Effect of trenbolone acetate plus estradiol on transcriptional regulation of metabolism pathways in bovine liver

2010 ◽  
Vol 2 (2) ◽  
Author(s):  
Christiane Becker ◽  
Irmgard Riedmaier ◽  
Martina Reiter ◽  
Ales Tichopad ◽  
Michael W. Pfaffl ◽  
...  
Keyword(s):  
Growth Factor ◽  
Insulin Receptor ◽  
Target Genes ◽  
Anabolic Steroids ◽  
Quantitative Polymerase Chain Reaction ◽  
Regulatory Protein ◽  
Bovine Liver ◽  
Control Group ◽  
Insulin Like Growth Factor ◽  
Trenbolone Acetate

AbstractThe use of anabolic steroids is forbidden for food producing animals in the EU. Owing to the advantages of anabolics for production profitability, illegal application is appealing. Anabolics are known to influence gene expression of several tissues. We focused on the liver because of its important role in nutrient and hormone metabolism. The aim of the present study was to find differentially regulated metabolic pathways, which might be used as treatment biomarkers.A total of 18 Nguni heifers were allocated equally to a control group and a treatment group and were implanted with Revalor H. Expression of 34 target genes was measured using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR).Upregulation of androgen receptor and insulin-like growth factor 1 (IGF-1) and downregulation of IGF-2, insulin-like growth factor binding protein 2, steroid hormone binding globulin, insulin receptor α, insulin receptor β, tyrosine aminotransferase, 17β-hydroxy steroid dehydrogenase 2,3-hydroxy-methylglutaryl-coenzym-A-synthase, cathepsin B, hepatocyte growth factor, steroidogenic acute regulatory protein, apolipoprotein 2 and tumor necrosis factor α was demonstrated.Several biochemical pathways showed different regulations on mRNA level under the influence of trenbolone acetate plus estradiol. The inhibition of nutrient metabolism and protein breakdown seems to support growth processes. IGF-1 plays an important role in growth and development and thus the upregulation of IGF-1 could be responsible for the stimulation of growth in treated animals. The upregulation of IGF-1 could also be revealed as a possible risk factor for the generation of artherosclerotic plaques, which are known as long-term side effects following the use of anabolic steroids. Principal components analysis of RT-qPCR results showed that both groups arrange together and can be clearly separated. Therefore, these might be used as possible biomarkers in bovine liver.

Long-term treadmill training ameliorates endothelium-dependent vasorelaxation mediated by insulin and insulin-like growth factor-1 in hypertension

2015 ◽  
Vol 119 (6) ◽  
pp. 663-669 ◽  
Author(s):  
Yi-Yuan Lin ◽  
Shin-Da Lee ◽  
Chia-Ting Su ◽  
Tsung-Lin Cheng ◽  
Ai-Lun Yang
Keyword(s):  
Growth Factor ◽  
Insulin Receptor ◽  
Treadmill Training ◽  
Control Group ◽  
Insulin Like Growth Factor ◽  
Hypertensive Rats ◽  
Protein Levels ◽  
Significant Difference ◽  
Nos Inhibitors

Dysfunction of insulin and insulin-like growth factor-1 (IGF-1) is associated with the pathophysiology of hypertension. The influence of long-term exercise on vascular dysfunction caused by hypertension remains unclear. We investigated whether long-term treadmill training improved insulin- and IGF-1-mediated vasorelaxation in hypertensive rats. Eight-week-old male spontaneously hypertensive rats (SHR) were randomly divided into sedentary and exercise (SHR-EX) groups. The SHR-EX group was trained on a treadmill for 60 min/day, 5 days/wk, for 8 wk. Wistar-Kyoto rats (WKY) were used as the normal control group. After training, aortic insulin- and IGF-1-mediated vasorelaxation was evaluated in organ baths. Additionally, the roles of phosphatidylinositol 3-kinase (PI3K), nitric oxide synthase (NOS), and aortic protein expression were examined in the three groups. Compared with sedentary SHR and WKY groups, insulin- and IGF-1-mediated vasorelaxation was significantly enhanced to a nearly normal level in the SHR-EX group. After endothelial denudation, blunted and comparable vasorelaxation was found among the three groups. Pretreatment with selective PI3K and NOS inhibitors attenuated insulin- and IGF-1-mediated vasorelaxation, and no significant difference was found among the three groups after the pretreatment. The aortic protein levels of the insulin receptor (IR), IGF-1 receptor (IGF-1R), insulin receptor substrate-1 (IRS-1), and endothelial NOS (eNOS) were also significantly increased in the SHR-EX group compared with the other two groups. These results suggested that treadmill training elicited the amelioration of endothelium-dependent insulin/IGF-1-mediated vasorelaxation partly via the increased activation of PI3K and NOS, as well as the enhancement of protein levels of IR, IGF-1R, IRS-1, and eNOS, in hypertension.

