Peer-reviewed veterinary case report
Metabolic changes in dogs with epilepsy on ketogenic MCT diet
By Law, Tsz Hong et al.·Published in The British journal of nutrition·2018·Royal Veterinary College, United Kingdom·View original on PubMed →
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Original publication title: Metabolic perturbations associated with the consumption of a ketogenic medium-chain TAG diet in dogs with idiopathic epilepsy.
- Species:
- dog
Plain-English summary
A group of dogs with idiopathic epilepsy (seizures with no known cause) was given a special diet high in medium-chain triglycerides (MCT) to see if it would help manage their condition. The dogs showed significant changes in their blood chemistry, indicating that the MCT diet affected their metabolism. Specifically, certain fatty acids were found in different amounts compared to when they were on a regular diet. This suggests that the MCT diet may have neuroprotective effects, potentially helping to improve seizure control in these dogs. Further research is needed to understand how these metabolic changes can enhance dietary treatments for epilepsy.
People also search for: dog epilepsy diet · ketogenic diet for dogs with seizures · medium-chain triglycerides for dog seizures
Abstract
Consumption of diets containing medium-chain TAG (MCT) has been shown to confer neuroprotective effects. We aim to identify the global metabolic perturbations associated with consumption of a ketogenic diet (medium-chain TAG diet (MCTD)) in dogs with idiopathic epilepsy. We used ultra-performance liquid chromatography-MS (UPLC-MS) to generate metabolic and lipidomic profiles of fasted canine serum and made comparisons between the MCTD and standardised placebo diet phases. We identified metabolites that differed significantly between diet phases using metabolite fragmentation profiles generated by tandem MS (UPLC-MS/MS). Consumption of the MCTD resulted in significant differences in serum metabolic profiles when compared with the placebo diet, where sixteen altered lipid metabolites were identified. Consumption of the MCTD resulted in reduced abundances of palmitoylcarnitine, octadecenoylcarnitine, stearoylcarnitine and significant changes, both reduced and increased abundances, of phosphatidylcholine (PC) metabolites. There was a significant increase in abundance of the saturated C17 : 0 fatty acyl moieties during the MCTD phase. Lysophosphatidylcholine (17 : 0) (P=0·01) and PC (17:0/20:4) (P=0·03) were both significantly higher in abundance during the MCTD. The data presented in this study highlight global changes in lipid metabolism, and, of particular interest, in the C17 : 0 moieties, as a result of MCT consumption. Elucidating the global metabolic response of MCT consumption will not only improve the administration of current ketogenic diets for neurological disease models but also provides new avenues for research to develop better diet therapies with improved neuroprotective efficacies. Future studies should clarify the involvement and importance of C17 : 0 moieties in endogenous MCT metabolic pathways.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/30001753/