Different choline supplement metabolism in adults using deuterium labelling

Area of Science:

• Nutritional Science
• Biochemistry
• Human Metabolism

Background:

• Choline deficiency causes liver, brain, and lung pathologies.
• Adequate choline is crucial for preterm infants and cystic fibrosis patients.
• This study investigates four deuterium-labeled (D9-) choline supplements administered enterally in adults.

Purpose of the Study:

• To analyze the assimilation of four different enterally administered deuterium-labeled (D9-) choline supplements in adults.
• To compare the bioavailability and metabolic fate of D9-choline chloride, D9-phosphorylcholine, D9-alpha-glycerophosphocholine (D9-GPC), and D9-1-palmitoyl-2-oleoyl-glycero-3-phosphoryl-choline (D9-POPC).
• To assess the impact of different choline formulations on plasma choline metabolites and trimethylamine N-oxide (TMAO) formation.

Main Methods:

• A prospective randomized cross-over study involving six healthy men.
• Administration of four single doses of D9-choline supplements (2.7 mg/kg) in a randomized order, 6 weeks apart.
• Plasma analysis via tandem mass spectrometry for D9-choline and its metabolites from 0.1 hours to 7 days post-intake.

Main Results:

• D9-POPC administration resulted in the latest peak concentrations of D9-choline and D9-betaine.
• D9-POPC and D9-phosphorylcholine led to significantly lower D9-trimethylamine (D9-TMAO) formation.
• The highest area under the curve (AUC) for plasma D9-phosphatidylcholine (D9-PC) was observed after D9-POPC administration, indicating efficient incorporation into PC following fatty acid remodeling.

Conclusions:

• D9-POPC supplementation results in a delayed but sustained increase in plasma D9-choline and D9-betaine, with a higher AUC for D9-PC.
• D9-POPC is remodeled based on enterocytic fatty acid availability, suggesting it can deliver specific fatty acids along with choline.
• D9-POPC is the most suitable choline supplement for increasing plasma PC concentrations, offering targeted fatty acid supply to organs with minimal TMAO production.