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为研究MED1如何影响血浆脂质代谢,以MED1肝脏特异性敲除鼠(MED1△Liv)为动物模型,禁食0、24、48、72 h,通过H&E染色切片观察了MED1△Liv鼠肝脏的形态学变化,运用甘油三酯和胆固醇酶试剂盒及FPLC方法分析了MED1△Liv和对照鼠(MED1fl/fl)血浆甘油三酯和胆固醇的水平以及脂蛋白的分布情况。研究结果显示,禁食72 h,与MED1fl/fl和PPARα-/-对照鼠相比,MED1△Liv鼠肝脏无脂肪沉积。禁食24、48、72 h,与MED1fl/fl鼠相比,MED1△Liv鼠血浆甘油三酯显著升高。禁食48 h和72 h,与MED1fl/fl鼠相比,MED1△Liv鼠血浆胆固醇显著升高。此外,饲喂条件下,MED1△Liv和MED1fl/fl鼠血浆脂蛋白分布无明显差异。然而,禁食24 h,MED1△Liv鼠中富含甘油三酯的极低密度脂蛋白高度积聚,表明MED1△Liv鼠呈现的高脂血症是由于极低密度脂蛋白的积聚引起,提示转录辅激活子MED1在富含甘油三酯的脂蛋白代谢中起关键调控作用。
To investigate how MED1 affects plasma lipid metabolism, MED1 liver-specific knockout mice (MED1ΔLiv) were used as animal models and fasted for 0, 24, 48 and 72 h. H & E staining sections were used to examine the liver The changes of plasma triglyceride and cholesterol and the distribution of lipoproteins in MED1 △ Liv and control (MED1fl / fl) were analyzed by using triglyceride and cholesterol enzyme kit and FPLC method. The results showed that, at 72 h after fasting, there was no fat deposition in the liver of MED1ΔLiv mice compared with MED1fl / fl and PPARα - / - control mice. Fasting 24,48,72 h, compared with MED1fl / fl mice, MED1 △ Livis plasma triglyceride significantly increased. After 48 and 72 h of fasting, plasma cholesterol was significantly increased in MED1ΔLiv mice compared with MED1fl / fl mice. In addition, there was no significant difference in plasma lipoprotein distribution between MED1ΔLiv and MED1fl / fl mice under feeding conditions. However, the fast accumulation of triglyceride-rich very-low-density lipoproteins in MED1ΔLiv mice at 24 h after fasting indicated that the hyperlipidemia in MED1ΔLiv mice was caused by the accumulation of very-low-density lipoprotein, suggesting transcription Secondary activator MED1 plays a key regulatory role in triglyceride-rich lipoprotein metabolism.