GPR120 controls neonatal brown adipose tissue thermogenic induction

Area of Science:

• Physiology
• Metabolism
• Endocrinology

Background:

• Adaptive thermogenesis in brown adipose tissue (BAT) is vital for neonatal survival.
• The role of specific receptors in this process is not fully understood.

Purpose of the Study:

• To investigate the role of G protein-coupled receptor protein 120 (GPR120) in neonatal adaptive thermogenesis.
• To determine the impact of GPR120 deficiency on BAT function and survival in newborn mice.

Main Methods:

• GPR120 expression analysis in neonatal mouse BAT.
• Assessment of cold tolerance and survival rates in GPR120-null neonates.
• Measurement of BAT heat production, uncoupling protein-1 expression, and fatty acid oxidation.
• Evaluation of fibroblast growth factor 21 (FGF21) gene expression and plasma levels.

Main Results:

• GPR120 expression is significantly induced in neonatal mouse BAT postnatally due to thermal stress.
• GPR120-null neonates exhibit impaired cold tolerance and reduced survival at lower temperatures.
• BAT heat production, uncoupling protein-1 expression, and fatty acid oxidation are diminished in GPR120-deficient pups.
• GPR120 deficiency leads to reduced FGF21 gene expression and plasma levels.

Conclusions:

• GPR120 is essential for adaptive thermogenesis in neonatal brown adipose tissue.
• GPR120 plays a critical role in regulating cold tolerance and metabolic adaptation in newborns.
• The GPR120-FGF21 axis may be important for neonatal thermoregulation.