Glycerol kinase activity in adenoma alveolar type II cells

Abstract

Although several in vivo [l-3] and whole-cell [4-121 studies have demonstrated lung tissue can incorporate glycerol into the glycerol backbone of lipids, the presence of glycerol kinase has not been conclusively demonstrated in the tissue [2,13-151. We have been particularly interested in the biosynthesis of dipahnitoyl-sn-glycero-3-phosphocholine, which is the major component of pulmonary surfactant and is synthesized by the alveolar type II cells. In previous studies [ 12,16-l 81 , pulmonary adenomas induced by urethan were demonstrated to be a useful model for studies of lipid metabolism in alveolar type II cells. These benign adenomas consist almost exclusively of type II cells that contain lamellar bodies [ 19,201 and synthesize surfactant as normal type II cells [12,16] . However, surfactant biosynthesis is more active in adenoma type II cells than in whole lung [12,18] where type II cells comprise only 10% of the cells [21] . We found that adenomas incubated in Krebs-Ringer phosphate buffer incorporated [2-3H, 1 ,3-14C]gly cerol into the glycerol moiety of phosphatidylcholine and other lipids [ 121. This finding implied glycerol kinase is present and led us to examine the type II cells for activity. In the studies reported here, we demonstrate the conversion of labeled glycerol to glycerophosphate by glycerol kinase in cell-free preparations from adenoma type II cells.