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Specific Aim 2 GH responses to GHRH in both healthy controls and in GH deficient patients correlate with expression and activity of the stimulatory G proteins, G alpha q and G alpha S. G protein levels correlate with gonadal steroid levels.
Specific Aim 3 Sexually dimorphic GH responses to GHRH are enhanced in Tanner Stage V compared to Tanner Stage 1 individuals
Growth hormone deficiency affects disproportionately more males than females. Although ascertainment bias plays a role in this sexual dimorphism, no plausible mechanism to fully explain this difference has been proposed.
This investigator initiated study will provide currently unavailable data on sexual/age differences in response to GH stimulation testing. Data obtained from the study may provide a basis for developing appropriate normal ranges for adult GH testing, may provide a plausible mechanism for the enhanced hormone responsiveness observed in females, and may provide data on when the sexual differences to GH stimulation may develop.
The objectives of this study are to:
1. Confirm the sexual dimorphism in growth hormone responses for adult growth hormone testing in healthy male and female subjects
2. Correlate peak Growth Hormone Releasing Hormone (GHRH)/arginine induced growth hormone responses with G protein levels in healthy subjects and in patients with a history of childhood GH deficiency
3. Determine whether sexual dimorphism is acquired during puberty
Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Pharmacodynamics Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Diagnostic
Growth Hormone Deficiency
GHRH/arginine stimulation testing
Children's Mercy Hospital
Children's Mercy Hospital Kansas City
Published on BioPortfolio: 2014-08-27T03:44:48-0400
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The biologically active fragment of human growth hormone-releasing factor, consisting of GHRH(1-29)-amide. This N-terminal sequence is identical in several mammalian species, such as human, pig, and cattle. It is used to diagnose or treat patients with GROWTH HORMONE deficiency.
A form of dwarfism caused by complete or partial GROWTH HORMONE deficiency, resulting from either the lack of GROWTH HORMONE-RELEASING FACTOR from the HYPOTHALAMUS or from the mutations in the growth hormone gene (GH1) in the PITUITARY GLAND. It is also known as Type I pituitary dwarfism. Human hypophysial dwarf is caused by a deficiency of HUMAN GROWTH HORMONE during development.
A 191-amino acid polypeptide hormone secreted by the human adenohypophysis (PITUITARY GLAND, ANTERIOR), also known as GH or somatotropin. Synthetic growth hormone, termed somatropin, has replaced the natural form in therapeutic usage such as treatment of dwarfism in children with growth hormone deficiency.
An autosomal recessive disorder characterized by short stature, defective GROWTH HORMONE RECEPTOR, and failure to generate INSULIN-LIKE GROWTH FACTOR I by GROWTH HORMONE. Laron syndrome is not a form of primary pituitary dwarfism (GROWTH HORMONE DEFICIENCY DWARFISM) but the result of mutation of the human GHR gene on chromosome 5.
A pituitary tumor that secretes GROWTH HORMONE. In humans, excess HUMAN GROWTH HORMONE leads to ACROMEGALY.
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