| First Author | Rowe GC | Year | 2009 |
| Journal | Endocrinology | Volume | 150 |
| Issue | 1 | Pages | 135-43 |
| PubMed ID | 18772235 | Mgi Jnum | J:146998 |
| Mgi Id | MGI:3839069 | Doi | 10.1210/en.2008-0678 |
| Citation | Rowe GC, et al. (2009) Increased energy expenditure and insulin sensitivity in the high bone mass DeltaFosB transgenic mice. Endocrinology 150(1):135-43 |
| abstractText | 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. |
