Step by Step
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Source and control
Growth hormone (GH, or somatotropin) is the most abundant hormone produced by the anterior pituitary's somatotroph cells. It's stimulated by GHRH, sleep (peaking during deep, stage 3/4 NREM sleep), exercise, stress, and hypoglycemia — and inhibited by somatostatin.
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Direct effects of GH
GH directly increases protein synthesis, increases fat mobilization (lipolysis), and increases blood glucose — this last effect makes GH "anti-insulin" or diabetogenic in its action.
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Indirect effects — via IGF-1
GH also stimulates the liver to produce IGF-1 (insulin-like growth factor 1), which promotes chondrocyte division, driving linear bone growth — but only before the epiphyseal growth plates close.
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Disorders of GH deficiency and excess
GH deficiency causes dwarfism (proportionate short stature). Excess GH during childhood (before epiphyseal closure) causes gigantism (excessive height). Excess GH in adults (after epiphyseal closure) causes acromegaly — enlarged hands, feet, jaw, tongue, and organs, since bones can no longer grow longer but can still grow in other ways. Treatment options include somatostatin analogs (like octreotide) or surgery.
Applied Walkthrough
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During deep sleep, GH release peaks, stimulating the liver to produce IGF-1 — which drives chondrocyte division and linear bone growth in a growing child, as long as the epiphyseal plates haven't yet closed.
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If a child's pituitary produces excessive GH before their epiphyseal plates close, the result is gigantism — significantly increased height, driven by prolonged linear bone growth.
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If instead an adult (whose epiphyseal plates have already closed) develops a GH-secreting tumor, linear bone growth is no longer possible — but bones can still thicken and soft tissues can still enlarge, producing the characteristic features of acromegaly: enlarged hands, feet, jaw, and tongue.
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This same adult's excess GH would also raise their blood glucose (its diabetogenic effect) and increase fat mobilization — illustrating that GH has metabolic effects distinct from its more famous growth-promoting role.
Exam Application
Exams test whether you understand the distinction between GH's direct metabolic effects and its indirect, IGF-1-mediated growth effects, and whether you can distinguish gigantism (excess GH before epiphyseal closure) from acromegaly (excess GH after epiphyseal closure).
⚠ Common Trap
The most common trap is confusing gigantism and acromegaly — both result from excess GH, but gigantism occurs specifically in children (before epiphyseal closure, allowing continued linear growth), while acromegaly occurs in adults (after epiphyseal closure, so growth manifests as enlargement of hands, feet, jaw, and organs instead of increased height).
✓ Quick Self-Check
1. What stimulates GH release?
GHRH, sleep (especially deep NREM sleep), exercise, stress, and hypoglycemia.
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2. What are GH's direct metabolic effects?
Increased protein synthesis, increased fat mobilization, and increased blood glucose (diabetogenic).
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3. What molecule mediates GH's growth-promoting effects, and where is it produced?
IGF-1, produced by the liver.
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4. What condition results from GH excess in childhood, versus in adulthood?
Gigantism in childhood (before epiphyseal closure); acromegaly in adulthood (after epiphyseal closure).
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5. What condition results from GH deficiency?
Dwarfism (proportionate short stature).
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