Growth Hormone & Anterior Pituitary Hormone Regulation
Somatotrophic Cells & Growth Hormone (GH)
- One of 5 anterior-pituitary cell types; most abundant.
- Secrete Growth Hormone (GH) (a.k.a. somatotropin) — most abundant anterior-pituitary hormone.
- GH acts on growth and metabolism.
Direct & Indirect Actions of GH
- Indirect (growth) actions – via Insulin-Like Growth Factors (IGFs)
- GH ➜ liver, bone, skeletal muscle, cartilage ➜ release of IGFs.
- IGFs stimulate bone lengthening, soft-tissue hypertrophy, protein synthesis, wound healing.
- Direct metabolic actions (energy-mobilising)
- Glucose-sparing effect
- ↓ glucose uptake in most cells so neurons can continue ATP production during scarcity.
- Lipolysis
- GH➜ adipocytes ➜ breakdown of triglycerides: (\text{TG}\rightarrow \text{Glycerol}+3\,\text{FA})
- Released fatty acids oxidised for ATP.
- Hepatic glucose output
- Stimulates glycogenolysis & gluconeogenesis ➜ ↑ blood glucose.
- Net result: ample ATP for the energy-intensive process of growth.
- Real-world illustration: Teenagers in growth spurts experience ↑ appetite to meet ATP/nutrient demand.
Stimuli That Increase GH Release
- Hypoglycaemia (\downarrow\text{[Glucose]}).
- ↓ blood fatty acids.
- ↑ blood amino acids (signals protein availability).
- Exercise, stress, deep sleep, puberty hormones, etc. (implied).
Hypothalamic–Pituitary Regulation Loop
- Step 1 – Hypothalamus
- Releases Growth Hormone-Releasing Hormone (GHRH) into the hypophyseal portal system.
- Step 2 – Anterior Pituitary (Somatotrophs)
- GHRH binds somatotrophs ➜ GH secretion.
- Step 3 – Target Actions
- Metabolic (direct) & Growth (via IGFs) as above.
- Negative Feedback
- ↑ GH & ↑ IGF levels ➜ inhibit GHRH release (hypothalamus).
- IGFs also directly inhibit GH secretion at the pituitary.
- Growth Hormone-Inhibiting Hormone (GHIH) / Somatostatin
- Secreted by hypothalamus when nutrient/energy levels are adequate or GH/IGF are high.
- Travels via the same portal system; suppresses GH release.
Key Principles & Clarifications
- Feedback is hormone-based, not organ-based: the hormone concentrations act as the signals.
- Typical endocrine pattern: stimulus ➜ hypothalamic releasing hormone ➜ anterior-pituitary hormone ➜ peripheral hormone ➜ negative feedback.
Quick Reference – Anterior Pituitary Hormones & Their Regulation
- GH (Growth Hormone)
- + by GHRH
- – by GHIH (somatostatin), ↑GH, ↑IGF
- TSH (Thyroid-Stimulating Hormone)
- + by TRH (Thyrotropin-Releasing Hormone)
- – by thyroid hormones (T₃/T₄)
- ACTH (Adrenocorticotropic Hormone)
- + by CRH (Corticotropin-Releasing Hormone)
- – by glucocorticoids, chiefly cortisol
- FSH (Follicle-Stimulating Hormone)
- + by GnRH (Gonadotropin-Releasing Hormone)
- – by estrogens (ovary) / inhibin (testis)
- LH (Luteinizing Hormone)
- + by GnRH
- – by estrogens, progesterone, testosterone
- PRL (Prolactin)
- + by PRH (Prolactin-Releasing Hormone)
- – by PIH (Dopamine) & ↑prolactin itself (autoinhibition)
Mnemonic – “TPFLAG” (Anterior-Pituitary Hormones)
- T – TSH
- P – Prolactin
- F – FSH
- L – LH
- A – ACTH
- G – GH
Practical/Clinical Connections
- GH deficiency in children ➜ dwarfism; excess ➜ gigantism.
- Adult excess ➜ acromegaly (enlarged hands, jaw, organs) owing to post-epiphyseal-plate closure.
- Somatostatin analogues used therapeutically to suppress GH (acromegaly) or other hypersecretory states.
- Exercise & sleep hygiene naturally augment physiologic GH spikes — exploited in paediatric endocrinology.