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Gene expression in liver tissue from Ghrh-KO and normal (wild-type) mice

gse51108

Description

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.

Overall Design

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.

Histogram

Data and Resources

Normalization Files [1]

Additional Info

Field Value
Source https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE51108
Type of Data

Expression profiling by array

Technology

Microarray

GSE Submission Date 23/09/2013
GSE Authors Liou,,Sun; William,R,Swindell
Dataset Last Updated December 1, 2020, 17:09 (UTC)
Dataset Created November 25, 2020, 18:05 (UTC)