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Discovery Sheds Lights on Glucose Control, Metformin

Dysregulation of LKB1 pathway could contribute to diabetes and cancer

THURSDAY, Nov. 24 (HealthDay News) -- A signaling pathway in the liver plays a critical role in controlling metabolism and blood-glucose levels, and is needed for activation of the type 2 diabetes drug metformin, according to research published online in the Nov. 24 issue of Sciencexpress.

Reuben Shaw, Ph.D., of The Salk Institute in La Jolla, Calif., and colleagues studied mice that were engineered to lack the LKB1 enzyme, which is a known tumor suppressor, in the liver but nowhere else in the body.

LKB1-deficient mice had almost completely inactive adenosine monophosphate-activated protein kinase (AMPK), high blood-glucose levels and increased expression of genes encoding enzymes involved in generating glucose from non-carbohydrate sources and generating fat from non-fat foods. The researchers also found that metformin had no effect in lowering blood-glucose levels in the mice.

"These findings reinforce the emerging intimate relationship that exists between physiological control of metabolism and cancer," the authors write. "The mTOR, insulin, and LKB1 pathways represent a fundamental eukaryotic network governing cell growth in response to environmental nutrients. Dysregulation of each contributes to both diabetes and cancer."

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