REDUCTION OF DIETARY OBESITY IN AP2-UCP TRANSGENIC MICE - PHYSIOLOGY AND ADIPOSE-TISSUE DISTRIBUTION

We seek to determine whether increased energy dissipation in adipose t issue can prevent obesity. Transgenic mice with C57BL6/J background an d the adipocyte lipid-binding protein (aP2) gene promoter directing ex pression of the mitochondrial uncoupling protein (UCP) gene in white a nd brown fat were used. Physiologically, UCP is essential for nonshive ring thermogenesis in brown fat. Mice were assigned to a chow or a hig h-fat (HF) diet at 3 mo of age. Over the next 25 wk, gains of body wei ght were similar in corresponding subgroups (n = 6-8) of female and ma le mice: 4-5 g in chow nontransgenic and transgenic, 20 g in HF nontra nsgenic, and 9-11 g in HF transgenic mice. The lower body weight gain in the HF transgenic vs. nontransgenic mice corresponded to a twofold lower feed efficiency. Gonadal fat was enlarged, but subcutaneous whit e fat was decreased in the transgenic vs. nontransgenic mice in both d ietary conditions. The results suggest that UCP synthesized from the a P2 gene promoter is capable of reducing dietary obesity.