Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

CRTC2 (TORC2) contributes to the transcriptional response to fasting in the liver but is not required for the maintenance of glucose homeostasis.

The liver contributes to glucose homeostasis by promoting either storage or production of glucose, depending on the physiological state. The cAMP response element-binding protein (CREB) is a principal regulator of genes involved in coordinating the hepatic response to fasting, but its mechanism of gene activation remains controversial. We derived CRTC2 (CREB-regulated transcription coactivator 2, previously TORC2)-deficient mice to assess the contribution of this cofactor to hepatic glucose metabolism in vivo. CRTC2 mutant hepatocytes showed reduced glucose production in response to glucagon, which correlated with decreased CREB binding to several gluconeogenic genes. However, despite attenuated expression of CREB target genes, including PEPCK, G6Pase, and PGC-1alpha, no hypoglycemia was observed in mutant mice. Collectively, these results provide genetic evidence supporting a role for CRTC2 in the transcriptional response to fasting, but indicate only a limited contribution of this cofactor to the maintenance of glucose homeostasis.

Pubmed ID: 19583954


  • Le Lay J
  • Tuteja G
  • White P
  • Dhir R
  • Ahima R
  • Kaestner KH


Cell metabolism

Publication Data

July 8, 2009

Associated Grants

  • Agency: NIDDK NIH HHS, Id: DK 049210
  • Agency: NIDDK NIH HHS, Id: P01 DK049210
  • Agency: NIDDK NIH HHS, Id: P01 DK049210-130013
  • Agency: NIDDK NIH HHS, Id: T32 DK007314

Mesh Terms

  • Animals
  • Fasting
  • Glucagon
  • Glucose
  • Glucose-6-Phosphatase
  • Liver
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Protein-Serine-Threonine Kinases
  • Trans-Activators
  • Transcription Factors
  • Transcription, Genetic