Research

Feeding and fasting controls liver expression of a regulator of G protein signaling (Rgs16) in periportal hepatocytes

Jie Huang¹ , Victor Pashkov¹ , Deborah M Kurrasch^1,2 , Kan Yu^1,3 , Stephen J Gold^4,5 and Thomas M Wilkie¹

¹  Department of Pharmacology, UT Southwestern Medical Center, 6001 Forest Park Dr., Dallas TX 75390-9041, USA

²  Department of Physiology, University of California, San Francisco 94143-2611, USA

³  Department of Neurology, University of Mississippi Medical Center, Jackson MS 39216, USA

⁴  Department of Psychiatry, UT Southwestern Medical Center, 6001 Forest Park Dr., Dallas TX 75390-9070, USA

⁵  Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, 3500 Camp Bowie Blvd., Ft. Worth TX 76107, USA

author email corresponding author email

Comparative Hepatology 2006, 5:8doi:10.1186/1476-5926-5-8

Published:	23 November 2006

Abstract

Background

Heterotrimeric G protein signaling in liver helps maintain carbohydrate and lipid homeostasis. G protein signaling is activated by binding of extracellular ligands to G protein coupled receptors and inhibited inside cells by regulators of G protein signaling (RGS) proteins. RGS proteins are GTPase activating proteins, and thereby regulate Gi and/or Gq class G proteins. RGS gene expression can be induced by the ligands they feedback regulate, and RGS gene expression can be used to mark tissues and cell-types when and where Gi/q signaling occurs. We characterized the expression of mouse RGS genes in liver during fasting and refeeding to identify novel signaling pathways controlling changes in liver metabolism.

Results

Rgs16 is the only RGS gene that is diurnally regulated in liver of ad libitum fed mice. Rgs16 transcription, mRNA and protein are up regulated during fasting and rapidly down regulated after refeeding. Rgs16 is expressed in periportal hepatocytes, the oxygen-rich zone of the liver where lipolysis and gluconeogenesis predominates. Restricting feeding to 4 hr of the light phase entrained Rgs16 expression in liver but did not affect circadian regulation of Rgs16 expression in the suprachiasmatic nuclei (SCN).

Conclusion

Rgs16 is one of a subset of genes that is circadian regulated both in SCN and liver. Rgs16 mRNA expression in liver responds rapidly to changes in feeding schedule, coincident with key transcription factors controlling the circadian clock. Rgs16 expression can be used as a marker to identify and investigate novel G-protein mediated metabolic and circadian pathways, in specific zones within the liver.