真鲷(Pagrus major)脂蛋白脂肪酶基因表达与内脏脂肪蓄积营养调控定量研究

采用竞争性PCR方法 ,进行 4种营养状况对真鲷脂蛋白脂肪酶 (LPL)基因mRNA表达水平与内脏脂肪蓄积影响的定量研究。结果表明 ,真鲷LPL基因在肝脏存在营养诱导性表达 ,饥饿、高脂食物均是其表达诱导因子 ;在腹腔肠系膜脂肪组织存在组成性表达 ,其表达水平受摄食状态的影响 ,但饲料脂肪水平却不起作用。当真鲷喂食高脂食物时 ,诱导产生的大量肝脏LPL将为肝脏提供更多的来源于食物的游离脂肪酸 ,使肝脏有可能出现营养诱导性脂肪蓄积 ,但真鲷腹腔肠系膜脂肪组织LPL基因表达水平未出现适应性变化 ,其腹腔肠系膜脂肪组织将不可能作为营养诱导性蓄脂器官。由于上述营养状况对真鲷体重、腹脂指数、肝指数均没有产生显著性影响 ,说明真鲷具有在不同营养状况下与哺乳类相似的维持其内脏脂肪蓄积稳定的代谢机制 ,推测真鲷应存在某种在功能上与哺乳类相似的肥胖基因。

NUTRITIONAL REGULATION OF LIPOPROTEIN LIPASE GENE EXPRESSION AND VISCERAL FAT DEPOSITION IN RED SEA BREAM (PAGRUS MAJOR)

To investigate the mechanism of visceral fat deposition in fish, the effects of dietary lipid level and feeding condition on lipoprotein lipase (LPL) gene expression in the liver and visceral adipose tissues of a marine fish, red sea bream Pagrus major were investigated by competitive polymerase chain reaction. Our quantitative results demonstrate that both dietary lipid level and feeding condition altered the liver LPL mRNA level, while only feeding condition but not dietary lipid level, caused changes in the visceral adipose LPL mRNA abundance. In the liver, high lipid diet significantly increased the LPL mRNA level under fed condition (at 5 hour post feeding). Although starvation (at 48 hour post feeding) drastically stimulated liver LPL gene expression in the fish fed low lipid diet, it had no effect in the fish fed high lipid diet. In the visceral adipose tissue, LPL mRNA number was significantly higher in fed condition than in starved condition, irrespective of the dietary lipid levels. The distinctive regulation of the LPL mRNA level in the two fat depot organs of red sea bream in response to dietary lipid, indicates that the liver may play a major role in nutrient induced lipid storage, whereas the visceral adipose tissue appears more like a constitutional fat depot organ. Our results on visceral fat deposition of the fish show that there was no significant change in the hepatosomatic index, the visceral adiposomatic index, or the body weight after the nutritional treatments. It is proposed that the fish liver may adapt to an excessive supply of lipid substrates by inducing UCP2 to facilitate substrate disposal. The ability of the fish to keep the balance between fat deposition and oxidation in such a way, similar to mammals, strongly suggests the possible existence of leptin homologue in the fish.