Peptide hormones Bind to cell surface receptors as they are hydrophilic and cannot cross the lipid membrane. Signal transduction typically via second messengers (e.g. cAMP, IP₃/DAG pathways). Examples: Insulin, ACTH, ADH, glucagon.
Steroid hormones Lipophilic: cross the cell membrane and bind to intracellular receptors (cytoplasmic or nuclear). Hormone–receptor complex acts as a transcription factor, regulating gene expression. Onset of action is delayed but prolonged. Examples: Cortisol, aldosterone, oestrogen, testosterone, vitamin D.
Amino acid–derived hormones Synthesised from tyrosine or tryptophan. Action varies: o Thyroxine (T₄) and triiodothyronine (T₃) act via nuclear receptors→ genomic effects. o Adrenaline and noradrenaline act via membrane receptors→ rapid non-genomic effects. Other examples: dopamine, melatonin.
Hormone resistance syndromes Target tissues are unresponsive to hormone action, despite normal or elevated levels. Common mechanisms: receptor defects or post-receptor signalling abnormalities. Examples: o Pseudohypoparathyroidism – resistance to PTH → hypocalcaemia, ↑PTH. o Type 2 diabetes mellitus – insulin resistance. o Androgen insensitivity syndrome – resistance to testosterone in XY individuals.
Feedback regulation Endocrine systems commonly regulated by negative feedback loops. Hormone secretion is inhibited by the downstream product. Example: Cortisol inhibits CRH and ACTH release via feedback on hypothalamus and pituitary. Some systems use positive feedback (e.g. oestrogen surge pre-ovulation increasing LH).
Pulsatile and circadian release Many hormones exhibit pulsatile or diurnal (circadian) secretion patterns. Maintains receptor sensitivity and physiological rhythm. Examples: o Growth hormone (GH) – released in pulses, especially during sleep. o Cortisol – peaks in early morning (∼8 AM), lowest at night →circadian rhythm. o LH/FSH – pulsatile secretion is essential for reproductive function.
