Loss of LKB1 in Beta Cells Enhances Glucose-Stimulated Insulin Secretion Despite Profound Mitochondrial Defects

Background: LKB1 regulates multiple aspects of pancreatic ß cell biology.

Results: LKB1 loss in ß cells leads to profound mitochondrial defects yet increases glucose-stimulated insulin secretion in a mitochondria-independent mechanism.

Conclusion: LKB1 is essential for mitochondrial maintenance and negatively regulates a distal step of insulin secretion.

Significance: LKB1 loss exposes powerful mechanisms of insulin secretion that can override defects in the classic triggering pathway.

A Swisa & etc. (2015). Loss of LKB1 in Beta Cells Enhances Glucose-Stimulated Insulin Secretion Despite Profound Mitochondrial Defects. JBC, doi:10.1074/jbc.M115.639237