BIO 304 · Human Anatomy & Physiology
Hormone Mechanisms
Endocrine System · Module 9
A reference for the Hormone Mechanisms video. Endocrine signaling is slow but global. Hormones travel in blood, bind specific receptors on or in target cells, and produce effects over minutes to days.
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- Distinguish steroid (lipid-soluble) from peptide (water-soluble) hormones by structure, transport, and receptor location.
- Compare second-messenger and direct gene activation pathways.
- Describe negative feedback control of hormone release using the HPA axis as an example.
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Two Hormone Classes
Peptide / amine hormones
- Examplesinsulin, glucagon, growth hormone, ADH, oxytocin, epinephrine, TSH
- Solubilitywater-soluble; circulate freely in plasma
- Receptor locationon cell surface
- Mechanismsecond messenger cascade
- Response speedfast (seconds to minutes)
- Durationshort; hormone is degraded relatively quickly
Steroid / thyroid hormones
- Examplescortisol, aldosterone, estrogen, testosterone, vitamin D, T₃/T₄
- Solubilitylipid-soluble; need transport proteins in plasma
- Receptor locationintracellular (cytoplasm or nucleus)
- Mechanismhormone-receptor complex binds DNA; modifies gene expression
- Response speedslow (hours)
- Durationlong; new proteins persist
Other modes
- Endocrinehormone travels via blood to distant target
- Paracrinelocal diffusion to nearby cell (histamine, prostaglandins)
- Autocrineacts on the cell that secreted it
Receptors & Feedback
Second messenger systems
- GPCR → cAMPepi on beta receptors; activates PKA → phosphorylates targets
- GPCR → IP₃ / DAG / Ca²⁺alpha-1 receptor; vasoconstriction
- Tyrosine kinase receptorinsulin, growth factors; receptor itself phosphorylates
- Amplificationone hormone → many enzymes → thousands of products
Direct gene activation
- Steroid diffuses through membranebinds cytoplasmic or nuclear receptor
- Receptor-hormone complexenters nucleus; binds hormone response element on DNA
- Transcription & translationnew proteins produced; effects unfold over hours
Control of release
- Humoralresponse to ion or nutrient level (parathyroid senses Ca²⁺)
- Hormonalone hormone triggers another (TRH → TSH → T₃/T₄)
- Neuralnerves stimulate gland (sympathetic to adrenal medulla)
Feedback
- Negative feedbackrising hormone shuts off its own release; the dominant mode
- Positive feedbackrising hormone amplifies release (LH surge at ovulation)
- HPA axis examplestress → CRH → ACTH → cortisol; cortisol inhibits CRH and ACTH
Receptor regulation
- Up-regulationlow hormone → more receptors expressed
- Down-regulationsustained high hormone → fewer receptors (insulin resistance)
- Permissivenessone hormone needs another to be present (cortisol allows epi action)
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