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Phosphatidylethanolamine methyltransferase activity in developing, demyelinating, and diabetic mouse brain
The Tohoku Journal of Experimental Medicine
|December 1, 1983
Summary
Phosphatidylethanolamine methyltransferase (PEMT) activity is elevated in actively myelinating and diabetic mouse brains, suggesting increased phosphatidylcholine synthesis is crucial for myelin repair and nerve function. Mecobalamin may supply essential methyl groups for this process.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Phosphatidylcholine (PC) is vital for cell membranes, including myelin.
- Phosphatidylethanolamine methyltransferase (PEMT) synthesizes PC via methylation of phosphatidylethanolamine.
- S-adenosylmethionine (AdoMet) serves as the methyl donor in this reaction.
Purpose of the Study:
- To investigate PEMT activity during active myelination and in diabetic mouse models.
- To explore the role of methyl group donors, such as mecobalamin, in brain PC synthesis.
Main Methods:
- Measurement of PEMT activity in microsome fractions of fetal, adult, and cuprizone-treated mouse brains.
- Analysis of PEMT activity in genetically diabetic (db/db) and streptozotocin-induced diabetic mice.
- Tracer studies using mecobalamin to track methyl group metabolism in brain slices.
Main Results:
- PEMT activity was significantly higher in actively myelinating fetal brains and during remyelination post-cuprizone treatment compared to normal adults.
- Diabetic mouse models exhibited elevated PEMT activity.
- Mecobalamin effectively transferred methyl groups for AdoMet synthesis, leading to choline and acetylcholine production in brain slices.
Conclusions:
- Increased PC synthesis, mediated by PEMT, is likely essential for myelin repair and maintaining nerve function in diabetic conditions.
- Mecobalamin may be a significant source of methyl groups for PC synthesis in the brain, particularly under metabolic stress.