scholarly journals miR-140 inhibits porcine fetal fibroblasts proliferation by directly targeting type 1 insulin-like growth factor receptor and indirectly inhibiting type 1 insulin-like growth factor receptor expression via SRY-box 4

2020 ◽  
Vol 33 (10) ◽  
pp. 1674-1682
Author(s):  
Hongwei Geng ◽  
Linlin Hao ◽  
Yunyun Cheng ◽  
Chunli Wang ◽  
Wenzhen Wei ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Growth Factor ◽  
Target Genes ◽  
Quantitative Polymerase Chain Reaction ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Luciferase Reporter ◽  
Insulin Like Growth Factor ◽  
Fetal Fibroblasts

Objective: This study aimed to elucidate the effect of miR-140 on the proliferation of porcine fetal fibroblasts (PFFs) and identify the target genes of miR-140 in PFFs.Methods: In this study, bioinformatics software was used to predict and verify target genes of miR-140. Quantitative polymerase chain reaction and western blot were used to detect the relationship between miR-140 and its target genes in PFFs. Dual luciferase reporter gene assays were performed to assess the interactions among miR-140, type 1 insulinlike growth factor receptor (IGF1R), and SRY-box 4 (SOX4). The effect of miR-140 on the proliferation of PFFs was measured by CCK-8 when PFFs were transfected with a miR-140 mimic or inhibitor. The transcription factor SOX4 binding to promoter of IGF1R was detected by chromatin immunoprecipitation assay (ChIP).Results: miR-140 directly targeted IGF1R and inhibited proliferation of PFFs. Meanwhile, miR-140 targeted transcription factor SOX4 that binds to promoter of porcine IGF1R to indirectly inhibit the expression of IGF1R. In addition, miR-140 inhibitor promoted PFFs proliferation, which is abrogated by SOX4 or IGF1R knockdown.Conclusion: miR-140 inhibited PFFs proliferation by directly targeting IGF1R and indirectly inhibiting IGF1R expression via SOX4, which play an important role in the development of porcine fetal.

scholarly journals Comparison of insulin-like growth factor I receptor and insulin receptor purified from human placental membranes.

1986 ◽  
Vol 261 (35) ◽  
pp. 16727-16731
Author(s):  
Y Fujita-Yamaguchi ◽  
T R LeBon ◽  
M Tsubokawa ◽  
W Henzel ◽  
S Kathuria ◽  
...  
Keyword(s):  
Growth Factor ◽  
Insulin Receptor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Placental Membranes ◽  
Growth Factor I

scholarly journals The Differential Effects of pp120 (Ceacam 1) on the Mitogenic Action of Insulin and Insulin-Like Growth Factor 1 Are Regulated by the Nonconserved Tyrosine 1316 in the Insulin Receptor

2000 ◽  
Vol 20 (11) ◽  
pp. 3896-3905 ◽  
Author(s):  
Payal Soni ◽  
Montaha Lakkis ◽  
Matthew N. Poy ◽  
Mats A. Fernström ◽  
Sonia M. Najjar
Keyword(s):  
Growth Factor ◽  
Insulin Receptor ◽  
Site Directed Mutagenesis ◽  
Insulin Like Growth Factor ◽  
Β Subunit ◽  
Conserved Domain ◽  
C Terminus ◽  
Mitogenic Action ◽  
The Difference ◽  
Differential Phosphorylation

ABSTRACT pp120 (Ceacam 1) undergoes ligand-stimulated phosphorylation by the insulin receptor, but not by the insulin-like growth factor 1 receptor (IGF-1R). This differential phosphorylation is regulated by the C terminus of the β-subunit of the insulin receptor, the least conserved domain of the two receptors. In the present studies, deletion and site-directed mutagenesis in stably transfected hepatocytes derived from insulin receptor knockout mice (IR−/−) revealed that Tyr1316, which is replaced by the nonphosphorylatable phenylalanine in IGF-1R, regulated the differential phosphorylation of pp120 by the insulin receptor. Similarly, the nonconserved Tyr1316 residue also regulated the differential effect of pp120 on IGF-1 and insulin mitogenesis, with pp120 downregulating the growth-promoting action of insulin, but not that of IGF-1. Thus, it appears that pp120 phosphorylation by the insulin receptor is required and sufficient to mediate its downregulatory effect on the mitogenic action of insulin. Furthermore, the current studies revealed that the C terminus of the β-subunit of the insulin receptor contains elements that suppress the mitogenic action of insulin. Because IR−/− hepatocytes are derived from liver, an insulin-targeted tissue, our observations have finally resolved the controversy about the role of the least-conserved domain of insulin and IGF-1Rs in mediating the difference in the mitogenic action of their ligands, with IGF-1 being more mitogenic than insulin.

Sign in / Sign up

Export Citation Format

Share Document