Journal
CELL METABOLISM
Volume 8, Issue 5, Pages 359-371Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2008.09.008
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Funding
- Banting and Best Diabetes Centre
- Canadian Diabetes Association
- Canadian Institutes for Health Research [MOP-10903]
- NIH [RO1 DK47425]
- Canada Research Chairs Program
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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 PPAR alpha-/- hepatocytes. These findings demonstrate that the Gcgr receptor is required for control of lipid metabolism during the adaptive metabolic response to fasting.
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