Metabolic perturbations associated with the consumption of a ketogenic medium-chain TAG diet in dogs with idiopathic epilepsy

被引:0
作者
Law, Tsz Hong [1 ,2 ]
Volk, Holger A. [1 ]
Pan, Yuanlong [3 ]
Zanghi, Brian [3 ]
Want, Elizabeth J. [2 ]
机构
[1] Royal Vet Coll, Dept Clin Sci & Serv, Hatfield AL9 7TA, Herts, England
[2] Imperial Coll, Div Integrat Syst Med & Digest Dis, London SW7 2AZ, England
[3] Nestle Purina Res, One Checkerboard Sq, St Louis, MO 63164 USA
基金
英国生物技术与生命科学研究理事会;
关键词
Ketogenic diets; Medium-chain TAG; Metabolic profiling; Odd-chain fatty acids; FATTY-ACIDS; SEIZURE CONTROL; REFRACTORY EPILEPSY; CANINE EPILEPSY; TRIGLYCERIDES; TRIHEPTANOIN; MODEL; MECHANISMS; PREVENTION; DISORDERS;
D O I
10.1017/S0007114518001617
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Consumption of diets containing medium-chain TAG (IvICT) has been shown to confer neuroprotective effects. We aim to identify the global metabolic pemirbations 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 MCID 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 palmitoylcamitine, octadecenoylcamitine, stearoylcamitine 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 'WAD 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.
引用
收藏
页码:484 / 490
页数:7
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