Chronic adult‐onset of growth hormone/IGF‐I hypersecretion improves cognitive functions and LTP and promotes neuronal differentiation in adult rats

2019 ◽  
Vol 229 (2) ◽  
Author(s):  
Juan Francisco Martín‐Rodríguez ◽  
Víctor Darío Ramos‐Herrero ◽  
Gloria G. Parras ◽  
Álvaro Flores‐Martínez ◽  
Ainara Madrazo‐Atutxa ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Neuronal Differentiation ◽  
Cognitive Functions ◽  
Adult Onset ◽  
Adult Rats ◽  
Igf I

Growth hormone and IGF-I modulate local cerebral glucose utilization and ATP levels in a model of adult-onset growth hormone deficiency

2006 ◽  
Vol 291 (3) ◽  
pp. E604-E610 ◽  
Author(s):  
William E. Sonntag ◽  
Colleen Bennett ◽  
Rhonda Ingram ◽  
Ashley Donahue ◽  
Jeremy Ingraham ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Glucose Metabolism ◽  
Glucose Utilization ◽  
Brain Aging ◽  
Hormone Deficiency ◽  
Adult Onset ◽  
Local Cerebral Glucose Utilization ◽  
Cerebral Glucose Utilization ◽  
Atp Levels ◽  
Igf I

Decreases in plasma IGF-I levels that occur with age have been hypothesized to contribute to the genesis of brain aging. However, support for this hypothesis would be strengthened by evidence that growth hormone (GH)/IGF-I deficiency in young animals produces a phenotype similar to that found in aged animals. As a result, we developed a unique model of adult-onset GH/IGF-I deficiency by using dwarf rats specifically deficient in GH and IGF-I. The deficiency in plasma IGF-I is similar to that observed with age (e.g., 50% decrease), and replacement of GH restores levels of IGF-I to that found in young animals with normal GH levels. The present study employs this model to investigate the effects of circulating GH and IGF-I on local cerebral glucose utilization (LCGU). Analysis of LCGU indicated that GH/IGF-I-deficient animals exhibit a 29% decrease in glucose metabolism in many brain regions, especially those involved in hippocampally dependent processes of learning and memory. Similarly, a high correlation between plasma IGF-I levels and glucose metabolism was found in these areas. The deficiency in LCGU was not associated with alterations in GLUT1, GLUT3, or hexokinase activity. A 15% decrease in ATP levels was also found in hippocampus of GH-deficient animals, providing compelling data that circulating GH and IGF-I have significant effects on the regulation of glucose utilization and energy metabolism in the brain. Furthermore, our results provide important data to support the conclusion that deficiencies in circulating GH/IGF-I contribute to the genesis of brain aging.

scholarly journals Human growth hormone and insulin-like growth factor-I inhibit erythropoietin secretion from the kidneys of adult rats

2005 ◽  
Vol 184 (1) ◽  
pp. 199-207 ◽  
Author(s):  
Motoi Sohmiya ◽  
Yuzuru Kato
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Rat Kidney ◽  
Infusion Pump ◽  
Insulin Like Growth Factor ◽  
Adult Rats ◽  
Adult Rat ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I

Growth hormone (GH) and insulin-like growth factor-I (IGF-I) play important roles in erythropoiesis and erythro-poietin (EPO) secretion. We examined the effects of GH and IGF-I on EPO production in adult rat kidney and liver in vivo and in vitro. Male Wistar rats aged 8–10 weeks were used. Recombinant human GH (hGH) was continuously infused (20 μg/kg per h) subcutaneously for 48 h using a micro-osmotic infusion pump. Octreotide (10 μg/kg) was subcutaneously injected every 12 h beginning 12 h before the hGH treatment. GH increased plasma EPO levels earlier than it increased plasma IGF-I levels. At 24 h, the IGF-I content in the liver and kidney was increased from 172.8±14.6 to 232.6±17.8 ng/g tissue (means±S.E.) and from 53.8±3.1 to 112.8±7.2 ng/g tissue, respectively. The EPO content in the liver was increased from 7.5±1.2 to 15.1±1.4 mIU/g tissue at 48 h, whereas the EPO content in the kidney was decreased at 12, 24, and 48 h after the start of hGH treatment. When the kidneys were organ-cultured, hGH considerably decreased EPO levels in the culture medium in a dose-related manner. The addition of anti-hGH IgG blunted the GH-induced inhibition of EPO secretion from the kidneys. IGF-I also decreased EPO levels in the medium in a dose-related manner. The addition of anti-IGF-I IgG blunted the IGF-I-induced inhibition of EPO secretion from the kidneys, whereas the GH-induced inhibition of EPO secretion was not affected. These findings suggest that both hGH and IGF-I have direct inhibitory effects on EPO secretion from adult rat kidneys.

