| First Author | Funda J | Year | 2022 |
| Journal | Dis Model Mech | Volume | 15 |
| Issue | 4 | PubMed ID | 35466996 |
| Mgi Jnum | J:344046 | Mgi Id | MGI:7275323 |
| Doi | 10.1242/dmm.049223 | Citation | Funda J, et al. (2022) Adipose tissue-specific ablation of PGC-1beta impairs thermogenesis in brown fat. Dis Model Mech 15(4):dmm049223 |
| abstractText | Impaired thermogenesis observed in mice with whole-body ablation of peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta; officially known as PPARGC1B) may result from impaired brown fat (brown adipose tissue; BAT) function, but other mechanism(s) could be involved. Here, using adipose-specific PGC-1beta knockout mice (PGC-1beta-AT-KO mice) we aimed to learn whether specific PGC-1beta ablation in adipocytes is sufficient to drive cold sensitivity. Indeed, we found that warm-adapted (30 degrees C) mutant mice were relatively sensitive to acute cold exposure (6 degrees C). When these mice were subjected to cold exposure for 7 days (7-day-CE), adrenergic stimulation of their metabolism was impaired, despite similar levels of thermogenic uncoupling protein 1 in BAT in PGC-1beta-AT-KO and wild-type mice. Gene expression in BAT of mutant mice suggested a compensatory increase in lipid metabolism to counteract the thermogenic defect. Interestingly, a reduced number of contacts between mitochondria and lipid droplets associated with low levels of L-form of optic atrophy 1 was found in BAT of PGC-1beta-AT-KO mice. These genotypic differences were observed in warm-adapted mutant mice, but they were partially masked by 7-day-CE. Collectively, our results suggest a role for PGC-1beta in controlling BAT lipid metabolism and thermogenesis. This article has an associated First Person interview with the first author of the paper. |
