title: Dietary sea cucumber cerebroside alleviates orotic acid-induced excess hepatic adipopexis in rats.
abstract: 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.
authors.affiliation: College of Food Science and Engineering, Ocean University of China, Qingdao, China.
authors.forename: Bei
authors.initials: B
authors.lastname: Zhang
authors.forename: Changhu
authors.initials: C
authors.lastname: Xue
authors.forename: Xiaoqian
authors.initials: X
authors.lastname: Hu
authors.forename: Jie
authors.initials: J
authors.lastname: Xu
authors.forename: Zhaojie
authors.initials: Z
authors.lastname: Li
authors.forename: Jingfeng
authors.initials: J
authors.lastname: Wang
authors.forename: Teruyoshi
authors.initials: T
authors.lastname: Yanagita
authors.forename: Yong
authors.initials: Y
authors.lastname: Xue
authors.forename: Yuming
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D000963:Antimetabolites / Q000008:administration & dosage*; D002334:Carnitine O-Palmitoyltransferase / Q000235:genetics / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002554:Cerebrosides / Q000008:administration & dosage*; D019587:Dietary Supplements; D064429:Fatty Acid Synthases / Q000378:metabolism; D005234:Fatty Liver / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D015870:Gene Expression; D005786:Gene Expression Regulation; D050356:Lipid Metabolism / Q000187:drug effects*; D050155:Lipogenesis / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D065626:Non-alcoholic Fatty Liver Disease; D009963:Orotic Acid; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012616:Sea Cucumbers / Q000737:chemistry*; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism
chemical_list: D000963:Antimetabolites; D002352:Carrier Proteins; D002554:Cerebrosides; C497389:Srebf1 protein, rat; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; C106092:microsomal triglyceride transfer protein; D009963:Orotic Acid; D002334:Carnitine O-Palmitoyltransferase; D064429:Fatty Acid Synthases