Activator of G protein signaling 3 null mice: I. Unexpected alterations in metabolic and cardiovascular function

被引:55
作者
Blumer, Joe B. [1 ,2 ]
Lord, Kevin [2 ]
Saunders, Thomas L. [3 ]
Pacchioni, Alejandra [5 ]
Black, Cory [4 ]
Lazartigues, Eric [2 ]
Varner, Kurt J. [2 ]
Gettys, Thomas W. [4 ]
Lanier, Stephen M. [1 ,2 ]
机构
[1] Med Univ S Carolina, Dept Cell & Mol Pharmacol & Expt Therapeut, Charleston, SC 29425 USA
[2] Louisiana State Univ, Hlth Sci Ctr, Dept Pharmacol & Expt Therapeut, New Orleans, LA 70112 USA
[3] Univ Michigan, Transgen Anim Model Core, Dept Internal Med, Ann Arbor, MI 48109 USA
[4] Pennington Biomed Res Ctr, Div Expt Obes, Baton Rouge, LA 70808 USA
[5] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA
关键词
D O I
10.1210/en.2008-0050
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Activator of G protein signaling (AGS)-3 plays functional roles in cell division, synaptic plasticity, addictive behavior, and neuronal development. As part of a broad effort to define the extent of functional diversity of AGS3-regulated-events in vivo, we generated AGS3 null mice. Surprisingly, AGS3 null adult mice exhibited unexpected alterations in cardiovascular and metabolic functions without any obvious changes in motor skills, basic behavioral traits, and brain morphology. AGS3 null mice exhibited a lean phenotype, reduced fat mass, and increased nocturnal energy expenditure. AGS3 null mice also exhibited altered blood pressure control mechanisms. These studies expand the functional repertoire for AGS3 and other G protein regulatory proteins providing unexpected mechanisms by which G protein systems may be targeted to influence obesity and cardiovascular function.
引用
收藏
页码:3842 / 3849
页数:8
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