Tissue acylcarnitine status in a mouse model of mitochondrial β-oxidation deficiency during metabolic decompensation due to influenza virus infection

Molecular Genetics and Metabolism
Tatiana N TarasenkoPeter J McGuire

Abstract

Despite judicious monitoring and care, patients with fatty acid oxidation disorders may experience metabolic decompensation due to infection which may result in rhabdomyolysis, cardiomyopathy, hypoglycemia and liver dysfunction and failure. Since clinical studies on metabolic decompensation are dangerous, we employed a preclinical model of metabolic decompensation due to infection. By infecting mice with mouse adapted influenza and using a pair-feeding strategy in a mouse model of long-chain fatty acid oxidation (Acadvl-/-), our goals were to isolate the effects of infection on tissue acylcarnitines and determine how they relate to their plasma counterparts. Applying statistical data reduction techniques (Partial Least Squares-Discriminant Analysis), we were able to identify critical acylcarnitines that were driving differentiation of our experimental groups for all the tissues studied. While plasma displayed increases in metabolites directly related to mouse VLCAD deficiency (e.g. C16 and C18), organs like the heart, muscle and liver also showed involvement of alternative pathways (e.g. medium-chain FAO and ketogenesis), suggesting adaptive measures. Matched correlation analyses showed strong correlations (r > 0.7) between pla...Continue Reading

Citations

May 6, 2019·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·Tatyana N TarasenkoPeter J McGuire
Apr 1, 2020·Journal of Agricultural and Food Chemistry·Grzegorz ZwierzchowskiBurim N Ametaj
Aug 17, 2021·Brain Communications·Kwangsik NhoUNKNOWN Alzheimer’s Disease Neuroimaging Initiative and on behalf of the Alzheimer Disease Metabolomics Consortium
Aug 17, 2021·Frontiers in Molecular Biosciences·Szymon MacioszekMichał J Markuszewski

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