Please note that we have stopped the regular imports of Gene Expression Omnibus (GEO) data into ArrayExpress. This may not be the latest version of this experiment.
E-GEOD-51108 - Gene expression in liver tissue from Ghrh-KO and normal (wild-type) mice
Released on 18 November 2013, last updated on 22 July 2015
The hypothalamus has recently emerged as a key regulator of metabolism and aging in mammals. We have examined the impact of targeted disruption of hypothalamic hypophysiotropic peptide: Growth Hormone-releasing Hormone (GHRH) in mice on longevity, and the putative mechanisms of delayed aging. GHRH knockout (KO) mice are remarkably long-lived and in comparison to genetically normal (wild type) animals exhibiting major shifts in the expression of genes related to xenobiotic detoxification, stress resistance, and insulin signaling. These mutant mice also have increased adiponectin levels and alterations in glucose homeostasis consistent with the removal of the counter-insulin effects of GH. While these effects overlap with those of caloric restriction (CR), we show that effects of CR and the GHRH mutation are additive, with lifespan of GHRH-KO mutants further increased by CR. We conclude that GHRH-KO mice feature perturbations in a network of signaling pathways related to stress resistance, metabolic control and inflammation, and therefore provide a new model that can be used to explore links between GHRH repression, downregulation of the somatotropic axis, and extended longevity. Hepatic tissue was obtained from 3 Ghrh-KO mice and 3 control (wild-type) mice (males). Expression in each sample was profiled using Affymetrix Mouse Genome 430 2.0 arrays.
transcription profiling by array
Growth hormone-releasing hormone disruption extends lifespan and regulates response to caloric restriction in mice. Sun LY, Spong A, Swindell WR, Fang Y, Hill C, Huber JA, Boehm JD, Westbrook R, Salvatori R, Bartke A.