Peer-reviewed veterinary case report
Gene changes in Miniature Schnauzers with high blood fat suggest clot
By Baker, Lauren A et al.·Published in PloS one·2024·Department of Animal and Dairy Sciences, United States·View original on PubMed →
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Original publication title: Whole blood gene expression analysis of spontaneous hypertriglyceridemia in dogs suggests an underlying pro-thrombotic process.
- Species:
- dog
Plain-English summary
A group of Miniature Schnauzers was studied for high triglyceride levels (hypertriglyceridemia), a condition that can lead to serious health issues. Researchers found that these dogs had changes in certain genes that suggest they might be at risk for blood clots and other complications. The findings indicate that the genetic factors causing high triglycerides in these dogs are similar to those seen in humans with metabolic syndrome. Understanding this could help in managing the health of affected dogs and potentially lead to better treatments.
People also search for: Miniature Schnauzer high triglycerides treatment · dog hypertriglyceridemia symptoms · genetic factors in dog health
Abstract
Hypertriglyceridemia (HTG) is influenced by multiple genetic and environmental factors. Spontaneous, idiopathic HTG is common in the Miniature Schnauzer dog and presumed to have a strong genetic influence in this breed. To define genes that are differentially expressed in dogs with HTG, we performed RNA sequencing on peripheral blood of 13 Miniature Schnauzers with HTG and 18 controls. We identified 110 differentially expressed genes (DEGs). Pathway analysis suggests an ongoing pro-thrombotic, endothelial activation process in dogs with HTG. The gene with the largest fold change (5.4 ± 1.4, Padj = 4.4E-04), SERPINE1, encodes plasminogen activator inhibitor 1 (PAI-1), a known risk factor for atherosclerosis and thrombosis. Other top DEGs, including SHANK3, MMRN1, and FZD7, are involved in endothelial activation. Two of the top DEGs, ARHGAP29 and ARHGAP21, inhibit pro-thrombotic pathways and are potentially protective of disease sequelae. Top DEGs, including SERPINE1 and ARHGAP21, have also been linked to metabolic syndrome or its features (e.g. insulin resistance) in humans and animal models. Our findings indicate that HTG in the Miniature Schnauzer dog has similar features to HTG and metabolic syndrome in humans, highlighting the potential use of the dog as a spontaneous model for further research into the etiology and effects of HTG.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/39531449/