AMPK as a metabolic tumor suppressor: control of metabolism and cell growth.
Background Hyperinsulinemia, hyperglycemia, and obesity have been identified as risk factors for a variety of cancers . Insulin inhibition (INSINH) can potentially limit cancer growth by factors including ketosis , and apoptosis secondary to fatty acid synthase inhibition  as well as intracellular potassium depletion . Furthermore, dysregulation of many signaling proteins downstream of the insulin/IGF receptors such as PI3K/Akt, mTOR (inhibition) and AMPK (amplification) is a major area of drug target development [5,6]. We performed a four week INSINH diet in patients with advanced cancers to study safety/feasibility and also to examine a change inF-2-fluoro, 2-deoxyglucose (FDG) uptake on PET scan as a surrogate measure for tumor response.