G protein-coupled receptor 12 deficiency results in dyslipidemia and obesity in mice

Biochem Biophys Res Commun. 2006 Sep 22;348(2):359-66. doi: 10.1016/j.bbrc.2006.07.090. Epub 2006 Jul 28.


Obesity has been proposed to be a result of an imbalance in the physiological system that controls and maintains the body energy homeostasis. Several G-protein coupled receptors (GPCRs) are involved in the regulation of energy homeostasis. To investigate the importance of GPCR12, mice deficient of this receptor (GPCR12 KO) were studied regarding metabolism. Expression of GPCR12 was found primarily in the limbic and sensory systems, indicating its possible involvement in motivation, emotion together with various autonomic functions, and sensory information processing. GPCR12 KO mice were found to have higher body weight, body fat mass, lower respiratory exchange ratio (RER), hepatic steatosis, and were dyslipidemic. Neither food intake nor energy in faeces was affected in the GPCR12 KO mice. However, lower energy expenditure was found in the GPCR12 KO mice, which may explain the obesity. In conclusion, GPCR12 is considered important for the energy balance since GPCR12 KO mice develop obesity and have lower energy expenditure. This may be important for future drugs that target this receptor.

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Body Composition
  • Body Weight
  • Carrier Proteins / biosynthesis
  • Cholesterol / blood
  • Dyslipidemias / etiology*
  • Dyslipidemias / genetics
  • Eating
  • Energy Metabolism
  • Female
  • Ion Channels
  • Male
  • Membrane Proteins / biosynthesis
  • Mice
  • Mice, Knockout
  • Mitochondrial Proteins
  • Obesity / genetics*
  • Receptors, G-Protein-Coupled / deficiency*
  • Triglycerides / metabolism
  • Uncoupling Protein 1


  • Blood Glucose
  • Carrier Proteins
  • Gpr12 protein, mouse
  • Ion Channels
  • Membrane Proteins
  • Mitochondrial Proteins
  • Receptors, G-Protein-Coupled
  • Triglycerides
  • Uncoupling Protein 1
  • Cholesterol