Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from human (h-) growth hormone-treated and untreated chimeric mouse liver repopulated with human hepatocytes

ABSTRACT: We generated h-hepatocyte chimeric mice with livers that were predominantly repopulated with h-hepatocytes in a h-growth hormone (GH)-deficient state. Using microarray profiles, comparison between h-hepatocytes from h-GH-treated and untreated mice identified 14 GH-up-regulated and four GH-down-regulated genes, including IGF-1, SOCS2, NNMT, IGFLS, P4AH1, SLC16A1, and SRD5A1, and FADS1 and AKR1B10, respectively. The chimeric mice were treated or untreated with h-GH at 2.5 mg/kg b.w. /day for 2 weeks before sacrifice. Hepatocytes or liver tissue were isolated from the mouse livers and their cDNAs were used for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: Fuyuki Miya

PROVIDER: E-GEOD-26224 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Growth hormone-dependent pathogenesis of human hepatic steatosis in a novel mouse model bearing a human hepatocyte-repopulated liver.

Tateno Chise C Kataoka Miho M Utoh Rie R Tachibana Asato A Itamoto Toshiyuki T Asahara Toshimasa T Miya Fuyuki F Tsunoda Tatsuhiko T Yoshizato Katsutoshi K

Endocrinology 20110208 4

Clinical studies have shown a close association between nonalcoholic fatty liver disease and adult-onset GH deficiency, but the relevant molecular mechanisms are still unclear. No mouse model has been suitable to study the etiological relationship of human nonalcoholic fatty liver disease and human adult-onset GH deficiency under conditions similar to the human liver in vivo. We generated human (h-)hepatocyte chimeric mice with livers that were predominantly repopulated with h-hepatocytes in a h ...[more]

PMID: 21303949

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Project description:E2 and GH are critical regulators of growth and intermediate metabolism in mammals. Hypothyroidism causes endocrine and metabolic disturbances in the liver with features that mimic deficiencies of E2 or GH signalling. In this work, we used the hypothyroid-orchiectomized (TXOX) adult rat model to evaluate the influence of E2 and GH on the liver in terms of global changes in gene expression. This study shows the changes in hepatic transcriptome that were provoked by E2 benzoate (50 ug/kg; sc; 5 days per week x 27 days), intermittent GH administration (0.3 mg/kg/day;sc injection divided into two daily injections x 7 days) or the combination of E2 plus GH in TXOX rats. E2 influenced the liver transcriptome, particularly genes involved in metabolism of lipids and endo-xenobiotics, and the GH-regulated endocrine, metabolic, gender, and immune responses. E2 did not prevent the inhibitory effects of GH on urea and amino acid metabolism-related genes. Notably, the combination of E2 and GH caused deleterious effects on transcriptional immune response. These results highlight the role of E2 as a critical regulator of liver metabolism in mammals and provide insights into the functional interplay between E2 and GH in the liver. Groups=4; Biological replicates = 4 per group; Samples=16; Reference samples=TXOX group. Adult (3 months old) male Sprague-Dawley rats (n=4 per group) were used throughout these experiments. The generation of TXOX was performed by adding methimazole (MMI; 0.05%) to the drinking water for 5 weeks starting on postnatal day (PND) 59 until sacrifice on PND94. Two weeks after starting MMI administration, male rats were castrated (OX) to make TXOX rats. Four days after OX, we began treatment with E2 benzoate (TXOXE2) or vehicle (TXOX) to TXOX rats for 20 days followed for 7 days by either vehicle plus GH (TXOXGH) or by E2 plus GH (TXOXE2GH). Twenty-four hours (in the case of E2) or twelve hours (in the case of GH) after the last injection, the animals were killed by exsanguinations. Portions of the liver were snap frozen in liquid nitrogen and stored at -80C until processed for mRNA analysis.

Dataset Information

Expression data from human (h-) growth hormone-treated and untreated chimeric mouse liver repopulated with human hepatocytes

Publications

Growth hormone-dependent pathogenesis of human hepatic steatosis in a novel mouse model bearing a human hepatocyte-repopulated liver.

Similar Datasets

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