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  • 标题:Upregulation of fatty acid synthesis and the suppression of hepatic triglyceride lipase as a direct cause of hereditary postprandial hypertriglyceridemia in rabbits
  • 本地全文:下载
  • 作者:Naoki Fukuda ; Tsunekata Ito ; Kazuo Ohwada
  • 期刊名称:Journal of Clinical Biochemistry and Nutrition
  • 印刷版ISSN:0912-0009
  • 电子版ISSN:1880-5086
  • 出版年度:2013
  • 卷号:53
  • 期号:2
  • 页码:114-121
  • DOI:10.3164/jcbn.13-21
  • 出版社:The Society for Free Radical Research Japan
  • 摘要:Rabbits with hereditary postprandial hypertriglyceridemia exhibit central obesity and are regarded as a reliable model for metabolic syndrome. This study was performed to gain insight into the affected process of lipid metabolism and into the causative genes of the postprandial hypertriglyceridemia rabbits. Eleven genes that play key roles in lipid metabolism were selected, their mRNA levels were assessed by quantitative PCR, and their expressions were compared among postprandial hypertriglyceridemia rabbits using Japanese white rabbits as the control. Two genes appeared to be in causal connection with postprandial hypertriglyceridemia, and these were regarded as likely candidates for the pathogenesis. One was the fatty acid synthase gene, which had an expression constitutively higher in postprandial hypertriglyceridemia rabbits than in Japanese white rabbits during the fasting state and reached quite high levels after feeding. The other was the gene for hepatic triglyceride lipase with an expression that was approximately one order lower than that found in the Japanese white rabbits. The low plasma hepatic triglyceride lipase activities were consistent with the low levels of the transcript in the livers of the postprandial hypertriglyceridemia rabbits. Thus, elevated fatty acid synthesis and defected lipid hydrolysis together would cause the postprandial hypertriglyceridemia in postprandial hypertriglyceridemia rabbits.
  • 关键词:postprandial hypertriglyceridemia;metabolic syndrome;hepatic triglyceride lipase;fatty acid synthase
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