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大量研究表明,高果糖可引起脂肪肝,但对肾脏脂质代谢的影响尚不清楚。该实验研究给予10%果糖水5周后诱导的脂肪肝大鼠肾脏的脂质代谢情况,并探讨其可能机制。将16只雄性SD大鼠随机分为正常组(con)和果糖组(fru),果糖组给予10%(W/V)果糖水,第5周末称体重、取血、处死,检测血浆GLU、TG、TC和INSULIN含量。取肾脏、肝脏和白色脂肪称重,采用形态学方法观察肝脏和肾脏脂质沉积情况,酶法测其TG、TC含量,以Real time-PCR检测肾脏、肝脏中脂质合成和脂质氧化相关基因水平,以Western blot检测肾、肝细胞核脂质合成转录因子的蛋白表达。结果显示,果糖组大鼠血浆TG、INSULIN明显升高,并出现肥胖体征,肝脏脂质沉积严重,其调控脂质合成的两个关键的转录因子ChREBP和SREBP1c mRNA和核蛋白表达都明显升高,并且它们靶向的脂质合成相关酶FAS、ACC1、SCD1 mRNA表达也显著增加。但是,在肾脏中,高果糖没有引起TG含量的变化,调控脂质重新合成的基因和蛋白的表达也未发生变化。因此,与果糖致脂肪肝不同,高果糖饮食并没有造成肾脏的脂质沉积和脂质合成相关基因、蛋白的变化。
A large number of studies have shown that high fructose can cause fatty liver, but the impact on renal lipid metabolism is unclear. This study investigated the effects of 10% fructose on the lipid metabolism in the kidneys of rats with fatty liver and the possible mechanism. Sixteen male Sprague-Dawley rats were randomly divided into normal group and fru group. Fructose group was given 10% (w / v) fructose water. Body weight was weighed at the end of the fifth week. Blood was collected and sacrificed. Plasma GLU, TG, TC and INSULIN content. The kidneys, liver and white fat were weighed. The liver and kidney lipid deposition was observed by morphological method. The contents of TG and TC were measured by enzymatic method. The lipid synthesis and lipid oxidation in kidney and liver were detected by Real time-PCR Western blot was used to detect the protein expression of nuclear lipid synthesis transcription factors in kidney and hepatocytes. The results showed that the TG and INSULIN levels in the fructose group were significantly increased, with obesity signs and severe liver lipid deposition. The two key transcription factors ChREBP and SREBP1c mRNA and nuclear protein expression that regulate lipid synthesis were significantly increased , And their targeted lipid synthesis related enzymes FAS, ACC1, SCD1 mRNA expression also increased significantly. However, in the kidneys, high fructose did not cause changes in TG content, and the expression of genes and proteins that regulate lipid recombination did not change either. Therefore, unlike fructose-induced fatty liver, high-fructose diet did not cause changes in kidney lipid deposition and lipid synthesis-related genes and proteins.