Methylmalonic acid metabolism and nervous-system fatty acids in cobalamin-deficient fruit bats receiving supplements of methionine, valine and isoleucine.

Cobalamin neuropathy was produced in Cape fruit bats (Rousettus aegyptiacus) by a cobalamin-free diet combined with intermittent exposure to nitrous oxide, which inactivates cobalamin. Cobalamin-deficient bats had low hepatic methylmalonyl-CoA mutase holoenzyme activity, with elevated plasma and urinary methylmalonic acid levels. No significant changes could be demonstrated in the concentration of odd- or branched-chain fatty acids in the nervous system.

Cobalamin neuropathy. Is S-adenosylhomocysteine toxicity a factor?

Cobalamin neuropathy was produced in cape fruit bats (Rousettus aegyptiacus) by a cobalamin-free diet combined with intermittent exposure to nitrous oxide, which inactivates cobalamin. There were no significant differences in S-adenosylmethionine/S-adenosylhomocysteine ratios in the central nervous system of cobalamin-deficient and cobalamin-replete bats. Taken with other data there are no grounds of support for a hypothesis that cobalamin neuropathy is the result of impaired methylation, however produced.

Both valine and isoleucine supplementation delay the development of neurological impairment in vitamin B12 deficient bats.

Supplementation of the diet with valine or isoleucine protects the fruit bat from neurological impairment associated with experimentally induced vitamin B12 deficiency. Valine and isoleucine are precursors in the vitamin B12 dependent propionic acid pathway and it is proposed that they exert their protective effect through stimulation of this pathway. This suggests that the previously observed protective effect of methionine may be mediated also through this pathway, since methionine may be metabolised via the transsulfuration pathway to propionyl CoA.

Demyelinisation in the spinal cord of vitamin B12 deficient fruit bats.

1. Vitamin B12 deficiency induced in the fruit bat by a combination of dietary deprivation and exposure to nitrous oxide (N2O) is accompanied by profound neurological impairment, thus providing an experimental model for the study of vitamin B12 neuropathy. 2.