scholarly journals Growth and Hepatic Insulin-Like Growth Factor-I Gene Expression in Dominant and Subordinate Oreochromis Niloticus L Under Limited Period of Physical Interaction

2021 ◽  
Vol 934 (1) ◽  
pp. 012005
Author(s):  
E M V Cruz ◽  
M C Manuel
Keyword(s):  
Gene Expression ◽  
Growth Rate ◽  
Mrna Expression ◽  
Oreochromis Niloticus ◽  
Physical Interaction ◽  
Factor I ◽  
Dominant Fish ◽  
Igf I ◽  
I Gene ◽  
Limited Period

Abstract Social stress is known to regulate several aspects of the teleost physiology. This study explored the influence of limited period of physical interaction on growth and hepatic insulin-like growth factor-I (IGF-I) messenger RNA (mRNA) expression of the fish. Twenty all-male Oreochromis niloticus were isolated for 10 days and were used in a social pair study. After the social interaction was settled, dominant and subordinate individuals in a pair were reared separately in one aquarium separated by glass divider. The fish were fed at the same rate daily to remove the possible effect of nutrition. The glass divider was removed 10 min daily for social interaction. Weight was monitored on Days 2, 7 and 14 during the experimental period, then hepatic IGF-I mRNA expression was quantified. During the 14 days social experiment, mean specific growth rate of dominant fish (1.6%·day−1) was significantly higher (P<0.01) than that of the subordinate fish (0.9%·day−1). Dominant fish also had 2.5 fold significantly higher (P<0.05) mean IGF-I mRNA expression than that of subordinate fish. These indicate that even under limited period of physical contact but with period of visual communication, social status regulates growth and hepatic IGF-I gene expression in this species of fish. There was also a significant positive correlation (r = 0.52; P<0.01) between growth and IGF-I mRNA level which supports the previous studies that hepatic IGF-I gene expression has a potential utility as an instantaneous growth rate indicator for O. niloticus.

Regulation of insulin-like growth factor-I gene expression by growth factors in cultured vascular smooth muscle cells

1990 ◽  
Vol 125 (3) ◽  
pp. 381-386 ◽  
Author(s):  
K. E. Bornfeldt ◽  
H. J. Arnqvist ◽  
G. Norstedt
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Basic Fgf ◽  
Aortic Smooth Muscle ◽  
Factor I ◽  
Igf I ◽  
I Gene

ABSTRACT The aim of this investigation was to study the regulation of insulin-like growth factor-I (IGF-I) gene expression in cultured rat aortic smooth muscle cells. Near-confluent cells were deprived of serum for 24 h and then exposed to IGF-I, insulin, serum, basic fibroblast growth factor (basic FGF), platelet-derived growth factor (PDGF-BB; consisting of B-chain homodimer) or GH for 24 h. Levels of IGF-I mRNA were measured by solution hybridization. The level of IGF-I mRNA was markedly decreased by 10% (v/v) newborn calf serum (78 ± 4 (s.e.m.) % decrease), 1 nmol basic FGF/1 (53 ± 8%), and 1 nmol PDGF-BB/1 (40 ± 3%) when measured after 24 h. The effect of PDGF-BB was significant after 6 h and became more marked after 24 h. GH (1 nmol/l or 0.1 μmol/l or insulin (1 nmol/l had no effect after 24 h, whereas IGF-I (1 nmol/l and insulin (10 μmol/l increased IGF-I mRNA 64 ± 20% and 46±14% respectively. The increase caused by IGF-I was demonstrated after 3 h, and was most marked after 24 h. Using Northern blot analysis of cultured aortic smooth muscle cells, IGF-I transcripts of 7-4, 1.7 and 1.1–0.8 kilobases were observed. Exposure of the cells to 10% serum, 1 nmol basic FGF/1 or 1 nmol PDGF-BB/1 for 48 h increased the cell number by 104 ±7%, 64 ± 3% and 61±22% respectively, while IGF-I, insulin and GH had little effect. In conclusion, IGF-I, and high concentrations of insulin, increased IGF-I mRNA in vascular smooth muscle cells, whereas factors which were stronger mitogens decreased IGF-I gene expression. Journal of Endocrinology (1990) 125, 381–386

Ovarian and hepatic insulin-like growth factor-I gene expression and associated metabolic responses in prepubertal gilts subjected to feed restriction and refeeding

