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Continuous GH treatment of old rat liver

ABSTRACT: Effect of continuous GH treatment on old rat liver. Male rats, 2-year-old, were treated with vehicle or human GH (0.34 microgram/gram body weight) for 3 weeks. Keywords: response of old rat liver to growth hormone

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE2962 | GEO | 2005/07/19

SECONDARY ACCESSION(S): PRJNA92637

REPOSITORIES: GEO

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Continuous GH treatment of old rat liver

Project description:Effect of continuous GH treatment on old rat liver. Male rats, 2-year-old, were treated with vehicle or human GH (0.34 microgram/gram body weight) for 3 weeks. Comparison of treated and untreated rats. Individual RNA were used for 4 microarray hybridization. Dye swapped.

2010-06-09 | E-GEOD-2962 | biostudies-arrayexpress

Sex-dependent and growth hormone (GH)-dependent gene expression

Project description:A series of dual-channel gene expression profiles obtained using MWG Rat 5K microarrays (~5535 unique rat genes) and MWG Rat Liver microarrays (~1353 unique rat genes with 999 of these genes also represented on the Rat 5K microarray) was used to examine the sex-dependent and GH-dependent differences in gene expression in adult rat liver. This series is comprised of 8 randomly chosen pairings of independent male and female rat liver cDNA samples and 8 randomly chosen pairings of independent male and continuous GH-treated male rat liver cDNA samples, totaling 16 samples. Half of the samples were hybridized to the MWG Rat 5K microarrays and the other half were hybridized to the MWG Rat Liver microarrays. Comparison of the set of sex-dependent genes with the set of GH-responsive genes shows that 90% of male-dominant genes are suppressed in male rats treated with a female pattern of GH. Approximately 73% of female-dominant genes were up-regulated in the continuous GH-treated male rats. Keywords = Growth hormone Keywords = liver sexual dimorphism Keywords = cytochrome P450 Keywords = liver gene expression Keywords = dual channel cDNA microarray Keywords: repeat sample

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Rattus norvegicus

Project description:Continuous GH treatment of old rat liver

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Proteomic changes of the liver in the absence of growth hormone (GH) actions

Project description:The liver is a central target organ of growth hormone (GH), which stimulates the synthesis of insulin-like growth factor 1 (IGF1) and affects multiple biochemical pathways. A systematic multi-omics analysis of GH actions in the liver has not been performed. GH receptor (GHR) deficiency is a unique model for studying consequences of lacking GH actions. In this study, we used molecular profiling techniques to capture a broad spectrum of these effects in the liver of a clinically relevant large animal model.

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GH directly inhibits steatosis and liver injury in a sex-dependent and IGF1-independent manner

Project description:A reduction in hepatocyte growth hormone (GH)-signaling promotes non-alcoholic fatty liver disease (NAFLD). However, debate remains as to the relative contribution of the direct effects of GH on hepatocyte function vs indirect effects, via alterations in insulin-like growth factor 1 (IGF1). To isolate the role of hepatocyte GH receptor (GHR) signaling, independent of changes in IGF1, mice with adult-onset, hepatocyte-specific GHR knockdown (aHepGHRkd) were treated with a vector expressing rat IGF1 targeted specifically to hepatocytes. Compared to GHR-intact mice, aHepGHRkd reduced circulating IGF1 and elevated GH. In male aHepGHRkd, the shift in IGF1/GH did not alter plasma glucose or non-esterified fatty acids (NEFA), but was associated with increased insulin, enhanced systemic lipid oxidation and reduced white adipose tissue (WAT) mass. Livers of male aHepGHRkd exhibited steatosis associated with increased de novo lipogenesis, hepatocyte ballooning and inflammation. In female aHepGHRkd, hepatic GHR protein levels were not detectable, but moderate levels of IGF1 were maintained, with minimal alterations in systemic metabolism and no evidence of steatosis. Reconstitution of hepatocyte IGF1 in male aHepGHRkd lowered GH and normalized insulin, whole body lipid utilization and WAT mass. However, IGF1 reconstitution did not reduce steatosis or eliminate liver injury. RNAseq analysis showed IGF1 reconstitution did not impact aHepGHRkd-induced changes in liver gene expression, despite changes in systemic metabolism. These results demonstrate the impact of aHepGHRkd is sexually dimorphic and the steatosis and liver injury observed in male aHepGHRkd mice is autonomous of IGF1, suggesting GH acts directly on the adult hepatocyte to control NAFLD progression.

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Response of liver-expressed genes (including lincRNAs) to continuous growth hormone (GH) infusion

Project description:Gene expression in livers of adult male mice subjected to continuous GH infusion using Alzet osmotic minipumps for 1, 4 or 7 days was assayed by RNA-seq, as part of a study of growth hormone regulation of hepatic lincRNAs (PMID:26459762) and protein-coding genes (PMID:28694329).

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Changes in chromatin accessibility in male mouse liver induced by naturally occurring endogenous pulses of plasma growth hormone (GH)-activated STAT5

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