Metformin Abolishes Increased Tumor FDG Uptake Associated With a High-Energy Diet

Insulin regulates glucose uptake by normal tissues. Although there is evidence that certain cancers are growth‐stimulated by insulin, the possibility that insulin influences tumor glucose uptake as assessed by 18F‐2‐Deoxy‐2‐Fluoro‐D‐Glucose Positron Emission Tomography (FDG‐PET) has not been studied in detail. We present a model of diet‐induced hyperinsulinemia associated with increased insulin receptor activation in neoplastic tissue, and with increased tumor FDG‐PET image intensity. Metformin, which has been associated with reduced cancer burden among diabetics, abolished the increase in insulin levels, tumor insulin receptor activation, and FDG‐PET signal associated with the high‐energy diet, but had no effect on these measurements in mice on a control diet. These findings suggest that for a subset of neoplasms, diet and insulin are variables that affect tumor FDG‐PET results, and have implications for design of clinical trials of metformin as an anti‐neoplastic agent.