1993 ◽  
Vol 139 (1) ◽  
pp. 143-152 ◽  
Author(s):  
S. T. Charlton ◽  
J. R. Cosgrove ◽  
D. R. Glimm ◽  
G. R. Foxcroft
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Follicular Fluid ◽  
Feed Restriction ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Plasma Gh ◽  
I Gene

ABSTRACT The effects of feed restriction and refeeding on ovarian and hepatic insulin-like growth factor-I (IGF-I) gene expression, systemic and ovarian IGF-I concentrations and on associated metabolic changes were measured in prepubertal gilts. Eleven pairs of littermate gilts (70·7 ± 4·7 kg) were placed on a maintenance level of feeding for 7 days (days 1–7). On day 8, littermates were either fed at a maintenance level of energy or fed to appetite for a further 6 days. Blood samples were taken on day 13 (07.00–16.00 h) to determine plasma insulin and IGF-I, and on day 14 (02.00–06.00 h) to determine plasma GH levels. Following slaughter on day 14, one ovary from each animal was retained to measure follicular fluid IGF-I and oestradiol concentrations. The remaining ovary and a sample of liver were retained for IGF-I mRNA analysis using a ribonuclease protection assay. Six days of refeeding significantly increased plasma IGF-I (P<0·005) and basal insulin (P<0·05) but there was no effect on plasma GH. Ovarian follicular volume and diameter were significantly larger after refeeding (P<0·05), with no effect on follicular fluid oestradiol concentrations. Mean follicular fluid IGF-I concentrations were unaffected by treatment. However, the relationships between individual follicular IGF-I concentrations, absolute follicular fluid IGF-I contents and follicle volume were affected by feeding level (P<0·05). Regression analysis of the same data also revealed that at this stage of maturity, small follicles had greater follicular fluid concentrations of IGF-I than larger follicles. Refeeding increased the amount of IGF-I mRNA in hepatic but not ovarian tissue. We conclude that there is differential regulation of the IGF-I gene in porcine hepatic and ovarian tissues, and that ovarian factors other than, or as well as, IGF-I are involved in the regulation of ovarian responses to refeeding. Journal of Endocrinology (1993) 139, 143–152

scholarly journals 20kDa Human Growth Hormone (20K hGH) Stimulates Insulin-Like Growth Factor-I (IGF-I) Gene Expression at Lower Concentrations than 22K hGH in hGH Receptor-Expressing Ba/F3 Cells

2000 ◽  
Vol 47 (SupplMarch) ◽  
pp. S37-S40 ◽  
Author(s):  
HIDEO YOSHIZATO ◽  
MINORU TANAKA ◽  
TAKAHIKO FUJIKAWA ◽  
YOSHIFUMI HIGASHIMOTO ◽  
AYAKO SHIMIZU ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Growth Factor ◽  
Human Growth Hormone ◽  
Human Growth ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
I Gene

scholarly journals Inhibition by Interleukin-1β and Tumor Necrosis Factor-α of the Insulin-Like Growth Factor I Messenger Ribonucleic Acid Response to Growth Hormone in Rat Hepatocyte Primary Culture*

Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 1078-1084 ◽  
Author(s):  
Jean-Paul Thissen ◽  
Josiane Verniers
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Mrna Levels ◽  
Factor I ◽  
Tnf Α ◽  
Igf I ◽  
Necrosis Factor ◽  
I Gene

Abstract The cytokines are the putative mediators of the catabolic reaction that accompanies infection and trauma. Evidence suggests that their catabolic actions are indirect and potentially mediated through changes in hormonal axis such as the hypothalamo-pituitary-adrenal axis. Insulin-like growth factor I (IGF-I) is a GH-dependent growth factor that regulates the protein metabolism. To determine whether cytokines can directly inhibit the production of IGF-I by the liver, we investigated the regulation of IGF-I gene expression by interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α (10 ng/ml) in a model of rat primary cultured hepatocytes. Hepatocytes were isolated by liver collagenase perfusion and cultured on Matrigel 48 h before experiments. Each experiment was performed in at least three different animals. In the absence of GH, IL-1β and TNF-α did not affect the IGF-I messenger RNA (mRNA) basal levels, whereas IL-6 increased it by a factor of 2.5 after 24 h (P &lt; 0.05). GH (500 ng/ml) alone stimulated the IGF-I gene expression markedly (5- to 10-fold increase) after 24 h (P &lt; 0.001). IL-1β, and TNF-α to a lesser extent, dramatically inhibited the IGF-I mRNA response to GH (IL-1β: −82%, P &lt; 0.001 and TNF-α: −47%, P &lt; 0.01). The half-maximal inhibition of the IGF-I mRNA response to GH was observed for a concentration of IL-1β between 0.1 and 1 ng/ml. Moreover, IL-1β abolished the IL-6-induced IGF-I mRNA response. In contrast, IL-6 did not impair the IGF-I mRNA response to GH. To determine the potential role of the GH receptor (GHR) and the GH-binding protein (GHBP) in this GH resistance, we assessed the GHR and GHBP mRNAs response to these cytokines. GH alone did not affect the GHR/GHBP mRNA levels. IL-1β markedly decreased the GHR and GHBP mRNA levels (respectively, −68% and −60%, P &lt; 0.05). Neither TNF-α nor IL-6 affected the GHR/GHBP gene expression. In conclusion, our results show that IL-1β, and TNF-α to a lesser extent, blunt the IGF-I mRNA response to GH. The resistance to GH induced by IL-1β might be mediated by a decrease of GH receptors, as suggested by the marked reduction of GHR mRNA. These findings suggest that decreased circulating IGF-I, in response to infection and trauma, may be caused by a direct effect of cytokines at the hepatocyte level.

