Pancreatic Neuroendocrine Tumors in Mice Lacking Glucagon Receptor
Author Information
Author(s): Yu Run, Dhall Deepti, Nissen Nicholas N., Zhou Cuiqi, Ren Song-Guang
Primary Institution: Cedars-Sinai Medical Center
Hypothesis
Defective glucagon signaling causes pancreatic neuroendocrine tumors (PNETs).
Conclusion
Defective glucagon signaling leads to the development of PNETs in Gcgr−/− mice, suggesting that complete inhibition of glucagon signaling may not be a safe approach to treat diabetes.
Supporting Evidence
- At 10–12 months, gross PNETs were detected in most Gcgr−/− pancreata.
- Normal islet morphology was observed in control mice, while Gcgr−/− mice showed dysplastic islets.
- Most PNETs in Gcgr−/− mice were glucagonomas.
Takeaway
Mice without a glucagon receptor develop tumors in their pancreas as they get older, which might happen in humans too if glucagon signaling is completely blocked.
Methodology
The study involved examining the pancreata of glucagon receptor-deficient mice over time to assess tumor development and related morphological changes.
Limitations
The study primarily focuses on a specific mouse model, which may not fully replicate human conditions.
Statistical Information
P-Value
p<0.001
Statistical Significance
p<0.001
Digital Object Identifier (DOI)
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