Loss of Lkb1 in adult β cells increases β cell mass and enhances glucose tolerance in mice

Fu, A. et al. (2009) Loss of Lkb1 in adult β cells increases β cell mass and enhances glucose tolerance in mice. Cell Metabolism, 10(4), pp. 285-295. (doi: 10.1016/j.cmet.2009.08.008)

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Publisher's URL: http://dx.doi.org/10.1016/j.cmet.2009.08.008


The Lkb1 tumor suppressor exerts its biological effects through phosphorylation and consequent activation of the AMP kinase (AMPK) family. Extensive genetic and biochemical evidence supports a role for Lkb1 in cell cycle arrest, establishment of cell polarity, and cellular energy metabolism. However, the role of Lkb1 and the AMPK family in β cell function in vivo has not been established. We generated conditional knockout mice with a deletion of the Lkb1 gene in the β cell compartment of pancreatic islets; these mice display improved glucose tolerance and protection against diet-induced hyperglycemia. Lkb1−/− β cells are hypertrophic because of elevated mTOR activity; they also proliferate more and secrete more insulin in response to glucose. These data indicate that inhibiting Lkb1 activity in β cells may facilitate β cell expansion and glucose tolerance in vivo.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Touyz, Professor Rhian
Authors: Fu, A., Ng, A.C., Depatie, C., Wijesekara, N., He, Y., Wang, G., Bardeesy, N., Scott, F.W., Touyz, R.M., Wheeler, M.B., and Screaton, R.A.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:Cell Metabolism
ISSN (Online):1932-7420
Published Online:06 October 2009

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