Uhal B D, Longmore W J
E.A. Doisy Department of Biochemistry, St. Louis University School of Medicine, MO.
Biochim Biophys Acta. 1988 Feb 4;958(2):279-88. doi: 10.1016/0005-2760(88)90186-5.
Glycerol utilization for phospholipid biosynthesis was examined in type II pneumocytes isolated from normal and streptozocinin-diabetic rats. With glucose in the incubation medium, incorporation of exogenous [1,3-14C]glycerol into disaturated phosphatidylcholine, total phosphatidylcholine (PC), phosphatidylglycerol (PG) and phosphatidylethanolamine (PE) was increased 4-fold in cells from diabetic rats. In the absence of glucose, glycerol incorporation was 5-fold greater than in its presence in cells from normal animals, but was further increased 2.2-fold in cells from diabetic rats. Insulin treatment of diabetic rats returned all incorporation rates to control values. The increased glycerol incorporation rates were not due to differences in either phospholipid turnover or the size of the glycerol 3-phosphate precursor pool. Kinetic analysis of glycerol entry into the acid-soluble cell fraction indicated that glycerol transport occurred largely by simple diffusion, and was not rate limiting for its entry into lipids. Glycerol entry into the total lipid fraction was saturable, reaching a Vmax of 48 pmol/micrograms DNA per h in normal cells and 120 pmol/micrograms DNA per h in cells from diabetic rats, with no change in the Km (0.31 mM). While glycerol oxidation was reduced 23% in cells from diabetic rats in the presence of glucose and by 44% in the absence of glucose, glycerol kinase activity in sonicates of cells from diabetic animals was increased 210% and was reversed by in vivo insulin treatment. These results suggest that glycerol utilization in type II pneumocytes is a hormonally regulated function of both glycerol oxidation and glycerol phosphorylation.
在从正常大鼠和链脲佐菌素诱导的糖尿病大鼠分离出的II型肺细胞中，研究了用于磷脂生物合成的甘油利用情况。在孵育培养基中有葡萄糖的情况下，糖尿病大鼠细胞中外源[1,3-¹⁴C]甘油掺入二饱和磷脂酰胆碱、总磷脂酰胆碱（PC）、磷脂酰甘油（PG）和磷脂酰乙醇胺（PE）的量增加了4倍。在没有葡萄糖的情况下，甘油掺入量比正常动物细胞中有葡萄糖时高5倍，但在糖尿病大鼠细胞中进一步增加了2.2倍。用胰岛素治疗糖尿病大鼠可使所有掺入率恢复到对照值。甘油掺入率增加并非由于磷脂周转或3-磷酸甘油前体池大小的差异。对甘油进入酸溶性细胞部分的动力学分析表明，甘油转运主要通过简单扩散发生，并且不是其进入脂质的限速步骤。甘油进入总脂质部分是可饱和的，正常细胞中达到的Vmax为每小时48 pmol/μg DNA，糖尿病大鼠细胞中为每小时120 pmol/μg DNA，Km（0.31 mM）没有变化。虽然在有葡萄糖存在的情况下，糖尿病大鼠细胞中的甘油氧化减少了23%，在没有葡萄糖的情况下减少了44%，但糖尿病动物细胞匀浆中的甘油激酶活性增加了210%，并且通过体内胰岛素治疗得以逆转。这些结果表明，II型肺细胞中的甘油利用是甘油氧化和甘油磷酸化的激素调节功能。
