Metformin abolishes increased tumor (18)F-2-fluoro-2-deoxy-D-glucose uptake associated with a high energy diet

Cell Cycle. 2011 Aug 15;10(16):2770-8. doi: 10.4161/cc.10.16.16219. Epub 2011 Aug 15.

Abstract

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 ( 18) F-2-Fluoro-2-Deoxy-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 abolished the diet-induced increases in serum insulin level, tumor insulin receptor activation and tumor FDG uptake associated with the high energy diet but had no effect on these measurements in mice on a control diet. These findings provide the first functional imaging correlate of the well-known adverse effect of caloric excess on cancer outcome. They demonstrate that, for a subset of neoplasms, diet and insulin are variables that affect tumor FDG uptake and have implications for design of clinical trials of metformin as an antineoplastic agent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animal Feed
  • Animals
  • Antineoplastic Agents / pharmacology
  • Blood Glucose / drug effects
  • Cell Line, Tumor
  • Cell Proliferation
  • Colonic Neoplasms / metabolism
  • Fluorine Radioisotopes / analysis
  • Fluorodeoxyglucose F18 / metabolism*
  • Glucose / metabolism
  • Hyperinsulinism / chemically induced
  • Insulin / blood*
  • Insulin / pharmacology
  • Metformin / pharmacology*
  • Mice
  • Mice, Inbred C57BL
  • Positron-Emission Tomography
  • Receptor, Insulin / metabolism
  • Signal Transduction

Substances

  • Antineoplastic Agents
  • Blood Glucose
  • Fluorine Radioisotopes
  • Insulin
  • Fluorodeoxyglucose F18
  • Metformin
  • Receptor, Insulin
  • Glucose