| First Author | Nonogaki K | Year | 2002 |
| Journal | Biochem Biophys Res Commun | Volume | 295 |
| Issue | 2 | Pages | 249-54 |
| PubMed ID | 12150939 | Mgi Jnum | J:108471 |
| Mgi Id | MGI:3624144 | Doi | 10.1016/s0006-291x(02)00665-4 |
| Citation | Nonogaki K, et al. (2002) Altered gene expressions involved in energy expenditure in 5-HT(2C) receptor mutant mice. Biochem Biophys Res Commun 295(2):249-54 |
| abstractText | Mice with a targeted null mutation of the serotonin 5-HT(2C) receptor gene exhibit hyperphagia that leads to a late-onset obesity. Here we show that oxygen consumption was decreased in fed and fasted obese mutants. No phenotypic differences were observed in uncoupling protein-1 (UCP-1) mRNA levels in brown adipose tissues and UCP-3 mRNA in skeletal muscle. UCP-2 mRNA levels were significantly increased in white adipose tissue (4-fold) and skeletal muscle (47%) in older obese mutant mice, whereas UCP-2 mRNA in liver are significantly increased in both young lean (54% increase) and older obese (52% increase) mutant mice. In contrast, 5-HT(2C) receptor mutants displayed age-dependent decreases in beta 3-adrenergic receptor (beta 3-AR) mRNA levels in white adipose tissue, however, no such changes were observed in brown adipose tissue. These results indicate that a mutation of 5-HT(2C) receptor gene leads to a secondary decrease in beta 3-AR gene expression that is related to enhanced adiposity. |
