| First Author | Quesada-López T | Year | 2019 |
| Journal | Am J Physiol Endocrinol Metab | Volume | 317 |
| Issue | 5 | Pages | E742-E750 |
| PubMed ID | 31361546 | Mgi Jnum | J:283695 |
| Mgi Id | MGI:6376837 | Doi | 10.1152/ajpendo.00081.2019 |
| Citation | Quesada-Lopez T, et al. (2019) GPR120 controls neonatal brown adipose tissue thermogenic induction. Am J Physiol Endocrinol Metab 317(5):E742-E750 |
| abstractText | Adaptive induction of thermogenesis in brown adipose tissue (BAT) is essential for the survival of mammals after birth. We show here that G protein-coupled receptor protein 120 (GPR120) expression is dramatically induced after birth in mouse BAT. GPR120 expression in neonatal BAT is the highest among GPR120-expressing tissues in the mouse at any developmental stage tested. The induction of GPR120 in neonatal BAT is caused by postnatal thermal stress rather than by the initiation of suckling. GPR120-null neonates were found to be relatively intolerant to cold: close to one-third did not survive at 21 degrees C, but all such pups survived at 25 degrees C. Heat production in BAT was significantly impaired in GPR120-null pups. Deficiency in GPR120 did not modify brown adipocyte morphology or the anatomical architecture of BAT, as assessed by electron microscopy, but instead impaired the expression of uncoupling protein-1 and the fatty acid oxidation capacity of neonatal BAT. Moreover, GPR120 deficiency impaired fibroblast growth factor 21 (FGF21) gene expression in BAT and reduced plasma FGF21 levels. These results indicate that GPR120 is essential for neonatal adaptive thermogenesis. |
