scholarly journals Exogenous growth hormone induces somatotrophic gene expression in neonatal liver and skeletal muscle

2000 ◽  
Vol 278 (4) ◽  
pp. R838-R844 ◽  
Author(s):  
A. J. Lewis ◽  
T. J. Wester ◽  
D. G. Burrin ◽  
M. J. Dauncey
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Intracellular Signaling ◽  
Posttranscriptional Regulation ◽  
Plasma Concentrations ◽  
Gh Treatment ◽  
Rnase Protection ◽  
Neonatal Pigs ◽  
Igf I

The extent to which the local somatotrophic axis is functional in extrahepatic tissues in the neonate is unclear. We therefore determined the expression of growth hormone (GH) receptor (GHR), and insulin-like growth factors I and II (IGF-I and IGF-II) mRNA in liver and skeletal muscle (longissimus) of neonatal pigs given daily intramuscular injections of either recombinant porcine GH (1 mg/kg body wt; n = 6) or saline ( n = 5) for 7 days. Exogenous GH increased plasma concentrations of GH 30-fold and IGF-I threefold. Abundances of specific mRNA in liver and muscle were measured by RNase protection assays (values are arbitrary density units). In liver, GH treatment increased GHR (6.0 vs. 9.7; P< 0.01) and IGF-I (5.2 vs. 49.0; P < 0.001) but not IGF-II (19.5 vs. 17.2) mRNA. In muscle, GH treatment increased IGF-I mRNA (13.3 vs. 22.8; P < 0.05) but not GHR (8.3 vs. 9.5) or IGF-II (16.1 vs. 16.9). These results demonstrate that exogenous GH can induce local somatotrophic function predominantly in liver but also in muscle of newborn pigs. Our novel finding on the selective increase in muscle IGF-I but not GHR gene expression suggests differences in posttranscriptional regulation and/or intracellular signaling mechanisms.

scholarly journals Growth hormone regulation of metabolic gene expression in muscle: a microarray study in hypopituitary men

2007 ◽  
Vol 293 (1) ◽  
pp. E364-E371 ◽  
Author(s):  
Klara Sjögren ◽  
Kin-Chuen Leung ◽  
Warren Kaplan ◽  
Margaret Gardiner-Garden ◽  
James Gibney ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Lipid Oxidation ◽  
Expression Profiles ◽  
Whole Body ◽  
Circadian Gene ◽  
Gh Treatment ◽  
Substrate Metabolism ◽  
Igf I

Muscle is a target of growth hormone (GH) action and a major contributor to whole body metabolism. Little is known about how GH regulates metabolic processes in muscle or the extent to which muscle contributes to changes in whole body substrate metabolism during GH treatment. To identify GH-responsive genes that regulate substrate metabolism in muscle, we studied six hypopituitary men who underwent whole body metabolic measurement and skeletal muscle biopsies before and after 2 wk of GH treatment (0.5 mg/day). Transcript profiles of four subjects were analyzed using Affymetrix GeneChips. Serum insulin-like growth factor I (IGF-I) and procollagens I and III were measured by RIA. GH increased serum IGF-I and procollagens I and III, enhanced whole body lipid oxidation, reduced carbohydrate oxidation, and stimulated protein synthesis. It induced gene expression of IGF-I and collagens in muscle. GH reduced expression of several enzymes regulating lipid oxidation and energy production. It reduced calpain 3, increased ribosomal protein L38 expression, and displayed mixed effects on genes encoding myofibrillar proteins. It increased expression of circadian gene CLOCK, and reduced that of PERIOD. In summary, GH exerted concordant effects on muscle expression and blood levels of IGF-I and collagens. It induced changes in genes regulating protein metabolism in parallel with a whole body anabolic effect. The discordance between muscle gene expression profiles and metabolic responses suggests that muscle is unlikely to contribute to GH-induced stimulation of whole body energy and lipid metabolism. GH may regulate circadian function in skeletal muscle by modulating circadian gene expression with possible metabolic consequences.

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.

Intravenous infusion of insulin-like growth factor I in fetal sheep reduces hepatic IGF-I and IGF-II mRNAs

1996 ◽  
Vol 271 (6) ◽  
pp. R1632-R1637 ◽  
Author(s):  
K. L. Kind ◽  
J. A. Owens ◽  
F. Lok ◽  
J. S. Robinson ◽  
K. J. Quinn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Factor ◽  
Intravenous Infusion ◽  
Feedback Inhibition ◽  
Fetal Liver ◽  
Plasma Concentrations ◽  
Insulin Like Growth Factor ◽  
Fetal Sheep ◽  
Igf I

