How p38δ Affects Insulin Secretion and Blood Sugar Levels
Author Information
Author(s): Sumara Grzegorz, Formentini Ivan, Collins Stephan, Sumara Izabela, Windak Renata, Bodenmiller Bernd, Ramracheya Reshma, Caille Dorothée, Jiang Huiping, Platt Kenneth A., Meda Paolo, Aebersold Rudolf, Rorsman Patrik, Ricci Romeo
Primary Institution: ETH Zurich
Hypothesis
Does the deletion of p38δ improve insulin secretion and glucose tolerance in mice?
Conclusion
Mice lacking p38δ show improved glucose tolerance and enhanced insulin secretion due to increased activity of protein kinase D (PKD).
Supporting Evidence
- Deletion of p38δ leads to enhanced insulin secretion from pancreatic β cells.
- p38δ null mice are protected against high-fat-feeding-induced insulin resistance.
- Inhibition of PKD1 reverses enhanced insulin secretion in p38δ-deficient islets.
- p38δ catalyzes an inhibitory phosphorylation of PKD1, affecting insulin secretion.
Takeaway
Scientists found that mice without a specific protein called p38δ can manage their blood sugar better because they release more insulin from their pancreas.
Methodology
The study involved generating p38δ null mice and assessing their glucose tolerance and insulin secretion through various tests.
Participant Demographics
The study involved male mice aged 8 weeks.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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