Laron syndrome – A case Report

JMS SKIMS ◽  
2017 ◽  
Vol 20 (2) ◽  
pp. 104-106
Author(s):  
Javaid Ahmad Bhat ◽  
Moomin Hussain Bhat ◽  
Hilal Bhat ◽  
Mona Sood ◽  
Shariq Rashid Masoodi
Keyword(s):  
Growth Hormone ◽  
Case Report ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Genetic Disorder ◽  
Female Child ◽  
Receptor Signaling ◽  
Laron Syndrome ◽  
Rare Genetic Disorder ◽  
Igf I

Background : Laron & colleagues (1966) reported a rare genetic disorder in Israliei Jewish sublings which was characterized by insensitivity to growth hormone due to abnormality in growth hormone receptor or post receptor signaling pathway.Case Report: We hereby report a case of a 5 year old female child who presented to us with features similar to Laron syndrome. The diagnosis was made & confirmed by various Lab. investigations like low IGF-I levels and managed accordingly. JMS 2017; 20 (2):104-106  

Biomarkers of Acromegaly and Growth Hormone Action

2020 ◽  
Vol 27 (12) ◽  
pp. 1231-1245
Author(s):  
Filippo Maffezzoni ◽  
Teresa Porcelli ◽  
Andrea Delbarba ◽  
Letizia Pezzaioli ◽  
Carlo Cappelli ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Biological Markers ◽  
Clinical Care ◽  
Hormone Deficiency ◽  
Surrogate Outcomes ◽  
Current State ◽  
Growth Hormone Action ◽  
Igf I ◽  
Definition Of

: Biological markers (biomarkers) play a key role in drug development, regulatory approval and clinical care of patients and are linked to clinical and surrogate outcomes. : Both acromegaly and Growth Hormone Deficiency (GHD) are pathological conditions related to important comorbidities that, in addition to having stringent diagnostic criteria, require valid markers for the definition of treatment, treatment monitoring and follow-up. GH and insulin-like growth factor-I (IGF-I) are the main biomarkers of GH action in children and adults while, in acromegaly, both GH and IGF-I are established biomarkers of disease activity. : However, although GH and IGF-I are widely validated biomarkers of GHD and acromegaly, their role is not completely exhaustive or suitable for clinical classification and follow-up. Therefore, new biological markers for acromegaly and GH replacement therapy are strongly needed. : The aim of this paper is to review and summarize the current state in the field pointing out new potential biomarkers for acromegaly and GH use/abuse.

Early increase in pulsatile growth hormone release after unilateral nephrectomy in adult rats

1994 ◽  
Vol 266 (4) ◽  
pp. F628-F632 ◽  
Author(s):  
A. Haramati ◽  
M. D. Lumpkin ◽  
S. E. Mulroney
Keyword(s):  
Growth Hormone ◽  
Early Time ◽  
Peak Level ◽  
Unilateral Nephrectomy ◽  
Sham Operation ◽  
Renal Growth ◽  
Adult Rats ◽  
Compensatory Renal Growth ◽  
Jugular Veins ◽  
Hypertrophic Response

Removal of one kidney results, within days, in accelerated growth of the remaining kidney. However, the mechanisms that underlie this compensatory renal hypertrophic response, particularly in the early time period following nephrectomy, are not understood. In this study we tested the hypothesis that removal of one kidney leads to a change in the pulsatile release of growth hormone (GH), which facilitates compensatory renal growth. Adult Wistar rats were implanted with Silastic cannulas in jugular veins and underwent either unilateral nephrectomy (UNX) or sham operation. Plasma levels of GH were determined 24 and 48 h after sham operation or UNX. Blood samples were taken every 20 min over a 6-h period from conscious, unrestrained animals. Pulsatile GH release was markedly elevated 24 h after UNX in both the amplitude of the surges as well as in the duration of release. Peak GH levels after 24 h were three- to fourfold higher in UNX rats compared with sham controls (417 +/- 75 vs. 119 +/- 23 ng/ml, P < 0.05). However, this enhanced release of GH appeared to be of short duration and began declining by 48 h post-UNX (peak level of 227 +/- 37 ng/ml, P < 0.05 vs. both 24 h UNX and sham controls). To examine whether this rise in GH release post-UNX contributed to the compensatory renal growth, rats underwent UNX and were immediately treated with an antagonist to GH-releasing factor (GRF-AN; i.e., [N-Ac-Tyr1,D-Arg2]GRF-(1-29) amide, 200 micrograms/kg twice daily), and the effects on GH release and renal growth were determined. Administration of GRF-AN significantly suppressed the increase in GH release post-UNX and was associated with a significant attenuation in renal growth 48 h post-UNX in GRF-AN-treated rats (8.7 +/- 2.6% vs. 22.7 +/- 3.0% in UNX controls, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Differential Diagnosis of the Short IGF-I-Deficient Child with Apparently Normal Growth Hormone Secretion

