» Articles » PMID: 20368432

Gene Knockout of Acc2 Has Little Effect on Body Weight, Fat Mass, or Food Intake

Overview
Specialty Science
Date 2010 Apr 7
PMID 20368432
Citations 54
Authors
Affiliations
Soon will be listed here.
Abstract

Deletion of acetyl CoA carboxylase-2 (Acc2) reportedly causes leanness in the setting of hyperphagia. To determine the cellular basis for these effects, we generated a mouse model in which Acc2 can be selectively deleted by the action of Cre recombinase. Deletion of Acc2 from skeletal muscle, the predominant site of Acc2 expression, had no effect on body weight, food intake, or body composition. When Acc2 was inactivated in the germline, Acc2 knockout (Acc2KO) mice displayed no differences in body weight, food intake, body composition, or glucose homeostasis as compared to controls on chow or high fat diet. Total malonyl CoA content and fatty acid oxidation rates in skeletal muscle of Acc2KO mice were unchanged, suggesting metabolic compensation in response to the loss of Acc2. The limited impact of Acc2 deletion on energy balance raises the possibility that selective pharmacological inhibition of Acc2 for the treatment of obesity may be ineffective.

Citing Articles

Carnitine palmitoyltransferase 1 facilitates fatty acid oxidation in a non-cell-autonomous manner.

Choi J, Smith D, Scafidi S, Riddle R, Wolfgang M Cell Rep. 2024; 43(12):115006.

PMID: 39671290 PMC: 11726389. DOI: 10.1016/j.celrep.2024.115006.


Effect of bariatric surgery on mitochondrial remodeling in human skeletal muscle: a narrative review.

Ge X, Wang Z, Song Y, Meng H Front Endocrinol (Lausanne). 2024; 15:1488715.

PMID: 39655345 PMC: 11625573. DOI: 10.3389/fendo.2024.1488715.


Mitochondrial fatty acid beta-oxidation: a possible therapeutic target for skeletal muscle lipotoxicity in peripheral artery disease myopathy.

Bradley C, Fletcher E, Wilkinson T, Ring A, Ferrer L, Miserlis D EXCLI J. 2024; 23:523-533.

PMID: 38741727 PMC: 11089102. DOI: 10.17179/excli2024-7004.


Molecular cloning and gene expression of acc2 from grass carp (Ctenopharyngodon idella) and the regulation of glucose metabolism by ACCs inhibitor.

Cao M, Li X, Dong L, Wen H, Jiang M, Lu X Mol Biol Rep. 2024; 51(1):402.

PMID: 38456942 DOI: 10.1007/s11033-024-09286-y.


Suppression of food intake by Glp1r/Lepr-coexpressing neurons prevents obesity in mouse models.

Rupp A, Tomlinson A, Affinati A, Yacawych W, Duensing A, True C J Clin Invest. 2023; 133(19).

PMID: 37581939 PMC: 10541203. DOI: 10.1172/JCI157515.


References
1.
Essop M, Camp H, Choi C, Sharma S, Fryer R, Reinhart G . Reduced heart size and increased myocardial fuel substrate oxidation in ACC2 mutant mice. Am J Physiol Heart Circ Physiol. 2008; 295(1):H256-65. PMC: 2494759. DOI: 10.1152/ajpheart.91489.2007. View

2.
Matzuk M, WAKIL S . Continuous fatty acid oxidation and reduced fat storage in mice lacking acetyl-CoA carboxylase 2. Science. 2001; 291(5513):2613-6. DOI: 10.1126/science.1056843. View

3.
Ruderman N, Flier J . Cell biology. Chewing the fat--ACC and energy balance. Science. 2001; 291(5513):2558-9. DOI: 10.1126/science.1060277. View

4.
Lewandoski M, Wassarman K, Martin G . Zp3-cre, a transgenic mouse line for the activation or inactivation of loxP-flanked target genes specifically in the female germ line. Curr Biol. 1997; 7(2):148-51. DOI: 10.1016/s0960-9822(06)00059-5. View

5.
Harwood Jr H . Acetyl-CoA carboxylase inhibition for the treatment of metabolic syndrome. Curr Opin Investig Drugs. 2004; 5(3):283-9. View