AI Article Synopsis
- GPR120 expression in brown adipose tissue (BAT) of newborn mice increases significantly after birth, largely due to thermal stress rather than feeding.
- GPR120-deficient neonates struggle with cold temperatures, with significant survival issues at lower temperatures, highlighting the receptor's role in thermogenesis.
- The absence of GPR120 does not change the structure of BAT but reduces crucial proteins and metabolism necessary for heat production, indicating its importance for healthy thermoregulation in newborns.
Article Abstract
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°C, but all such pups survived at 25°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.
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| http://dx.doi.org/10.1152/ajpendo.00081.2019 | DOI Listing |
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