scholarly journals Growth hormone improves short-term growth in patients with temple syndrome

2019 ◽  
Author(s):  
Brightman DS ◽  
Lokulo-Sodipe O ◽  
Searle B ◽  
Mackay DJG ◽  
Davies JH ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Short Term ◽  
Temple Syndrome

scholarly journals Growth Hormone Improves Short-Term Growth in Patients with Temple Syndrome

2018 ◽  
Vol 90 (6) ◽  
pp. 407-413 ◽  
Author(s):  
Diana S. Brightman ◽  
Oluwakemi Lokulo-Sodipe ◽  
Beverly A. Searle ◽  
Deborah J.G. Mackay ◽  
Justin H. Davies ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Short Stature ◽  
Growth Hormone Treatment ◽  
Standard Deviation Score ◽  
Uniparental Disomy ◽  
Hormone Treatment ◽  
Height Velocity ◽  
Short Term ◽  
Temple Syndrome ◽  
Hands And Feet

Background/Aims: Temple syndrome is an imprinting disorder caused by maternal uniparental disomy of chromosome 14 (mat UPD14), paternal deletion of 14q32 or paternal hypomethylation of the intergenic differentially methylated region (MEG3/DLK1 IG-DMR). Patients with Temple syndrome have pre- and postnatal growth restriction, short stature, hypotonia, small hands and feet and precocious puberty. We sought to determine whether treatment with growth hormone improves growth outcomes in patients with Temple syndrome. Methods: This was a retrospective observational study reviewing the medical records of 14 patients with Temple syndrome, 7 of whom were treated with growth hormone. Results: After 1 year of growth hormone treatment, the height standard deviation score (SDS) increased a median of 1.31 SDS with a median increased height velocity of 5.30 cm/year. Conclusions: These results suggest short-term improvement in height SDS with growth hormone treatment similar to the response in patients treated under the small for gestational age indication. We recommend considering growth hormone therapy in all patients with Temple syndrome who have short stature.

Different short-term effect of protein and carbohydrate intake on TSH, growth hormone (GH), insulin, C-peptide, and glucagon in humans

1990 ◽  
Vol 50 (7) ◽  
pp. 801-805 ◽  
Author(s):  
L. E. Matzen ◽  
B. B. Andersen ◽  
B. G. Jensen ◽  
H. J. Gjessing ◽  
S. H. Sindrup ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Term Effect ◽  
Carbohydrate Intake ◽  
Short Term ◽  
C Peptide ◽  
Short Term Effect

scholarly journals Impairment of Host Liver Repopulation by Transplanted Hepatocytes in Aged Rats and the Release by Short-Term Growth Hormone Treatment

2017 ◽  
Vol 187 (3) ◽  
pp. 553-569 ◽  
Author(s):  
Peggy Stock ◽  
Maximilian Bielohuby ◽  
Martin S. Staege ◽  
Mei-Ju Hsu ◽  
Martin Bidlingmaier ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Treatment ◽  
Hormone Treatment ◽  
Aged Rats ◽  
Host Liver ◽  
Short Term ◽  
Liver Repopulation

Short-Term Tools to Measure Responsiveness to Growth Hormone Replacement

2001 ◽  
Vol 55 (2) ◽  
pp. 40-43 ◽  
Author(s):  
Jens O.L. Jørgensen ◽  
Troels K. Hansen ◽  
Flávia Lucia Conceição ◽  
Jens J. Christensen ◽  
Nina Vahl ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Hormone Replacement ◽  
Growth Hormone Replacement ◽  
Short Term

Growth hormone, cortisol, or both are involved in defense against, but are not critical to recovery from, hypoglycemia

1991 ◽  
Vol 260 (3) ◽  
pp. E395-E402 ◽  
Author(s):  
P. J. Boyle ◽  
P. E. Cryer
Keyword(s):  
Growth Hormone ◽  
Plasma Glucose ◽  
Low Doses ◽  
Short Term ◽  
Control Subjects ◽  
Glucose Recovery ◽  
Do So

