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Growth hormone (hGH)
Growth - Biochemical Basics
Growth is stimulated and controlled by the anabolic and mitogenic activity of growth hormone and insulin-like growth factors (IGFs, insulin-like growth factors). From a physiological point of view, hGH has general anabolic effects (e.g. increased glucose uptake, protein synthesis, lipolysis). Its main task is to stimulate bone growth in adolescents through the following biochemical processes:
- The hypothalamus releases GHRH (growth hormone releasing hormone).
- GHRH stimulates the release of hGH by the pituitary gland.
- hGH reaches the liver and other tissues through the blood.
- The liver and other tissues respond to hGH by synthesizing IGF-1, an insulin-like growth factor.
- IGF-1 stimulates the cells at the growth centers of the bones and thus leads to linear bone growth.
Molecular forms of growth hormone
Human growth hormone (hGH) occurs in two different molecular forms with a molecular mass of 20 kDa and 22 kDa, respectively. Over 90% of circulating hGH consists of the 22 kDa isoform, which is composed of 191 amino acids. The 20 kDa isoform is released together with the 22 kDa isoform. It is a replacement product of the hGH gene of the pituitary gland, which lacks amino acid residues 32-46. It corresponds to approximately 10% of the total circulating hGH. It is assumed that the biological activity of both forms is comparable.
Synthesis and secretion of growth hormone
The synthesis of hGH is controlled by hypothalamic and peripheral signals. It is promoted by GHRH (growth hormone releasing hormone), ghrelin3, sleep, physical activity, insulin, low blood sugar levels, increased androgen secretion during puberty and stimulation tests with arginine, clonidine or insulin. The release of hGH is inhibited by somatostatin, glucose, glucocorticoids, fatty acids, L-dopa and beta blockers and regulated by circulating hGH and IGF-1 concentrations through a negative feedback mechanism. In addition, the secretion of hGH is influenced by additional hormone signals, sex steroids and thyroid hormones.
In the blood, growth hormone is bound to growth hormone binding protein (GHBP). GHBP acts as an intravascular hormone store, which attenuates the fluctuations to which hGH, which is released in a pulsatile manner from the anterior pituitary gland, is subject. Secretion occurs in a pulsatile manner or with several daily peaks, which results in hGH plasma concentrations between 5 and 45 ng / mL, which only normalize to a base concentration of usually below 5 ng / mL after 10 to 30 minutes. Base levels of hGH are highest in early childhood and decrease with age. They reach the nadir in the sixth decade of life. In older men, the hGH secretion is 1/5 to 1/20 of that observed in young adults. The hGH release decreases twice as fast in men as in women, so that after the age of 50 the hGH release in women is higher than in men. The age ‐ dependent decrease in hGH secretion is related to the decreasing GHRH and increasing somatostatin secretion. Decreasing production of sex steroids, less physical activity, and changes in sleep behavior can also contribute to lowering hGH levels during aging. The GH secretion, which changes with increasing age, is associated with a progressive loss of muscle mass and strength, a decrease in physical performance, an increase in body fat and a decrease in bone mineral density (BMD).
Clinical results regarding growth hormone concentrations should be interpreted with caution as they may vary depending on the time of day, gender, age and many other internal and external factors (physical activity, stress, hypoglycaemia, etc.).
Excess growth hormone
Excess growth hormone is typically accompanied by gigantism and acromegaly. Gigantism is abnormal, highly proportioned growth that occurs due to excessive hGH and IGF-1 effects during childhood when the epiphyseal plates are still open and leads to tall stature. Acromegaly describes the same dysfunction caused by hGH and IGF-1 excess in adulthood when the epiphyseal cartilage is closed. It is often caused by hGH-secreting somatotropic adenomas of the anterior pituitary gland. The clinical manifestations of acromegaly range from insidious signs, such as: Excessive acral growth and coarsening of facial features lead to significant metabolic, cardiovascular and respiratory manifestations, leading to increased morbidity and mortality.
Growth hormone deficiency (GHD)
Growth hormone deficiency in children inhibits the growth in length of bones. In adults, severe growth hormone deficiency is associated with decreased muscle strength and bone mass, insulin sensitivity, abdominal obesity and increased cardiovascular risk factors (e.g. abnormal fat distribution, arteriosclerosis). As the growth hormone deficiency progresses, renal, skeletal and intestinal cells become insensitive to parathyroid hormone (PTH) in adults, leading to a mild form of PTH resistance and increased PTH concentrations in the serum. Along with a decrease in the sensitivity of the target organs, the calcemic response to PTH is delayed.
Stimulation and suppression tests in the diagnosis of growth hormone disorders
The diagnosis of growth hormone deficiency or excess is based on clinical auxological criteria and an NMR spectroscopy of the pituitary gland. It is confirmed by determining the hGH concentration in the serum using stimulation or suppression tests (i.e. a combination of arginine and GHRH (hGH releasing hormone), clonidine or insulin).
For a correct assessment, the hGH base concentrations and the concentrations after stimulation and suppression should be measured. The cutoff levels for the diagnosis of hGH deficiency can vary depending on the type of stimulation test and are influenced by the body mass index (BMI). Guidelines on cutoff levels should be found in the literature.
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