scholarly journals Dairy cows experience selective reduction of the hepatic growth hormone receptor during the periparturient period

2004 ◽  
Vol 181 (2) ◽  
pp. 281-290 ◽  
Author(s):  
J Wook Kim ◽  
RP Rhoads ◽  
SS Block ◽  
TR Overton ◽  
SJ Frank ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Dairy Cows ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Late Pregnancy ◽  
Target Tissue ◽  
Ghr Gene ◽  
Igf I

At parturition, dairy cows experience a 70% reduction in plasma IGF-I. This reduction coincides with decreased abundance of GHR1A, the liver-specific transcript of the growth hormone receptor (GHR) gene, suggesting impaired growth hormone-dependent synthesis of IGF-I. It is not immediately obvious that the periparturient reduction in GHR1A is sufficient to reduce hepatic GHR abundance. This is because approximately 50% of total GHR mRNA abundance in prepartum liver is accounted for by ubiquitously expressed transcripts which remain collectively unchanged at parturition. In addition, the possibility that parturition alters GHR expression in other growth hormone target tissue has not been examined. To address these questions, we measured GHR gene expression and GHR protein in liver and skeletal muscle of four dairy cows on days -35,+3 and+56 (relative to parturition on day 0). Hepatic GHR abundance and GHR1A transcripts were lower on day+3 than on day -35 and returned to late pregnancy value by day+56. Additional studies in two other groups of cows indicated that the hepatic levels of the GHR protein recovered substantially within 10 days after parturition. These changes occurred without variation in the abundance of HNF4, a liver-enriched transcription factor activating the promoter responsible for GHR1A synthesis. In contrast to liver, levels of GHR gene expression and GHR protein were identical on days -35,+3 and+56 in skeletal muscle. These data suggest a role for the GHR in regulating tissue-specific changes in growth hormone responsiveness in periparturient dairy cows.

Perinatal ontogeny of porcine growth hormone receptor gene expression is modulated by thyroid status

1996 ◽  
Vol 134 (4) ◽  
pp. 524-531 ◽  
Author(s):  
C Duchamp ◽  
KA Burton ◽  
P Herpin ◽  
MJ Dauncey
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Growth Hormone Receptor ◽  
Receptor Gene ◽  
Thyroid Status ◽  
Ghr Gene ◽  
Growth Hormone Receptor Gene ◽  
Receptor Gene Expression ◽  
Hormone Receptor Gene

Duchamp C, Burton KA, Herpin P, Dauncey MJ, Perinatal ontogeny of porcine growth hormone receptor gene expression is modulated by thyroid status. Eur J Endocrinol 1996;134:524–31 The ontogeny of growth hormone receptors (GHR) represents a critical stage in growth and metabolism. We have investigated the perinatal ontogeny of hepatic and skeletal muscle GHR gene expression in piglets, and its modulation by GH and thyroid hormones. Test piglets were rendered hypothyroid in late gestation by feeding the sow a high-glucosinolate rapeseed meal. Plasma and tissue samples were obtained from test and control piglets at various ages between 80 days of fetal life (80F) and 2 days postnatally. Plasma hormone levels were determined by radioimmunoassay and GHR mRNA by RNase protection assays. In controls, plasma thyroxine (T4) and 3,5,3′-triiodothyronine (T3) levels increased between 80F and birth and the early postnatal period was characterized by a marked surge in plasma T3. Test piglets were hypothyroid at 110F with total T4, total T3 and free T3 levels being reduced by 28, 53 and 33% respectively. By contrast, the postnatal increase in T3 was more marked in test than in control animals. Plasma GH levels decreased over the perinatal period and there was no effect of treatment. Hepatic GHR mRNA was at the lower limit of detection at 80F but by 11 OF was expressed in both groups of animals. However, fetal hypothyroidism at 11 OF resulted in a marked 70% decrease in hepatic GHR mRNA (p < 0.01). The higher postnatal rise in T3 in test piglets was accompanied by a recovery of hepatic GHR mRNA levels. By contrast with liver, skeletal muscle (longissimus dorsi) expressed high levels of GHR mRNA at 80F and hypothyroidism induced a 68% increase in GHR mRNA (p < 0.001). The present results suggest that thyroid hormones may modulate the perinatal ontogeny of GHR gene expression, in addition to other hormonal factors, and that this modulation is tissue-specific. MJ Dauncey, Department of Cellular Physiology, The Babraham Institute, Cambridge CB2 4AT, UK

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.

ORIGINAL ARTICLE: Associations of the growth hormone receptor (GHR) gene polymorphisms with adiposity and IGF-I activity in adolescents

2010 ◽  
Vol 73 (3) ◽  
pp. 313-322 ◽  
Author(s):  
Janice L. Y. Mong ◽  
Maggie C. Y. Ng ◽  
Georgia S. Guldan ◽  
Claudia H. T. Tam ◽  
Heung Man Lee ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Receptor ◽  
Gene Polymorphisms ◽  
Growth Hormone Receptor ◽  
Ghr Gene ◽  
Igf I

scholarly journals Growth hormone receptor gene expression in the skeletal muscle of normal and double-muscled bovines during foetal development

2005 ◽  
Vol 45 (4) ◽  
pp. 393-403 ◽  
Author(s):  
Anne Listrat ◽  
Jean François Hocquette ◽  
Brigitte Picard ◽  
François Ménissier ◽  
Jean Djiane ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Receptor Gene ◽  
Foetal Development ◽  
Growth Hormone Receptor Gene ◽  
Receptor Gene Expression ◽  
Hormone Receptor Gene

scholarly journals Growth Hormone Receptor Gene is Essential for Chicken Mitochondrial Function In Vivo and In Vitro

2019 ◽  
Vol 20 (7) ◽  
pp. 1608 ◽  
Author(s):  
Bowen Hu ◽  
Shuang Hu ◽  
Minmin Yang ◽  
Zhiying Liao ◽  
Dexiang Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Mitochondrial Function ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Ghr Gene ◽  
Chicken Skeletal Muscle

The growth hormone receptor (GHR) gene is correlated with many phenotypic and physiological alternations in chicken, such as shorter shanks, lower body weight and muscle mass loss. However, the role of the GHR gene in mitochondrial function remains unknown in poultry. In this study, we assessed the function of mitochondria in sex-linked dwarf (SLD) chicken skeletal muscle and interfered with the expression of GHR in DF-1 cells to investigate the role of the GHR gene in chicken mitochondrial function both in vivo and in vitro. We found that the expression of key regulators of mitochondrial biogenesis and mitochondrial DNA (mtDNA)-encoded oxidative phosphorylation (OXPHOS) genes were downregulated and accompanied by reduced enzymatic activity of OXPHOS complexes in SLD chicken skeletal muscle and GHR knockdown cells. Then, we assessed mitochondrial function by measuring mitochondrial membrane potential (ΔΨm), mitochondrial swelling, reactive oxygen species (ROS) production, malondialdehyde (MDA) levels, ATP levels and the mitochondrial respiratory control ratio (RCR), and found that mitochondrial function was impaired in SLD chicken skeletal muscle and GHR knockdown cells. In addition, we also studied the morphology and structure of mitochondria in GHR knockdown cells by transmission electron microscopy (TEM) and MitoTracker staining. We found that knockdown of GHR could reduce mitochondrial number and alter mitochondrial structure in DF-1 cells. Above all, we demonstrated for the first time that the GHR gene is essential for chicken mitochondrial function in vivo and in vitro.

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