Targeting Glucose Metabolism May Help Treat ADPKD.

Researchers have found that defective glucose metabolism is involved in the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD), and that inhibiting glycolysis with 2-deoxyglucose in a mouse model of the disease leads to lower kidney weight, volume, cystic index, and proliferation rates. The defective glucose metabolism linked with ADPKD depends on the extracellular signal-related kinase pathway acting in a dual manner by inhibiting the liver kinase B1–AMP-activated protein kinase axis while activating the mTOR complex 1-glycolytic cascade. The Nature Medicine findings indicate that targeting defective glucose metabolism may be an effective therapeutic strategy against ADPKD.