Deletion of LKB1 in adult β cells led to cellular hypertrophy (due to increased mTORC1 activity, secondary to inactivation of AMPK), increased β cell proliferation, dramatic alteration of β cell polarity (due to inactivation of MARK2), and increased glucose-stimulated insulin secretion, leading to accelerated clearance of glucose in vivo and to protection against high fat diet-induced glucose intolerance. This evidence concerns the gene STK11 and Glucose intolerance.