Omega-3 could improve phospholipid deterioration observed in autism
Abnormal metabolism of phospholipids is a major component in many neurodevelopmental disorders, including autism. Concentrations of propionic acid, or propanoic acid (a short-chain fatty acid produced in the intestine as a metabolite of Clostridium difficile spp.) are higher in the stools of individuals with autism than in their control peers. In rodents, oral administration of this acid produces behavioural abnormalities (deterioration in social interaction, hyperactivity and repetitive behaviours) and biochemical, physiological and histopathological characteristics (oxidative stress, neuroinflammation, neurochemical and metabolic lipid alterations, neuron loss and astrogliosis) similar to those observed in autism. For this reason they can be used as a model for understanding altered fatty acid metabolism in autism.
In a study designed to investigate alterations to phospholipid metabolism in the brain using a rat autism model and to explore possible beneficial effects of omega-3 fatty acids (ω-3 FA) and vitamin B12, five groups of rats were defined: 1) control; 2) rat autism model (rats treated with a neurotoxic dose of propionic acid for three days; 3) rats treated with a neurotoxic dose of propionic acid who subsequently received vitamin B12 for 30 days; 4) rats treated with a neurotoxic dose of propionic acid who were subsequently treated with ω-3 FA for 30 days; and 5) rats treated with a neurotoxic dose of propionic acid who subsequently received ω-3 FA and vitamin B12 for 30 days.
Concentrations of phospholipids, phospholipase A2 and cytosolic phospholipase A2 were measured in the homogenised brain of all groups: a reduction in phospholipid concentrations and a significant increase in cytosolic phospholipase A2 were observed in all groups; however, both ω-3 FA and vitamin B12 were effective in reducing the neurotoxic effect of propionic acid.
The authors concluded that both ω-3 FA and vitamin B12, separately or combined, could play a role in improving phospholipid deterioration observed in autism.