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Increase in liver cytosolic lipases activities and VLDL-TAG secretion rate do not prevent the non-alcoholic fatty liver disease in cafeteria diet-fed rats
Biochimie ( IF 3.3 ) Pub Date : 2018-04-26
Anderson Fernandes de Melo, Carolina Campos Lima Moreira, Camila Ferreira Sales, Thiago Rentz, Helena Fonseca Raposo, Maria Antonieta Rissato Garófalo, Leida Maria Botion, Isis do Carmo Kettelhut, Helena Coutinho Franco de Oliveira, Valéria Ernestânia Chaves

We have previously shown that the cafeteria diet increases body fat mass, triacylglycerol (TAG) and insulin plasma levels, glucose uptake by white and brown adipose tissues, as well as the sympathetic activity to both adipose tissues in Wistar rats. The metabolic pathways responsible for the development of non-alcoholic fatty liver disease (NAFLD) were examined in cafeteria diet-fed rats. After 3 weeks offering cafeteria diet, we evaluated: (i) activity of the sympathetic nervous system by norepinephrine turnover rates; (ii) de novo fatty acid synthesis in vivo using 3H2O; (iii) secretion of very low density lipoprotein (VLDL)-TAG secretion measuring serum TAG levels after administration of lipase lipoprotein inhibitor, (iv) liver cytosolic lipases activity and (v) liver mRNA expression of enzymes involved in lipids secretion and oxidation by RT-PCR. The cafeteria diet induced an increase in TAG (120%) and cholesterol (30%) liver contents. Cafeteria diet did not change the sympathetic nervous system activity to liver, but induced a marked increase in the lipogenesis (approximately four-fold) and significant increase in cytosolic lipases activities (46%) and VLDL-TAG secretion (22%) compared to control diet-fed rats. The cafeteria diet also increased the microsomal triglyceride transfer protein (30%) and carnitine palmitoyltransferase I (130%) mRNA expression but decreased the apolipoprotein B100 (26%) mRNA expression. Our findings demonstrate that the increase in the cytosolic lipases activities and VLDL-TAG secretion rates were not able to compensate for the increased lipogenesis rates induced by the cafeteria diet, resulting in NAFLD.



中文翻译:

食堂饮食喂养的大鼠中肝细胞脂肪酶活性的增加和VLDL-TAG分泌率的增加并不能预防非酒精性脂肪肝

先前我们已经表明,食堂饮食会增加Wistar大鼠体内的脂肪量,三酰甘油(TAG)和胰岛素血浆水平,白色和棕色脂肪组织的葡萄糖摄取以及对两种脂肪组织的交感活性。在食堂饮食喂养的大鼠中检查了负责发展非酒精性脂肪肝疾病(NAFLD)的代谢途径。提供食堂饮食3周后,我们评估:(i)去甲肾上腺素周转率引起的交感神经系统活动;(ii)使用3H 2 O在体内从头合成脂肪酸;(iii)施用脂肪酶脂蛋白抑制剂后,测量血清TAG水平的极低密度脂蛋白(VLDL)-TAG分泌,(iv)肝细胞脂肪酶活性和(v)逆转录-聚合酶链反应(RT-PCR)参与脂质分泌和氧化的酶的肝mRNA表达。自助餐厅饮食引起TAG(120%)和胆固醇(30%)肝含量的增加。自助餐厅饮食未改变对肝脏的交感神经系统活动,但与对照组相比,脂肪生成显着增加(约四倍),胞质脂肪酶活性(46%)和VLDL-TAG分泌显着增加(22%)饮食喂养的大鼠。食堂饮食还增加了微粒体甘油三酸酯转移蛋白(30%)和肉碱棕榈酰转移酶I(130%)mRNA表达,但降低了载脂蛋白B100(26%)mRNA表达。

更新日期:2018-04-27
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