Liver contains the highest concentrations of insulin-like growth factor (IGF) I mRNA in adult rats and sheep and is a major source of circulating IGF-I. In rats, inhibition of hepatic IGF-I production by exogenous IGF-I has been reported. In fetal sheep, skeletal muscle and liver are major sites of IGF-I synthesis and potential sources of circulating IGF-I. To determine whether feedback inhibition of IGF gene expression in fetal liver or muscle by IGF-I occurs, IGF-I and IGF-II mRNAs were measured in these tissues after intravenous infusion of recombinant human IGF-I into fetal sheep. Infusion of IGF-I (26 +/- 4 micrograms.h-1.kg-1; n = 6) or saline (n = 6) commenced on day 120 of pregnancy (term = 150 days) and continued for 10 days. Plasma concentrations of IGF-I were threefold higher in infused fetuses at 130 days of gestation (P < 0.0003), whereas those of IGF-II were unchanged. IGF-I infusion reduced the relative abundance of IGF-I mRNA (P < 0.0002) and IGF-II mRNA (P < 0.01) in fetal liver by approximately 50% but did not alter IGF-I or IGF-II mRNA in skeletal muscle. These results indicate that IGF-I inhibits the expression of both IGF-I and IGF-II genes in fetal liver and that IGF gene expression in fetal liver and muscle is differentially regulated by IGF-I.

scholarly journals FNDC5 relates to skeletal muscle IGF-I and mitochondrial function and gene expression in obese men with reduced growth hormone

2016 ◽  
Vol 26 ◽  
pp. 36-41 ◽  
Author(s):  
Suman Srinivasa ◽  
Caroline Suresh ◽  
Jay Mottla ◽  
Sulaiman R. Hamarneh ◽  
Javier E. Irazoqui ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Mitochondrial Function ◽  
Igf I

scholarly journals Functional deficits and insulin-like growth factor-I gene expression following tourniquet-induced injury of skeletal muscle in young and old rats

2008 ◽  
Vol 105 (4) ◽  
pp. 1274-1281 ◽  
Author(s):  
David W. Hammers ◽  
Edward K. Merritt ◽  
Wayne Matheny ◽  
Martin L. Adamo ◽  
Thomas J. Walters ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Intracellular Signaling ◽  
Ischemia Reperfusion ◽  
Force Production ◽  
Histological Evaluation ◽  
Igf I ◽  
Old Rats ◽  
I Gene ◽  
Recovery Groups

This study investigated the effect of age on recovery of skeletal muscle from an ischemia-reperfusion (I/R)-induced injury. Young (6 mo old) and old (24–27 mo old) Sprague-Dawley rats underwent a 2-h bout of hindlimb ischemia induced by a pneumatic tourniquet (TK). The TK was released to allow reperfusion of the affected limb, and animals were divided into 7- and 14-day recovery groups. Maximum plantar flexor force production was assessed in both 7- and 14-day recovery groups of both ages, followed by histological evaluation. Subsequent analysis of IGF-I gene expression and intracellular signaling in 7-day recovery muscles was performed by RT-PCR and Western blotting, respectively. Old rats had significantly greater deficits in force production and exhibited more evidence of histological pathology than young at both 7 and 14 days postinjury. In addition, old rats demonstrated an attenuated upregulation of IGF-I mRNA and induction of proanabolic signaling compared with young in response to injury. We conclude that aged skeletal muscle exhibits more damage and/or defective regeneration following I/R and identify an age-associated decrease in local IGF-I responsiveness as a potential mechanism for this phenomenon.

Stimulation of the renin-angiotensin system by growth hormone in Lewis dwarf rats

1993 ◽  
Vol 265 (2) ◽  
pp. E332-E339 ◽  
Author(s):  
B. Wyse ◽  
M. Waters ◽  
C. Sernia
Keyword(s):  
Growth Hormone ◽  
Plasma Concentrations ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Ii Receptor ◽  
Gh Treatment ◽  
Angiotensin System ◽  
Lewis Rats ◽  
Renin Angiotensin ◽  
Igf I

A genetically growth hormone (GH)-deficient strain of Lewis rats was used to test the hypothesis that the actions of GH on electrolyte and fluid homeostasis are mediated by the renin-angiotensin-aldosterone system (RAAS). Dwarf rats injected with recombinant bGH (2 mg.kg-1 x day-1) for 7 days (group GH1+) and 28 days (group GH4+), respectively, were compared with saline-injected dwarf (group GH-) and normal (group N) Lewis rats. GH decreased Na+ excretion and increased renal glomerular filtration rate in dwarf rats. The dietary intake and plasma concentrations of Na+ and K+ remained unchanged. GH increased plasma insulin-like growth factor I (IGF-I) concentrations in dwarf rats (GH - = 109 +/- 9, GH1+ = 184 +/- 5, GH4+ = 189 +/- 28, N = 477 +/- 29 ng/ml plasma). Plasma angiotensinogen increased towards the levels found in normal Lewis rats (GH- = 859 +/- 38, GH1+ = 906 +/- 18, GH4+ = 1,027 +/- 19, N = 1497 +/- 80 ng angiotensin I/ml plasma); plasma renin activity increased above that of the normal Lewis (GH- = 10.2 +/- 0.6, GH1+ = 11.7 +/- 0.7, GH4+ = 16.7 +/- 2.4, N = 10.6 +/- 0.8 ng angiotensin I.ml plasma-1 x h-1). Plasma aldosterone, corticosterone, and triodothyronine concentrations were unchanged by GH treatment. Angiotensin II receptor densities in GH- rats (liver = 356 +/- 23, kidney = 228 +/- 28, adrenal = 478 +/- 58 fmol/mg protein) were upregulated by GH (GH4+ rats; liver = 573 +/- 27, kidney = 360 +/- 86, adrenal = 721 +/- 78 fmol/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Growth Hormone Treatment Prevents the Decrease in Insulin-Like Growth Factor I Gene Expression in Patients Undergoing Abdominal Surgery1

