Peer-reviewed veterinary case report
Gene study on pancreatic atrophy causing digestion issues in German
By Clark, Leigh Anne et al.·Published in Mammalian genome : official journal of the International Mammalian Genome Society·2005·Department of Pathobiology, United States·View original on PubMed →
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Original publication title: Linkage analysis and gene expression profile of pancreatic acinar atrophy in the German Shepherd Dog.
- Species:
- dog
Plain-English summary
A German Shepherd dog with pancreatic acinar atrophy (PAA) was found to have a genetic issue affecting its pancreas, leading to problems digesting food. This condition is the most common cause of exocrine pancreatic insufficiency in this breed. Researchers identified a specific gene that may be linked to this disease, but they did not find a mutation that directly causes PAA. Understanding this genetic link could help in developing better treatments or management strategies for affected dogs in the future.
People also search for: German Shepherd pancreatic disease · dog digestive problems · exocrine pancreatic insufficiency treatment
Abstract
Pancreatic acinar atrophy (PAA) is a degenerative disease of the exocrine pancreas and is the most common cause of exocrine pancreatic insufficiency in the German Shepherd Dog. Analyses of inheritance have shown that a single gene segregating in an autosomal recessive fashion is causative for PAA. To date the gene and causative mutation have not been determined. To identify a region of interest and/or candidate genes, we conducted linkage and gene expression studies. Analysis of 384 microsatellite markers resulted in a maximum two-point LOD score of 2.5 for FH2107 on CFA03. We used an oligonucleotide array to generate gene expression profiles for normal and affected pancreata. It revealed 244 genes with greater than two-fold difference in expression levels. Five genes of interest were further assessed by TaqMan quantitative real-time RT-PCR that confirmed trends observed using the microarray. One gene, gp25L, located on CFA03, was found to be downregulated by more than 500-fold in affected pancreata and was further investigated as a candidate gene. Sequence data did not reveal a mutation in the coding sequence that segregates with PAA.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/16341675/