ArticlePathoGenetics2009
Pancreatic islet expression profiling in diabetes-prone C57BLKS/J mice reveals transcriptional differences contributed by DBA loci, including Plagl1 and Nnt.
Article in PathoGenetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- Comparison of the characteristics of non-alcoholic fatty liver disease in C57BL/6J-LeprExperimental animals · 2025Article
- Gestational diabetes mellitus causes genome hyper-methylation of oocyte via increased EZH2.Nature communications · 2025Article
- Humanization of the mdx Mouse Phenotype for Duchenne Muscular Dystrophy Modeling: A Metabolic Perspective.Journal of neuromuscular diseases · 2023Review
- Metabolic differences and differentially expressed genes between C57BL/6J and C57BL/6N mice substrains.PloS one · 2022Article
- Increased glycolysis affects β-cell function and identity in aging and diabetes.Molecular metabolism · 2022Article
- Genome wide analysis of gene expression changes in skin from patients with type 2 diabetes.PloS one · 2020Article
- Article
- Attention to Background Strain Is Essential for Metabolic Research: C57BL/6 and the International Knockout Mouse Consortium.Diabetes · 2016Review
- Zac1 Regulates the Differentiation and Migration of Neocortical Neurons via Pac1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Vitamin E and vitamin C do not reduce insulin sensitivity but inhibit mitochondrial protein expression in exercising obese rats.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2015Article
- Similarity in Transcytosis of nNOSα in Enteric Nerve Terminals and Beta Cells of Pancreatic Islet.Frontiers in medicine · 2014Review
- Divergent compensatory responses to high-fat diet between C57BL6/J and C57BLKS/J inbred mouse strains.American journal of physiology. Endocrinology and metabolism · 2013Article
- Animal models of human genetic diseases: do they need to be faithful to be useful?Molecular genetics and genomics : MGG · 2011Review
- Synergy analysis reveals association between insulin signaling and desmoplakin expression in palmitate treated HepG2 cells.PloS one · 2011Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundC57BLKS/J (BLKS) mice are susceptible to islet exhaustion in insulin-resistant states as compared with C57BL6/J (B6) mice, as observed by the presence of the leptin receptor (Lepr) allele, Leprdb/db. Furthermore, DBA2/J (DBA) mice are also susceptible to beta-cell failure and share 25% of their genome with BLKS; thus the DBA genome may contribute to beta-cell dysfunction in BLKS mice.
resultsHere we show that BLKS mice exhibit elevated insulin secretion, as evidenced by improved glucose tolerance and increased islet insulin secretion compared with B6 mice, and describe interstrain transcriptional differences in glucose response. Transcriptional differences between BLKS and B6 mice were identified by expression profiling of isolated islets from both strains. Genomic mapping of gene expression differences demonstrated a significant association of expression differences with DBA loci in BLKS mice (P = 4x10-27).
conclusionTwo genes, Nicotinamide nucleotide transhydrogenase (Nnt) and Pleiomorphic adenoma gene like 1 (Plagl1), were 4 and 7.2-fold higher respectively in BLKS islets, and may be major contributors to increased insulin secretion by BLKS islets. Contrary to reports for B6 mice, BLKS mice do not harbor a mutant Nnt gene. We detected 16 synonymous polymorphisms and a two-amino acid deletion in the Plagl1 gene in BLKS mice. Several inflammatory glucose-responsive genes are expressed at a higher level in BLKS, suggesting an inflammatory component to BLKS islet dysfunction. This study describes physiological differences between BLKS and B6 mice, and provides evidence for a causative role of the DBA genome in beta-cell dysfunction in BLKS mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.