, phosphoinositide metabolism with neurotransmission, hormonal, and other

, either choline oxidation or thesecretion of PC in the bile, and to a lesser extent, by the intestinal mucosa. Cholineimbalances can be compensated by adaptive increases in PEMT activity, byrecycling of choline, decreased oxidation of choline, reabsorption of biliaryPC (95% of bile phospholipids is PC, of which about 40% return to the liver),and by redistribution of tissue choline to maintain homeostasis  particularly in the brain and liver. 44 Regarding the fetus, infant and youngchild, and phospholipids in the brain increase two-fold in the cortex andthree-fold in the white matter from the 10th 482 week of gestation to the ageof two years. The studies have also shown that a relative continuous decreaseof choline phosphoglycerides, from 50% of total phospholipids in the cerebralcortex of the fetus to 45% in 485 infants at term and 38% in children at twoyears of age.

In this study, SPM shows a continuous 486 increase, from 3% oftotal phospholipids in the cerebral cortex of the fetus to 5% in infants atterm and 487 10% in children at two years of age 45. Phosphatidylethanolamine(PE):  Phosphatidylethanolamine N-methyltransferase(PEMT) activity in the diabetic mouse brain was determined as a possible markerof demyelination. As animal models for diabetes mellitus, we used geneticallytransmitted diabetic mice C57BL/KsJ-db/db, and streptozotocin induced diabeticmice.

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Enzyme activity was much lower in the brains of these mice than in thoseof developing and demyelinating mice but significantly higher than in normaladult mouse brains 46.Phosphatidylinositol (PI): Phospholipase C (PLCB1, PLCD1) is a critical enzyme thatintegrates phosphoinositide metabolism with neurotransmission, hormonal, andother signaling processes. PLC can be activated by G-protein mechanisms coupledto muscarinic cholinergic M1,3,5, dopaminergic D2,3,4,serotonergic 5-HT2A,C, and other post-synaptic neuroreceptors, or tohormone receptors .

PLC cleaves membrane PI(4,5)P2 to form twoimportant second messengers, cytosol-soluble inositol 1,4,5-trisphosphate(Ins(1,4,5)P3, or IP3) and membrane-bound diacylglycerol(DAG) 47,48,49,50.  Further,According to research by Lee et al. mice had a reducedcontent of ARA in PI and had deficits in cortical lamination during braindevelopment, delayed neuronal processes in the cortex, and reduced neuriteoutgrowth in vitro. Mice died within a month and showed atrophyof the cerebral cortex and hippocampus.

These results demonstrate theimportance of ARA-containing PI in normal cortical development in mice. Byeliminating Lysophosphatidylinositol-acyltransferase-1 (LPIAT1)in mice, the enzyme responsible for the incorporation of ARA into PI, it wasshown that the ARA-containing PI is essential for brain development in mammals51. 

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