肪肝大鼠的预防作用。方法将雄性Wistar大鼠随机分为四组,分别为正常对照组,NAFLD模型组和两个SCC治疗组,SCC分别为0.006%和0.03%。通过向大鼠施用1%乳清酸(OA)建立脂肪肝模型。 10天后,检测血清和肝脂质水平。并测定血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)的活性。此外,为获得潜在的机制,还测定了与肝脂质代谢相关的关键酶和基因表达的变化。结果饮食中SCC含量为0.006%和0.03%可以改善脂肪肝大鼠肝脂质的积累。施用SCC可提高OA喂养大鼠的血清甘油三酸酯(TG)水平以及ALT,AST活性。 SCC处理抑制了脂肪酸合成酶(FAS),苹果酸酶(ME)和葡萄糖6-磷酸脱氢酶(G6PDH)等肝脂肪酶的活性。饲喂SCC的大鼠中FAS,ME,G6PDH和固醇调节元件结合蛋白(SREBP-1c)的基因表达也降低。但是,饮食中的SCC并不会影响肝脏中肉碱棕榈酰转移酶(CPT)的活性和mRNA表达。此外,在喂食SCC的大鼠中观察到微粒体甘油三酸酯转移蛋白(MTP)活性的抑制。结论这些结果表明,饮食性SCC可以抑制肝脏脂肪生成基因的表达和酶活性,并增强肝脏的TG分泌,从而减轻肝脏脂肪变性。

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