We tested the hypotheses that growth hormone, cortisol, or both are involved in defense against but are not critical to recovery from prolonged hypoglycemia and that the putative roles of these hormones in defense against prolonged hypoglycemia are permissive rather than direct. To do so we studied control subjects (n = 10) and patients with growth hormone and cortisol deficiencies resulting from hypopituitarism both in the untreated state (n = 7) and with prestudy and basal intrastudy growth hormone and cortisol replacement (n = 6). Postabsorptive plasma glucose, insulin, glucagon, and epinephrine concentrations were no different in the untreated patients and controls. Twelve-hour insulin infusions, in low doses adjusted over the 1st 2 h to produce plasma glucose concentrations of 3.6 mmol/l (65 mg/dl) and then fixed at that dose, resulted in significantly (P less than 0.0001) lower late plasma glucose concentrations in the patients, without and with replacement. The 12-h plasma glucose concentrations were 2.9 +/- 0.1 mmol/l (53 +/- 1 mg/dl) in the control subjects, 2.4 +/- 0.1 mmol/l (43 +/- 2 mg/dl; P less than 0.001 vs. control) in the deficient patients, and 2.5 +/- 0.1 mmol/l (45 +/- 2 mg/dl; P less than 0.01 vs. control) in the replaced patients. Rates of glucose recovery from hypoglycemia after discontinuation of insulin were identical in all three studies. Thus growth hormone, cortisol, or probably both play a demonstrable role in defense against prolonged, in contrast to short-term, hypoglycemia in humans. This does not appear to be the result of permissive actions of the hormones and is therefore best attributed to their increments during hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth Hormone Enhances Excitatory Synaptic Transmission in Area CA1 of Rat Hippocampus

2006 ◽  
Vol 95 (5) ◽  
pp. 2962-2974 ◽  
Author(s):  
Ghada S. Mahmoud ◽  
Lawrence M. Grover
Keyword(s):  
Growth Hormone ◽  
Synaptic Transmission ◽  
Pi3 Kinase ◽  
Janus Kinase ◽  
Excitatory Synaptic Transmission ◽  
Common Mechanism ◽  
Hippocampal Function ◽  
Short Term ◽  
Area Ca1 ◽  
Short Term Effects

The hippocampus produces growth hormone (GH) and contains GH receptors, suggesting a potential role for GH signaling in the regulation of hippocampal function. In agreement with this possibility, previous investigations have found altered hippocampal function and hippocampal-dependent learning and memory after chronic GH administration or deficiency. In this study we applied GH to in vitro rat hippocampal brain slices, to determine whether GH has short-term effects on hippocampal function in addition to previously documented chronic effects. We found that GH enhanced both AMPA- and NMDA-receptor–mediated excitatory postsynaptic potentials (EPSPs) in hippocampal area CA1, but did not alter GABAA-receptor–mediated inhibitory synaptic transmission. GH enhancement of excitatory synaptic transmission was gradual, requiring 60–70 min to reach maximum, and occurred without any change in paired-pulse facilitation, suggesting a possible postsynaptic site of action. In CA1 pyramidal neurons, GH enhancement of EPSPs was correlated with significant hyperpolarization and decreased input resistance. GH enhancement of EPSPs required Janus kinase 2 (JAK2), phosphatidylinositol-3 (PI3) kinase, mitogen-activated protein (MAP) kinase kinase (MEK), and synthesis of new proteins. Although PI3 kinase and MEK were required for initiation of GH effects on excitatory synaptic transmission, they were not required for maintained enhancement of EPSPs. GH treatment and tetanus-induced long-term potentiation were mutually occluding, suggesting a common mechanism or mechanisms in both forms of synaptic enhancement. Our results demonstrate that GH has powerful short-term effects on hippocampal function, and extend the timescale for potential roles of GH in regulating hippocampal function and hippocampal-dependent behaviors.

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