Increased energy expenditure and insulin sensitivity in the high bone mass DeltaFosB transgenic mice.

Academic Article

Abstract

  • Obesity and osteoporosis are major health issues affecting millions of individuals. Transgenic mice overexpressing DeltaFosB, an activator protein-1 transcription factor, under the control of the enolase 2 (ENO2) promoter exhibit both an increase in bone density and a decrease in adipose mass. Here we demonstrate that DeltaFosB overexpression increases fatty-acid oxidation and energy expenditure, leading to a decrease in adipocyte size and adipose mass. In addition, the ENO2-DeltaFosB mice exhibit increased insulin sensitivity and glucose tolerance. Targeted overexpression of DeltaFosB in adipocytes using the adipocyte protein 2 promoter failed to induce changes in fat or in bone, showing that the effect on metabolic activity is not due to cell-autonomous effects of DeltaFosB within adipocytes. Detailed analysis of the ENO2-DeltaFosB mice demonstrated that energy expenditure was increased in muscle, independent of locomotor activity. These findings provide evidence that signaling downstream of DeltaFosB is a potential target for not only osteoporosis but also obesity and diabetes.
  • Authors

    Keywords

  • Animals, Bone Density, Energy Intake, Energy Metabolism, Fatty Acids, Insulin, Mice, Mice, Transgenic, Obesity, Organ Size, Osteocalcin, Phosphopyruvate Hydratase, Polymerase Chain Reaction, Proto-Oncogene Proteins c-fos
  • Digital Object Identifier (doi)

    Author List

  • Rowe GC; Choi CS; Neff L; Horne WC; Shulman GI; Baron R
  • Start Page

  • 135
  • End Page

  • 143
  • Volume

  • 150
  • Issue

  • 1