Chu S W, Geyer R P
Biochim Biophys Acta. 1982 Jan 15;710(1):63-70. doi: 10.1016/0005-2760(82)90190-4.
The synthesis and turnover of phosphatidylinositol as well as clearance were studied in the intestines of lipodystrophic gerbils treated with or without an intraperitoneal dose of myo-inositol by monitoring the incorporation of 32Pi and the retention of absorbed [1-14C] palmitic acid. 1. myo-Inositol deficiency produced an intestinal lipodystrophy with a large lipid accumulation and a decreased level of phosphatidylinositol. Upon myo-inositol repletion, the intestinal phosphatidylinositol rapidly returned to the control level by h, at which time the removal of excess lipid still remained in a lag phase. 2. myo-Inositol injection caused an increase in the incorporation of 32Pi into phosphatidylinositol mainly due to an increased phosphatidylinositol synthesis de novo. As a result, the turnover of phosphatidylinositol molecules might increase because of an expanded pool size. 3. The stimulation of phosphatidylinositol synthesis was then followed by an enhanced clearance of absorbed [14C] palmitate and by an intestinal recovery which was monitored by the loss of accumulated triacylglycerol. 4. This study indicates that myo-inositol availability appears to regulate the in vivo biosynthesis of phosphatidylinositol which, in turn, may play a crucial role in normal lipid transport across gerbil intestine.
