, phosphoinositide metabolism with neurotransmission, hormonal, and other

, either choline oxidation or the
secretion of PC in the bile, and to a lesser extent, by the intestinal mucosa. Choline
imbalances can be compensated by adaptive increases in PEMT activity, by
recycling of choline, decreased oxidation of choline, reabsorption of biliary
PC (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 young
child, and phospholipids in the brain increase two-fold in the cortex and
three-fold in the white matter from the 10th 482 week of gestation to the age
of two years. The studies have also shown that a relative continuous decrease
of choline phosphoglycerides, from 50% of total phospholipids in the cerebral
cortex of the fetus to 45% in 485 infants at term and 38% in children at two
years of age. In this study, SPM shows a continuous 486 increase, from 3% of
total phospholipids in the cerebral cortex of the fetus to 5% in infants at
term and 487 10% in children at two years of age 45.

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Phosphatidylethanolamine
(PE):  Phosphatidylethanolamine N-methyltransferase
(PEMT) activity in the diabetic mouse brain was determined as a possible marker
of demyelination. As animal models for diabetes mellitus, we used genetically
transmitted diabetic mice C57BL/KsJ-db/db, and streptozotocin induced diabetic
mice. Enzyme activity was much lower in the brains of these mice than in those
of developing and demyelinating mice but significantly higher than in normal
adult mouse brains 46.

Phosphatidylinositol (PI): Phospholipase C (PLCB1, PLCD1) is a critical enzyme that
integrates phosphoinositide metabolism with neurotransmission, hormonal, and
other signaling processes. PLC can be activated by G-protein mechanisms coupled
to muscarinic cholinergic M1,3,5, dopaminergic D2,3,4,
serotonergic 5-HT2A,C, and other post-synaptic neuroreceptors, or to
hormone receptors . PLC cleaves membrane PI(4,5)P2 to form two
important 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 reduced
content of ARA in PI and had deficits in cortical lamination during brain
development, delayed neuronal processes in the cortex, and reduced neurite
outgrowth in vitro. Mice died within a month and showed atrophy
of the cerebral cortex and hippocampus. These results demonstrate the
importance of ARA-containing PI in normal cortical development in mice. By
eliminating Lysophosphatidylinositol-acyltransferase-1 (LPIAT1)
in mice, the enzyme responsible for the incorporation of ARA into PI, it was
shown that the ARA-containing PI is essential for brain development in mammals
51. 

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