PUBLICATION
SOCS1 and SOCS3 are the main negative modulators of the somatotrophic axis in liver of homozygous GH-transgenic zebrafish (Danio rerio)
- Authors
- Studzinski, A.L., Almeida, D.V., Lanes, C.F., Figueiredo, M.D., and Marins, L.F.
- ID
- ZDB-PUB-081031-2
- Date
- 2009
- Source
- General and comparative endocrinology 161(1): 67-72 (Journal)
- Registered Authors
- Almeida, Daniela Volcan, Figueiredo, Marcio de Azevedo, Lanes, Carlos Frederico Ceccon, Marins, Luis Fernando, Studzinski, Ana Lupe Motta
- Keywords
- GH-transgenic zebrafish, Homozygous, Somatotrophic axis regulation, Growth, Suppressor of cytokine signaling
- MeSH Terms
-
- Growth Hormone/physiology*
- Zebrafish/genetics
- STAT5 Transcription Factor/metabolism
- Suppressor of Cytokine Signaling Proteins/physiology*
- Animals
- Insulin-Like Growth Factor I/metabolism
- Janus Kinase 2/metabolism
- Animals, Genetically Modified
- Zebrafish Proteins/metabolism
- Zebrafish Proteins/physiology*
- Homozygote
- Liver/drug effects
- Liver/metabolism*
- PubMed
- 18955058 Full text @ Gen. Comp. Endocrinol.
Citation
Studzinski, A.L., Almeida, D.V., Lanes, C.F., Figueiredo, M.D., and Marins, L.F. (2009) SOCS1 and SOCS3 are the main negative modulators of the somatotrophic axis in liver of homozygous GH-transgenic zebrafish (Danio rerio). General and comparative endocrinology. 161(1):67-72.
Abstract
Homozygote individuals (HO) of the GH-transgenic zebrafish lineage (F0104), despite expressing double the amount of growth hormone (GH) in relation to the hemizygote (HE) individuals, presented smaller growth in relation to the last, and similar to the non-transgenic (NT) group. Through the analysis of the expression of genes of the somatotrophic axis in the livers of HO and NT individuals, it was verified that GHR, JAK2 and STAT5.1 did not present significant differences among the analyzed genotypes (NT and HO). However, in the IGF-I gene expression, an accentuated decrease was observed in group HO (p<0.01), suggesting a resistance effect to excess GH. This resistance could be related to the insufficient amount of energy for supporting the accelerated metabolic demand caused by excess circulating GH. Analysis of the genes involved in the regulation of GH signalization by dephosphorylation (PTP-H1 and PTP-1B) did not show any significant alteration when comparing groups HO and NT. However, the analysis of the SOCS1 and SOCS3 genes showed an induction in homozygotes of 2.5 times (p<0.01) and 4.3 times (p<0.05), respectively, in relation to non-transgenics. The results of the present work demonstrate that, in homozygotes, GH signaling is reduced by the action of the SOCS1 and SOCS3 proteins.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping