| First Author | Longuet C | Year | 2008 |
| Journal | Cell Metab | Volume | 8 |
| Issue | 5 | Pages | 359-71 |
| PubMed ID | 19046568 | Mgi Jnum | J:143752 |
| Mgi Id | MGI:3828901 | Doi | 10.1016/j.cmet.2008.09.008 |
| Citation | Longuet C, et al. (2008) The glucagon receptor is required for the adaptive metabolic response to fasting. Cell Metab 8(5):359-71 |
| abstractText | Glucagon receptor (Gcgr) signaling maintains hepatic glucose production during the fasting state; however, the importance of the Gcgr for lipid metabolism is unclear. We show here that fasted Gcgr-/- mice exhibit a significant increase in hepatic triglyceride secretion and fasting increases fatty acid oxidation (FAO) in wild-type (WT) but not in Gcgr-/- mice. Moreover fasting upregulated the expression of FAO-related hepatic mRNA transcripts in Gcgr+/+ but not in Gcgr-/- mice. Exogenous glucagon administration reduced plasma triglycerides in WT mice, inhibited TG synthesis and secretion, and stimulated FA beta oxidation in Gcgr+/+ hepatocytes. The actions of glucagon on TG synthesis and FAO were abolished in PPARalpha-/- hepatocytes. These findings demonstrate that the Gcgr receptor is required for control of lipid metabolism during the adaptive metabolic response to fasting. |
