Growth Hormone
Growth Hormone (GH), also called somatotropin, is a 191-amino-acid peptide hormone secreted by somatotroph cells of the anterior pituitary gland. It is the body’s primary anabolic hormone, regulating growth, body composition, and metabolism throughout life.
Structure of human growth hormone (somatotropin) — a single-chain protein with two disulfide bonds
Hypothalamus–Pituitary Control (Somatotropic Axis)
GH secretion is regulated by two hypothalamic releasing hormones in opposition:
- GHRH (Growth Hormone-Releasing Hormone): stimulates GH release from somatotrophs
- Somatostatin (SST): inhibits GH release
- Ghrelin (from stomach): potent GH secretagogue via GHS-R receptors
GH release is pulsatile — not continuous. The largest pulse occurs ~1 hour after sleep onset, during slow-wave (deep) sleep. Sleep quality therefore directly affects GH output.
IGF-1 Mediation
Most growth-promoting effects of GH are indirect, mediated by Insulin-like Growth Factor 1 (IGF-1):
GH → liver (and other tissues) → IGF-1 → target tissues (muscle, bone, cartilage)
IGF-1 acts via its own receptor (IGF-1R), a tyrosine kinase, to stimulate cell proliferation and differentiation. A negative feedback loop: IGF-1 inhibits GHRH and stimulates somatostatin.
Anabolic Effects
| Target | Effect |
|---|---|
| Bone | ↑ chondrocyte proliferation → longitudinal growth; ↑ bone density in adults |
| Muscle | ↑ protein synthesis, ↑ amino acid uptake, anti-catabolic |
| Fat tissue | ↑ lipolysis → ↓ adipose mass (especially visceral fat) |
| Liver | ↑ IGF-1 production, gluconeogenesis, glycogenolysis |
| Immune system | Modulates T-cell and NK-cell activity |
GH is counter-regulatory to insulin: it promotes glucose production and can induce insulin resistance at high doses.
Pulsatile Release and Sleep
During childhood and adolescence, ~70% of daily GH is secreted during nocturnal slow-wave sleep. Factors that increase GH:
- Sleep (especially stage N3 / deep sleep)
- Exercise (especially high-intensity)
- Fasting/hypoglycemia
- Stress (acute)
- Puberty (estrogen and testosterone amplify GH pulses)
Factors that suppress GH:
- Obesity (particularly visceral fat)
- Hyperglycemia
- Aging (GH declines ~15% per decade after age 30 — “somatopause”)
Childhood vs. Adult Roles
In childhood/adolescence: GH drives linear bone growth via epiphyseal growth plates. Once growth plates fuse (end of puberty), linear growth stops.
In adults: GH maintains muscle mass, bone density, fat distribution, and metabolic rate. Adult GH deficiency causes increased visceral fat, reduced muscle, fatigue, and cardiovascular risk.
Pathology: Deficiency vs. Excess
| Condition | Cause | Effect |
|---|---|---|
| GH deficiency (childhood) | Pituitary tumor, genetic, idiopathic | Short stature, delayed puberty |
| GH deficiency (adult) | Pituitary damage | ↑ fat, ↓ muscle, osteoporosis, fatigue |
| Gigantism | GH excess before growth plate fusion | Excessive height (rare; e.g., pituitary adenoma) |
| Acromegaly | GH excess after fusion | Enlarged hands/feet/jaw, coarse features, organ enlargement, cardiovascular risk |
Clinical Use
- Recombinant GH (somatropin): Used in GH deficiency, Turner syndrome, Prader-Willi, chronic kidney disease, and HIV-associated wasting
- GH as performance-enhancing drug: Widely misused in sport — improves lean body mass and recovery, but detection via IGF-1 and GH biomarkers
- Pegvisomant: GH receptor antagonist used in acromegaly treatment
- Somatostatin analogs (octreotide): Suppress GH in acromegaly
see also
Tags: HormoneNeurotransmitter science ai-generated
Superlink: 052 🫧Hormone und Neurotransmitter
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Erstellt: 03-09-22 16:07