High Glucose Concentrations Stimulate Renal Papillary Phosphatidylcholine Biosynthesis

Abstract

The effects of a high glucose concentration (HGC) on renal phosphatidylcholine (PtdCho) biosynthesis were studied. In control rats, HGC increased papillary PtdCho biosynthesis. In chronic diabetic rats, an increase above that induced by diabetes was observed. Such glucose-responsive phospholipid pools were shown to be transient in adult control rats, while in acute diabetic and aged control and chronic diabetic rats they seem to be of slow breakdown or permanent. Deoxyglucose evokes the HGC effect only in the presence of 5 mM glucose. Neomycin, which blocks phospholipase C action, corrected the HGC effect in control and chronic diabetic rats, but not the increase due to diabetes. CDP-choline: 1,2-diacylglycerol cholinephosphotransferase activity was increased by both in vivo and simulated diabetes. Therefore, transient high extracellular glucose levels promote a reversible increase in papillary ³²P-PtdCho, while diabetes causes an irreversible increase resulting in PtdCho accumulation, possibly related to papillary necrosis.

Myo-Inositol Moderates Glucose-Induced Effects on Human Placental 13C-Arachidonic Acid Metabolism

“…This lack of change with very high glucose mirrors published findings where 20 mM glucose was found to have little impact on overall 14 C-AA uptake by primary cytotrophoblasts [ 48 ]. One possible explanation for increased PC and LPC may be increases in the activity of phosphocholine cytidylyltransferase or phosphatidylethanolamine N-methyltransferase, which catalyze the rate limiting steps in PC synthesis, and which are known to be upregulated by hyperglycemia or glucose treatment in a range of tissue types [ 49 , 50 , 51 ]. However, alterations in these genes would not explain why other lipids are decreased by 10 mM but not 17 mM glucose.…”