scholarly journals Defining human insulin-like growth factor I gene regulation

2016 ◽  
Vol 311 (2) ◽  
pp. E519-E529 ◽  
Author(s):  
Aditi Mukherjee ◽  
Damir Alzhanov ◽  
Peter Rotwein
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Biological Effects ◽  
Model Systems ◽  
Trophic Factors ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
I Gene

Growth hormone (GH) plays an essential role in controlling somatic growth and in regulating multiple physiological processes in humans and other species. Insulin-like growth factor I (IGF-I), a conserved, secreted 70-amino acid peptide, is a critical mediator of many of the biological effects of GH. Previous studies have demonstrated that GH rapidly and potently promotes IGF-I gene expression in rodents and in some other mammals through the transcription factor STAT5b, leading to accumulation of IGF-I mRNAs and production of IGF-I. Despite this progress, very little is known about how GH or other trophic factors control human IGF1 gene expression, in large part because of the absence of any cellular model systems that robustly express IGF-I. Here, we have addressed mechanisms of regulation of human IGF-I by GH after generating cells in which the IGF1 chromosomal locus has been incorporated into a mouse cell line. Using this model, we found that physiological levels of GH rapidly stimulate human IGF1 gene transcription and identify several potential transcriptional enhancers in chromatin that bind STAT5b in a GH-regulated way. Each of the putative enhancers also activates a human IGF1 gene promoter in reconstitution experiments in the presence of the GH receptor, STAT5b, and GH. Thus we have developed a novel experimental platform that now may be used to determine how human IGF1 gene expression is controlled under different physiological and pathological conditions.

scholarly journals Control of ovine hepatic growth hormone receptor and insulin-like growth factor I by thyroid hormones in utero

2000 ◽  
Vol 278 (6) ◽  
pp. E1166-E1174 ◽  
Author(s):  
A. J. Forhead ◽  
J. Li ◽  
J. C. Saunders ◽  
M. J. Dauncey ◽  
R. S. Gilmour ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Growth Factor ◽  
Thyroid Hormones ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Igf I ◽  
I Gene

By use of RNase protection assays, hepatic growth hormone receptor (GHR) and insulin-like growth factor I (IGF-I) mRNA abundances were measured in sheep fetuses after experimental manipulation of fetal plasma thyroid hormone concentrations by fetal thyroidectomy (TX) and exogenous infusion of triiodothyronine (T3) and cortisol. TX abolished the normal prepartum rise in hepatic GHR abundance but had little effect on hepatic GHR gene expression at 127–130 days (term 145 ± 2 days). By contrast, it upregulated basal IGF-I expression in immature fetal liver by increasing both Class 1 and Class 2 transcript abundance but had no further effects on IGF-I gene mRNA levels at 142–145 days. Raising plasma T3 to prepartum values by exogenous infusion of either T3 or cortisol into immature intact fetuses prematurely raised hepatic GHR and IGF-I mRNA abundances to values similar to those seen in intact fetuses at 142–145 days. In TX fetuses, cortisol infusion increased hepatic GHR mRNA but not total IGF-I mRNA abundance at 127–130 days. These findings show that thyroid hormones have an important role in the regulation of hepatic GHR and IGF-I gene expression in fetal sheep during late gestation and suggest that T3 mediates the maturational effects of cortisol on the hepatic somatotropic axis close to term.

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