2021 ◽  
pp. 1-24
Author(s):  
Jan M. Wit ◽  
Sjoerd D. Joustra ◽  
Monique Losekoot ◽  
Hermine A. van Duyvenvoorde ◽  
Christiaan de Bruin
Keyword(s):  
Growth Hormone ◽  
Differential Diagnosis ◽  
Growth Hormone Secretion ◽  
Normal Growth ◽  
Stimulation Test ◽  
Healthy Children ◽  
Genetic Causes ◽  
Gh Secretion ◽  
Igf I

The current differential diagnosis for a short child with low insulin-like growth factor I (IGF-I) and a normal growth hormone (GH) peak in a GH stimulation test (GHST), after exclusion of acquired causes, includes the following disorders: (1) a decreased spontaneous GH secretion in contrast to a normal stimulated GH peak (“GH neurosecretory dysfunction,” GHND) and (2) genetic conditions with a normal GH sensitivity (e.g., pathogenic variants of <i>GH1</i> or <i>GHSR</i>) and (3) GH insensitivity (GHI). We present a critical appraisal of the concept of GHND and the role of 12- or 24-h GH profiles in the selection of children for GH treatment. The mean 24-h GH concentration in healthy children overlaps with that in those with GH deficiency, indicating that the previously proposed cutoff limit (3.0–3.2 μg/L) is too high. The main advantage of performing a GH profile is that it prevents about 20% of false-positive test results of the GHST, while it also detects a low spontaneous GH secretion in children who would be considered GH sufficient based on a stimulation test. However, due to a considerable burden for patients and the health budget, GH profiles are only used in few centres. Regarding genetic causes, there is good evidence of the existence of Kowarski syndrome (due to <i>GH1</i> variants) but less on the role of <i>GHSR</i> variants. Several genetic causes of (partial) GHI are known (<i>GHR</i>, <i>STAT5B</i>, <i>STAT3</i>, <i>IGF1</i>, <i>IGFALS</i> defects, and Noonan and 3M syndromes), some responding positively to GH therapy. In the final section, we speculate on hypothetical causes.

scholarly journals Regulation of GH and GH Signaling by Nutrients

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1376
Author(s):  
Marina Caputo ◽  
Stella Pigni ◽  
Emanuela Agosti ◽  
Tommaso Daffara ◽  
Alice Ferrero ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Insulin Signaling ◽  
Current Knowledge ◽  
Nutrient Sensing ◽  
Feedback Mechanisms ◽  
Nutrition Management ◽  
Prevention And Treatment ◽  
Igf I ◽  
Macro And Micronutrients ◽  
Energy Deprivation

Growth hormone (GH) and insulin-like growth factor-1 (IGF-I) are pleiotropic hormones with important roles in lifespan. They promote growth, anabolic actions, and body maintenance, and in conditions of energy deprivation, favor catabolic feedback mechanisms switching from carbohydrate oxidation to lipolysis, with the aim to preserve protein storages and survival. IGF-I/insulin signaling was also the first one identified in the regulation of lifespan in relation to the nutrient-sensing. Indeed, nutrients are crucial modifiers of the GH/IGF-I axis, and these hormones also regulate the complex orchestration of utilization of nutrients in cell and tissues. The aim of this review is to summarize current knowledge on the reciprocal feedback among the GH/IGF-I axis, macro and micronutrients, and dietary regimens, including caloric restriction. Expanding the depth of information on this topic could open perspectives in nutrition management, prevention, and treatment of GH/IGF-I deficiency or excess during life.

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