Betaine delays the onset of neurological impairment in nitrous oxide-induced vitamin B-12 deficiency in fruit bats.
The mechanism whereby vitamin B-12 deficiency leads to neurological changes in humans is still uncertain. Nitrous oxide (N2O), which inactivates vitamin B-12 in vivo, results in neurological impairment leading to ataxia and death in the fruit bat Rousettus . These changes were prevented by the injection of the vitamin. The effect of dietary betaine (a catalytic product of choline) or methionine supplementation was studied in bats exposed to N2O. Supplementation with betaine resulted in less weight loss and delayed onset of neurological impairment when compared with unsupplemented animals. Supplementation with methionine at similar concentrations (600 mg/kg fruit and 2 g/kg fruit) was more effective in preventing weight loss and delaying the onset of neurological impairment than the corresponding levels of betaine. These results suggest that dietary betaine was effective in increasing that part of methionine synthesis that is not dependent on vitamin B-12 in N2O-exposed bats with impairment of the vitamin B-12-dependent methionine synthase reaction.
D000818:Animals; D001259:Ataxia / Q000139:chemically induced / Q000517:prevention & control*; D001622:Betaine / Q000494:pharmacology*; D001835:Body Weight; D002685:Chiroptera / Q000502:physiology*; D004032:Diet; D006710:Homocysteine / Q000097:blood; D008715:Methionine / Q000097:blood / Q000494:pharmacology; D009609:Nitrous Oxide; D014806:Vitamin B 12 Deficiency / Q000139:chemically induced / Q000503:physiopathology*
D006710:Homocysteine; D001622:Betaine; D008715:Methionine; D009609:Nitrous Oxide