1998 ◽  
Vol 83 (5) ◽  
pp. 1566-1572
Author(s):  
Ragnar Bjarnason ◽  
Ruth Wickelgren ◽  
Majlis Hermansson ◽  
Folke Hammarqvist ◽  
Björn Carlsson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Parenteral Nutrition ◽  
Major Surgery ◽  
Control Group ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Gh Treatment ◽  
Igf I ◽  
I Gene

Acquired GH resistance together with reduced skeletal muscle mass are found in patients with increased protein catabolism due, for example, to sepsis, trauma, or major surgery. Both administration of glutamine-containing parenteral nutrition and GH treatment have been found to diminish this catabolism. The effects of GH are mediated in part by insulin-like growth factor I (IGF-I) that is produced in the liver and locally in GH target tissues. The aim of this study was to investigate the effect of GH treatment on expression of the IGF-I gene and GH receptor (GHR) gene in skeletal muscle after major surgery. A new quantitative RT-PCR-based assay was established to measure IGF-I gene expression. Metabolically healthy patients, without significant preoperative weight loss, who were undergoing elective abdominal surgery were included in the study. Five patients (one woman and four men) were treated with daily injections of GH (0.3 IU/kg·day) in addition to being given total parenteral nutrition including glutamine (0.28 g/kg·day). The control group consisted of eight patients (three women and five men), who were given glutamine-enriched total parenteral nutrition but no GH. A muscle biopsy was taken from the lateral portion of the quadriceps femoris muscle preoperatively (day 0) after induction of anesthesia. A second biopsy was taken under local anesthesia on postoperative day 3. Total ribonucleic acid (RNA) was extracted from the muscle biopsies, and IGF-I messenger RNA (mRNA) and GHR mRNA were measured by competitive quantitative RT-PCR assays. IGF-I mRNA and GHR mRNA levels were related to the expression of a housekeeping gene (cyclophilin). In the control group, IGF-I mRNA levels decreased from 1505 ± 265 (mean ± sem) transcripts/cpm cyclophilin on day 0 to 828 ± 172 on day 3 (P &lt; 0.05). In contrast, IGF-I mRNA levels did not change in the GH-treated group (1188 ± 400 transcripts/cpm cyclophilin on day 0 vs. 1089± 342 transcripts/cpm cyclophilin on day 3). No statistically significant changes were seen in GHR expression. We conclude that administration of GH prevents the reduction in IGF-I gene expression in skeletal muscle after abdominal surgery.

Growth hormone increases IGF-I, collagen I and collagen III gene expression in dwarf rat skeletal muscle

1995 ◽  
Vol 115 (2) ◽  
pp. 187-197 ◽  
Author(s):  
Victoria J. Wilson ◽  
Marcus Rattray ◽  
Chris R. Thomas ◽  
Barbara H. Moreland ◽  
Dennis Schulster
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Collagen I ◽  
Rat Skeletal Muscle ◽  
Collagen Iii ◽  
Igf I

Efficacy of long-term growth hormone therapy in short non-growth hormone-deficient children

2017 ◽  
Vol 30 (2) ◽  
Author(s):  
Lucia Schena ◽  
Cristina Meazza ◽  
Sara Pagani ◽  
Valeria Paganelli ◽  
Elena Bozzola ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Final Height ◽  
Standard Deviation Score ◽  
Bone Age ◽  
Gh Treatment ◽  
Short Children ◽  
Igf I ◽  
Height Gain ◽  
The Cost

AbstractBackground:In recent years, several studies have been published showing different responses to growth hormone (GH) treatment in idiopathic short stature children. The aim of the present study was to investigate whether non-growth-hormone-deficient (non-GHD) short children could benefit from long-term GH treatment as GHD patients.Methods:We enrolled 22 prepubertal children and 22 age- and sex-matched GHD patients, with comparable height, body mass index (BMI), bone age, and insulin-like growth factor 1 (IGF-I) circulating levels. The patients were treated with recombinant human GH (rhGH) and followed until they reach adult height.Results:During GH treatment, the two groups grew in parallel, reaching the same final height-standard deviation score (SDS) and the same height gain. On the contrary, we found significantly lower IGF-I serum concentrations in non-GHD patients than in GHD ones, at the end of therapy (p=0.0055).Conclusions:In our study, the response to GH treatment in short non-GHD patients proved to be similar to that in GHD ones. However, a careful selection of short non-GHD children to be treated with GH would better justify the cost of long-term GH therapy.

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