| First Author | Delezie J | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 16888 |
| PubMed ID | 33060645 | Mgi Jnum | J:299016 |
| Mgi Id | MGI:6472324 | Doi | 10.1038/s41598-020-73794-7 |
| Citation | Delezie J, et al. (2020) PGC-1beta-expressing POMC neurons mediate the effect of leptin on thermoregulation in the mouse. Sci Rep 10(1):16888 |
| abstractText | The arcuate nucleus (ARC) of the hypothalamus is a key regulator of food intake, brown adipose tissue (BAT) thermogenesis, and locomotor activity. Whole-body deficiency of the transcriptional coactivator peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator-1beta (PGC-1beta) disrupts mouse circadian locomotor activity and BAT-regulated thermogenesis, in association with altered gene expression at the central level. We examined whether PGC-1beta expression in the ARC is required for proper energy balance and locomotor behavior by generating mice lacking the PGC-1beta gene specifically in pro-opiomelanocortin (POMC) neurons. POMC neuron-specific deletion of PGC-1beta did not impact locomotor behavior, food intake, body composition, energy fuel utilization and metabolic rate in fed, 24-h fasted and 24-h refed conditions. In contrast, in the fed state, deletion of PGC-1beta in POMC cells elevated core body temperature during the nighttime period. Importantly, this higher body temperature is not associated with changes in BAT function and gene expression. Conversely, we provide evidence that mice lacking PGC-1beta in POMC neurons are more sensitive to the effect of leptin on heat dissipation. Our data indicate that PGC-1beta-expressing POMC neurons are part of a circuit controlling body temperature homeostasis and that PGC-1beta function in these neurons is involved in the thermoregulatory effect of leptin. |
