Gene Expression Differences in Diabetes-Prone Mice
Author Information
Author(s): Anderson Abraham A, Helmering Joan, Juan Todd, Li Chi-Ming, McCormick Jocelyn, Graham Melissa, Baker Daniel M, Damore Michael A, Véniant Murielle M, Lloyd David J
Primary Institution: Amgen Inc.
Hypothesis
The DBA genome contributes to islet dysfunction in diabetes-prone C57BLKS/J mice.
Conclusion
The study identifies significant transcriptional differences in islet function between BLKS and B6 mice, suggesting a role for DBA loci in β-cell dysfunction.
Supporting Evidence
- BLKS mice showed elevated insulin secretion compared to B6 mice.
- Transcriptional differences were linked to DBA loci.
- Plagl1 and Nnt were significantly higher in BLKS islets.
- Inflammatory gene expression was higher in BLKS mice.
- Islet dysfunction in BLKS mice was associated with DBA genetic contributions.
Takeaway
This study looked at how certain genes in mice that are prone to diabetes work differently than in other mice, which helps us understand diabetes better.
Methodology
The study involved gene expression profiling of isolated islets from BLKS and B6 mice under different glucose conditions.
Limitations
The study primarily focuses on two mouse strains and may not generalize to other models of diabetes.
Participant Demographics
The study used male mice aged 12 weeks.
Statistical Information
P-Value
4×10-27
Statistical Significance
p<0.001
Digital Object Identifier (DOI)
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