Methionine-choline deprivation alters liver and brain acetylcholinesterase activity in C57BL6 mice

Abstract

Choline and methionine are precursors of acetylcholine, whose hydrolysis is catalyzed by acetylcholinesterase (AChE). Considering the possibility of their common deficiency, we investigated the influence of methionine-choline deprivation on AChE activity in liver and various brain regions (hypothalamus, hippocampus, cerebral cortex and striatum) in mice fed with methionine-choline deficient (MCD) diet. Male C57BL/6 mice (n = 28) were randomly and equally divided into following groups: control group fed with standard diet for 6 weeks (C) and groups fed with MCD diet for 2 weeks (MCD2), 4 weeks (MCD4) and for 6 weeks (MCD6). After the diet, mice were sacrificied and AChE activity in liver and brain was determined spectrophotometrically. Hepatic AChE activity was higher in MCD2, MCD4 and MCD6 compared to control (p < 0.01), with most prominent increase in MCD6. AChE activity in hypothalamus was higher in MCD4 and MCD6 vs. control (p < 0.05 and p < 0.01, respectively), as well as in MCD6 compared to MCD4 (p < 0.01). In hippocampus, increase in AChE activity was shown in MCD6 compared to control (p < 0.01). In cortex and striatum, increase in AChE activity was noted in MCD6 compared to control (p < 0.05). Our findings indicate the increase of hepatic and brain AChE activity in mice caused by methionine-choline deprivation.

Cerebrolysin Use in Patients with Liver Damage—A Translational Study

“…The main drawback of the MCD diet model is that mice develop a different metabolic profile than humans [11,12]. Another drawback of the model is that many cellular metabolisms rely on methionine and choline [13,14] and, as such, can interfere with basic molecular findings. For example, methionine is an essential amino acid involved in various processes such as cellular growth and development and protein and enzyme synthesis [13].…”

Circulating choline pathway nutrients and risk of moyamoya disease

“…Second, choline and betaine are important sources of 1-carbon units ( 11 , 13 , 16 ), when choline stores are inadequate, methylation of Hcy to methionine is decreased resulting in increased Hcy, and increased Hcy has been related to greater risk of MMD ( 9 ). Additionally, choline deficiency increases the activity of acetylcholinesterase ( 21 ), and serum cholinesterase activities reflect the intensity of the neuroinflammatory response in patients with stroke ( 22 ). Moreover, choline and betaine are metabolites of the choline pathway associated with decreased cardiovascular risks and recurrent strokes ( 23 , 24 ).…”

Untargeted metabolomics analysis of rat hippocampus subjected to sleep fragmentation

“…In addition, J o u r n a l P r e -p r o o f 15 methionine is an acetylcholine precursor. Acetylcholinesterase (AChE) activity, a crucial enzyme that hydrolyzes acetylcholine, was increased in hippocampi of mice subjected to dietary restriction of methionine (Vucevic et al, 2016). Because methionine is an acetylcholine precursor and its deficiency resulted in increased activation of AChE, a decrease in methionine level in the hippocampus of rats subjected to SF may indicate the impaired status of cholinergic neurotransmission in hippocampus subjected to long-term SF.…”