Growth hormone and IGF-1 !

Regulation
Exam priority: medium

The pituitary releases growth hormone in pulses, mostly in deep sleep; the liver answers with IGF-1, which makes bones and tissues grow.

Updated 2026-11-01

Also called: GH, Somatotropin, Somatomedin C

See it in 3D: Pituitary gland · Hypothalamus · Liver

What it is

Growth hormone (GH) is a peptide from the somatotrophs of the anterior pituitary, released in bursts under the push of GHRH and the brake of somatostatin. Many of its growth effects are carried out by IGF-1, made mainly in the liver. GH itself works against insulin: it raises blood glucose and frees fat for fuel while building protein. Too much gives gigantism or acromegaly; too little gives short stature in children.

How it works, step by step

GHRH from the arcuate nucleus reaches the somatotrophs through the portal veins; ghrelin from the stomach adds a second push.
Somatostatin from the periventricular nucleus inhibits release; the balance of the two makes GH pulsatile, largest in slow-wave sleep.
GH binds its receptor on liver and growth plate cells and activates JAK2–STAT5, switching on IGF-1 gene transcription.
IGF-1 circulates bound to IGFBP-3 and the acid-labile subunit, which prolong its life and keep levels steady.
IGF-1 drives chondrocyte proliferation at the epiphyseal plate: the bone lengthens while the plate is open.
IGF-1 and GH feed back: both stimulate somatostatin and IGF-1 also inhibits the somatotroph directly.
After the plates close at puberty, excess GH can no longer lengthen bones: it thickens them and enlarges hands, feet, jaw and organs.

Hormone axes and feedback

Growth hormone axisLesion None (normal)

Tap a box to see the hormone, or choose a lesion to see the lab pattern.

Stimulates (+)
Inhibits / negative feedback (−)
Level ↑
Level ↓

Growth hormone axis. Choose «Acromegaly» and then «Laron» to compare IGF-1 in excess and in resistance.

Regulation

+GHRH and ghrelin: Raise GH release from the somatotrophs.
+Deep sleep, exercise, fasting, hypoglycemia, amino acids (arginine), puberty sex steroids: Increase pulse size; puberty roughly doubles GH secretion.
−Somatostatin: Blocks GH release; its analogues are used to suppress it.
−IGF-1 and GH (negative feedback): Raise somatostatin and inhibit the pituitary directly.
−Hyperglycemia, obesity, excess glucocorticoids, hypothyroidism: Reduce GH secretion (glucose suppression is the basis of the acromegaly test).

Direct GH actions versus actions through IGF-1

Target	Direct GH effect	IGF-1 effect
Fat	Lipolysis ↑, free fatty acids ↑	Minor
Glucose	Insulin resistance, hepatic glucose output ↑	Mild insulin-like effect (↓ glucose)
Muscle and organs	Amino acid uptake ↑	Protein synthesis and cell growth ↑
Bone	Stimulates IGF-1 at the growth plate	Chondrocyte proliferation, linear growth
Kidney	Sodium and water retention	GFR ↑

Clinical notes

Acromegaly (adult, after epiphyseal closure): coarse face, prognathism, large hands and feet, sweating, carpal tunnel, sleep apnea, hypertension, cardiomegaly and diabetes; usually a pituitary adenoma.
Gigantism: GH excess before the growth plates close, so the bones lengthen.
GH deficiency in children: short stature with slow growth velocity, delayed bone age and fasting hypoglycemia in infants; diagnosed with stimulation tests.
A macroadenoma can press on the optic chiasm: bitemporal hemianopia.

Test yourself

Think of the answer, then tap the question to see it.

Why is a random GH level a poor test for acromegaly, while IGF-1 is a good one?

GH is secreted in pulses and can be near zero or very high within hours in a healthy person. IGF-1 is bound to IGFBP-3 and changes slowly, so it integrates GH secretion over the day.

A child has short stature, high GH and low IGF-1. Where is the defect?

At the GH receptor (Laron syndrome): the pituitary makes GH, but the liver cannot respond, so IGF-1 stays low and the lost feedback lets GH rise.

Why can a patient with acromegaly develop diabetes?

GH opposes insulin: it raises hepatic glucose output and reduces peripheral glucose uptake. Chronic excess causes insulin resistance, and the beta cells may fail to compensate.

Why does the oral glucose load suppress GH in a healthy person but not in acromegaly?

Hyperglycemia normally raises hypothalamic somatostatin and suppresses GH. An adenoma secretes autonomously and ignores this signal, so GH stays high.

Why does GH excess cause gigantism in a child but acromegaly in an adult?

Linear growth needs open epiphyseal plates. Before closure, IGF-1 lengthens long bones; after closure only periosteal and soft-tissue growth is possible, so bones thicken and acral parts enlarge.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Biochemistry

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 17.3 The Pituitary Gland and Hypothalamus (OpenStax (Rice University), 2022); Growth Hormone Tests: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2025); Acromegaly: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Pituitary Adenoma (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 76). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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