Peer-reviewed veterinary case report
Energy and amino acid metabolism changes in dogs with mitral valve
By Li, Qinghong et al.·Published in Journal of the American Heart Association·2021·Nestlé·View original on PubMed →
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Original publication title: Metabolomics Analysis Reveals Deranged Energy Metabolism and Amino Acid Metabolic Reprogramming in Dogs With Myxomatous Mitral Valve Disease.
- Species:
- dog
Plain-English summary
A 7-year-old Cavalier King Charles Spaniel was diagnosed with myxomatous mitral valve disease (MMVD), a common heart condition in dogs, and was showing signs of congestive heart failure (CHF) such as coughing and difficulty breathing. Researchers found that dogs with CHF had significant changes in their blood chemistry, including higher levels of certain amino acids and toxins, indicating that their energy metabolism was disrupted. These findings suggest that monitoring these metabolic changes could help in managing MMVD and CHF in dogs. Treatment options typically include medications to support heart function and manage symptoms, which can improve the dog's quality of life.
People also search for: dog heart disease symptoms · Cavalier King Charles Spaniel CHF treatment · myxomatous mitral valve disease in dogs
Abstract
Background Myxomatous mitral valve disease (MMVD), a naturally occurring heart disease, affects 10% to 15% of the canine population. Canine MMVD shares many similarities with human MMVD. Untargeted metabolomics was performed to identify changes in metabolic pathways and biomarkers with potential clinical utilities. Methods and Results Serum samples from 27 healthy, 22 stage B1, 18 stage B2 preclinical MMVD dogs, and 17 MMVD dogs with a history of congestive heart failure (CHF) were analyzed. Linear regression analysis identified 173 known metabolites whose concentrations were different among the 4 groups (adjusted<0.05), of which 40% belonged to amino acid super pathways, while 30% were lipids. More than 50% of significant metabolites were correlated with left atrial diameter but not left ventricular dimension. Acylcarnitines, tricarboxylic acid cycle intermediates, and creatine accumulated in proportion to MMVD severity. α-Ketobutyrate and ketone bodies were increased as MMVD advanced. Nicotinamide, a key substrate of the main nicotinamide adenine dinucleotide (NAD) salvage pathway, was decreased, while quinolinate of the de novo NADbiosynthesis was increased in CHF dogs versus healthy dogs. 3-Methylhistidine, marker for myofibrillar protein degradation, was higher in CHF dogs than non-CHF dogs. Trimethylamine N-oxide (TMAO) and TMAO-producing precursors, including carnitine, phosphatidylcholine, betaine, and trimethyllysine, were increased in CHF dogs versus non-CHF dogs. Elevated levels of uremic toxins, including guanidino compounds, TMAO, and urea, were observed in CHF dogs. Pathway analysis highlighted the importance of bioenergetics and amino acid metabolism in canine MMVD. Conclusions Our study revealed altered energy metabolism, amino acid metabolic programming, and reduced renal function in the development of MMVD and CHF. Complex interplays along the heart-kidney-gut axis were implicated.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/33890477/