RasGAP-Derived Fragment N Increases the Resistance of Beta Cells towards Apoptosis in NOD Mice and Delays the Progression from Mild to Overt Diabetes
2011

Fragment N Protects Beta Cells in Diabetic Mice

Sample size: 44 publication 10 minutes Evidence: moderate

Author Information

Author(s): Bulat Natasa, Jaccard Evrim, Peltzer Nieves, Khalil Hadi, Yang Jiang-Yan, Dubuis Gilles, Widmann Christian

Primary Institution: University of Lausanne, Lausanne, Switzerland

Hypothesis

Does fragment N provide a protective role against apoptosis in beta cells during the development of type 1 diabetes?

Conclusion

Fragment N significantly increases the time that NOD-RIPN mice can remain free of overt diabetes once they start to lose their ability to maintain normal blood sugar levels.

Supporting Evidence

  • Islets from NOD-RIPN mice were more resistant to apoptosis than control NOD islets.
  • NOD-RIPN mice maintained a longer period of normo-glycemia compared to control NOD mice.
  • Fragment N did not affect the extent of immune cell infiltration in the islets.

Takeaway

Researchers found that a special protein called fragment N helps protect insulin-producing cells in mice from dying, which can delay diabetes.

Methodology

The study involved creating a transgenic mouse model (NOD-RIPN) and assessing the effects of fragment N on beta cell apoptosis and diabetes progression through various experimental techniques.

Limitations

Fragment N was expressed in only about 40% of beta cells, which may limit its overall protective effect.

Participant Demographics

NOD mice, both male and female, were used in the study.

Statistical Information

P-Value

p<0.05

Confidence Interval

95% CI

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0022609

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