| First Author | Nolan MA | Year | 2004 |
| Journal | Mol Endocrinol | Volume | 18 |
| Issue | 9 | Pages | 2302-11 |
| PubMed ID | 15192081 | Mgi Jnum | J:92076 |
| Mgi Id | MGI:3051721 | Doi | 10.1210/me.2004-0194 |
| Citation | Nolan MA, et al. (2004) The Role of Uncoupling Protein 1 in the Metabolism and Adiposity of RII{beta}-Protein Kinase A-Deficient Mice. Mol Endocrinol 18(9):2302-2311 |
| abstractText | Mice lacking the RIIbeta regulatory subunit of protein kinase A exhibit a 50% reduction in white adipose tissue stores compared with wild-type littermates and are resistant to diet-induced obesity. RIIbeta(-/-) mice also have an increase in resting oxygen consumption along with a 4-fold increase in the brown adipose-specific mitochondrial uncoupling protein 1 (UCP1). In this study, we examined the basis for UCP1 induction and tested the hypothesis that the induced levels of UCP1 in RIIbeta null mice are essential for the lean phenotype. The induction of UCP1 occurred at the protein but not the mRNA level and correlated with an increase in mitochondria in brown adipose tissue. Mice lacking both RIIbeta and UCP1 (RIIbeta(-/-)/Ucp1(-/-)) were created, and the key parameters of metabolism and body composition were studied. We discovered that RIIbeta(-/-) mice exhibit nocturnal hyperactivity in addition to the increased oxygen consumption at rest. Disruption of UCP1 in RIIbeta(-/-) mice reduced basal oxygen consumption but did not prevent the nocturnal hyperactivity. The double knockout animals also retained the lean phenotype of the RIIbeta null mice, demonstrating that induction of UCP1 and increased resting oxygen consumption is not the cause of leanness in the RIIbeta mutant mice. |
