Upregulation of fatty acid synthesis and the suppression of hepatic triglyceride lipase as a direct cause of hereditary postprandial hypertriglyceridemia in rabbits
Upregulation of fatty acid synthesis and the suppression of hepatic triglyceride lipase as a direct cause of hereditary postprandial hypertriglyceridemia in rabbits
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DOI：
10.3164/jcbn.13-21
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发表时间：
2013-09-01
影响因子：
2.4
通讯作者：
Fujii, Junichi
中科院分区：
文献类型：
--
作者：
Fukuda, Naoki;Ito, Tsunekata;Fujii, Junichi
遗传性餐后高胆固醇血症兔表现为向心性肥胖，被认为是代谢综合征的可靠模型。本研究旨在了解餐后高脂血症家兔的脂代谢过程和致病基因。选择11个在脂质代谢中起关键作用的基因，通过定量PCR评估其mRNA水平，并以日本白色兔为对照，比较其在餐后高脂血症兔中的表达。两个基因似乎与餐后高胆固醇血症有因果关系，这些基因被认为是可能的发病机制的候选者。一个是脂肪酸合成酶基因，在禁食状态下，该基因在餐后高脂血症兔中的表达组成性高于日本白色兔，并且在进食后达到相当高的水平。另一个是肝甘油三酯脂肪酶基因，其表达比日本白色兔中发现的低约一个数量级。低血浆肝甘油三酯脂肪酶活性与餐后高胆固醇血症兔肝脏中低水平的转录本一致。因此，脂肪酸合成增加和脂质水解缺陷共同导致餐后高甘油三酯血症。
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.