急性和慢性乙醇摄入对仓鼠肝脏甘油脂质生物合成的影响。
The effect of acute and chronic ethanol intake on hepatic glycerolipid biosynthesis in the hamster.
作者信息
Lamb R G, Wood C K, Fallon H J
出版信息
J Clin Invest. 1979 Jan;63(1):14-20. doi: 10.1172/JCI109268.
The effect of acute and chronic ethanol intake on hepatic glycerolipid biosynthesis in the hamster was studied by in vivo and in vitro techniques. The results were compared with those from control hamsters receiving isocaloric amounts of glucose. Both chronic and acute ethanol intake elevated serum and hepatic triglyceride concentrations and induced a rapid rise in the capacity of neutral glycerolipid formation from sn[1,3-14C]glycerol-3-phosphate by hamster liver homogenate and microsomal fractions. Ethanol intake also produced a corresponding increase in the incorporation of [1,3-14C]glycerol into hepatic neutral glycerolipids by the intact animal. The ethanol-induced rise in the capacity of neutral glycerolipid production by liver as measured in vivo and in vitro correlated well with an increase in hepatic phosphatidate phosphohydrolase activity. Therefore, the rise in hepatic and serum triglyceride levels associated with ethanol intake may be explained in part by an increase in the activity of the enzyme.
通过体内和体外技术研究了急性和慢性乙醇摄入对仓鼠肝脏甘油脂质生物合成的影响。将结果与接受等热量葡萄糖的对照仓鼠的结果进行了比较。急性和慢性乙醇摄入均提高了血清和肝脏甘油三酯浓度，并导致仓鼠肝脏匀浆和微粒体部分从sn[1,3-14C]甘油-3-磷酸形成中性甘油脂质的能力迅速增加。乙醇摄入还使完整动物将[1,3-14C]甘油掺入肝脏中性甘油脂质中的量相应增加。体内和体外测量的乙醇诱导的肝脏中性甘油脂质产生能力的增加与肝脏磷脂酸磷酸水解酶活性的增加密切相关。因此，与乙醇摄入相关的肝脏和血清甘油三酯水平的升高可能部分归因于该酶活性的增加。
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