The Glucagon Receptor Is Required for the Adaptive Metabolic Response to Fasting
(2008) In Cell Metabolism 8(5). p.359-371- Abstract
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 PPARα-/- hepatocytes. These... (More)
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 PPARα-/- hepatocytes. These findings demonstrate that the Gcgr receptor is required for control of lipid metabolism during the adaptive metabolic response to fasting.
(Less)
- author
- Longuet, Christine ; Sinclair, Elaine M. ; Maida, Adriano ; Baggio, Laurie L. ; Maziarz, Marlena LU ; Charron, Maureen J. and Drucker, Daniel J.
- publishing date
- 2008-11-05
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- HUMDISEASE
- in
- Cell Metabolism
- volume
- 8
- issue
- 5
- pages
- 13 pages
- publisher
- Cell Press
- external identifiers
-
- pmid:19046568
- scopus:54849431792
- ISSN
- 1550-4131
- DOI
- 10.1016/j.cmet.2008.09.008
- language
- English
- LU publication?
- no
- id
- f6ccc5fd-21d3-4215-9d5f-5625aeb9f976
- date added to LUP
- 2019-08-05 13:18:46
- date last changed
- 2024-04-16 18:16:57
@article{f6ccc5fd-21d3-4215-9d5f-5625aeb9f976,
abstract = {{<p>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 PPARα-/- hepatocytes. These findings demonstrate that the Gcgr receptor is required for control of lipid metabolism during the adaptive metabolic response to fasting.</p>}},
author = {{Longuet, Christine and Sinclair, Elaine M. and Maida, Adriano and Baggio, Laurie L. and Maziarz, Marlena and Charron, Maureen J. and Drucker, Daniel J.}},
issn = {{1550-4131}},
keywords = {{HUMDISEASE}},
language = {{eng}},
month = {{11}},
number = {{5}},
pages = {{359--371}},
publisher = {{Cell Press}},
series = {{Cell Metabolism}},
title = {{The Glucagon Receptor Is Required for the Adaptive Metabolic Response to Fasting}},
url = {{http://dx.doi.org/10.1016/j.cmet.2008.09.008}},
doi = {{10.1016/j.cmet.2008.09.008}},
volume = {{8}},
year = {{2008}},
}