Lipid Composition of the Brain in the Vitamin B₁₂‐Deficient Fruit Bat (Rousettus aegyptiacus) with Neurological Impairment

Abstract

The Egyptian fruit bat Rouseitus aegyptiacus develops severe vitamin BIZ deficiency when fed a diet of fresh peeled fruit and water. In a group of bats fed this diet, B,, concentrations in the serum and brain were low, and neurological impairment, evidenced by deficient or absent hindlimb groping or grasping ability and climbing difficulties, was manifest. Control bats fed the identical diet supplemented with BIZ showed no such changes. Fatty acid analysis of whole brain homogenates showed a higher level of 2 0 4 in the deficient group. Phosphatidylcholine showed a marginally higher percentage of 18:3. The total percentage of branched chain fatty acids of phosphatidylethanolamine was four times higher in deficient brains, comprising 2% of the total. Sphingomyelin showed a slightly higher percentage of 1S:O, and a significantly lower percentage of long chain fatty acids C-24 and longer (p < 0.01). The compositions of nonhydroxy fatty acids in cerebroside were unchanged. Examination of phospholipids showed that 8.9 ? 0.4% of total phosphorus was present as sphingomyelin in deficient bats, compared with 11.9 5 1.2% in control animals (p < 0.05). There were no statistically significant differences in the concentrations of total brain lipid, protein, phospholipid, glycosphingolipid, cholesterol and plasmalogen between B,,-deficient and control bats. Key Words: Lipids-Myelin-Brain-Fatty acids-Fruit bats-Vitamin B,,. van der Westhuyzen J. et al. Lipid composition of the brain in the vitamin B,,-deficient fruit bat (Rousettus aegyptiacus) with neurological impairment. Abbreviutions used: BHT, 2.6-di-rerr-Butyl-4-methylphenol; MMA-CoA, Methylmalonyl coenzyme A .

Nitrous oxide-induced B12 deficiency myelopathy: Perspectives on the clinical biochemistry of vitamin B12

“…Mainly, there is no compelling evidence of a constant finding of increased odd chain and branched chain fatty acids in the neural tissues of animals with B 12 deficiency myelopathy. For example, in the fruit bat model, while there is decreased activity of MMCoAM and an increase in serum and urine methylmalonic acid, there are no significant differences in the brain or spinal cord lipid profiles in either odd chain or branched chain fatty acids [12,[30][31][32]. Additionally, further study of human data provides strong evidence against the AdoB 12 -MMCoAM hypothesis.…”

Local Cerebral Glucose Utilization in Two Models of B12 Deficiency

“…has been until recently the only method that permitted production of the neurological and histopathological sequelae of BI2 deficiency (Agamanolis et al, 1976;Fehling et al, 1978;van der Westhuyzen et al, Prolonged dietary deprivation of vitamin B 1981). Much shorter exposure to nitrous oxide hastens this process considerably.…”

“…Production of an animal model of vitamin B12 deficiency through dietary deprivation requires lengthy preparation. Rats bred from vitamin BIZdepleted dams develop neurological signs only after 7 months on a B,,-deficient diet (Fehling et al, 1978), whereas the Egyptian fruit bat develops vitamin B,, deficiency and neurological impairment following 285-560 days of dietary deprivation of vitamin B,, (van der Westhuyzen et al, 1981). The monkey requires 4 years on a deficient diet to develop neurological manifestations and demyelinating lesions of the CNS (Agamanolis et al, 1976).…”

Adaptive Evolution of the Myo6 Gene in Old World Fruit Bats (Family: Pteropodidae)

“…Besides, fruits are also lacking many essential vitamins, especially fat-soluble vitamins such as vitamin D and vitamin B 12 [39]. Captive pteropodids fed on fruit-only diets show nutrient deficiencies and even neurological impairment caused by vitamin B 12 deficiency [40], [41]. Hence, how Old World fruit bats subsist on diets with low contents of protein and essential nutrients has long been of interest, and earlier studies focusing on behavior and physiology revealed some clues [42], [43], [44].…”