Summary
Since acyl groups of phosphatidylinositol (PI) are enriched in stearic (18:0) and arachidonic (20:4) acids, and these fatty acids are preferentially released during cerebral ischemia, a metabolic relationship between PI and the free fatty acid (FFA) release is suggested. However, several lines of evidence have pointed against a direct involvement of the PI in this event. In our studies, ischemia elicited an increase in the level of diacylglycerols (DG) enriched in 18:0 and 20:4, but the level of PI in rat brain synaptosomes was not changed. Furthermore, active hydrolysis of PI by phosphodiesterase could not be demonstrated in synaptosomes under physiologically feasible conditions, although incubation of the same fraction resulted in a two-fold increase in DG. When rats pre-labeled with 32Pi were subjected to post-decapitative ischemic treatment, radioactivity of phosphatidylinositol 4,5-bisphosphate (PI P2) and phosphatidate (PA) in synaptosomes was decreased, but that of PI increased. These results suggest that an increase in enzymic degradation of these lipids coupled with hydrolysis of DG by DG lipase may account for the increase in DG and FFA enriched in 18:0 and 20:4 during the early phase of cerebral ischemia.
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Sun, G.Y., Tang, W., Huang, S.FL., Foudin, L. (1985). Is Phosphatidylinositol Involved in the Release of Free Fatty Acids in Cerebral Ischemia?. In: Bleasdale, J.E., Eichberg, J., Hauser, G. (eds) Inositol and Phosphoinositides. Experimental Biology and Medicine, vol 6. Humana Press. https://doi.org/10.1007/978-1-4612-5184-2_33
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DOI: https://doi.org/10.1007/978-1-4612-5184-2_33
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