Endocrine Physiology (Part 1)

Ultimate purpose of hormone secretion = activate a receptor and provoke a cellular response (or be converted to an active form that can do so).
Sensitivity of a target cell depends on number & specificity of its receptors.
- Up-regulation: cell inserts/expresses more receptors → higher probability of hormone binding → larger response.
- Down-regulation: cell removes/internalises receptors → reduced sensitivity.
Key take-away: the body can modulate potency of a fixed hormone concentration simply by changing receptor density.

Hormones rarely act in isolation; multiple signals can converge on the same tissue.
Figure discussed: Thyroid Hormone (TH) and Epinephrine (Epi) impacting lipolysis.
- TH alone → almost no fatty-acid (FA) release (purple baseline).
- Epi alone → modest FA release.
- Sequence TH ➜ up-regulates β-adrenergic receptors ➜ Epi applied later binds more efficiently ➜ large FA release (synergistic/permissive effect).
Clinical relevance: patients with altered thyroid status often show exaggerated or blunted responses to catecholamines.

Secreting excess hormone (hypersecretion) can induce disease states – collectively labelled pharmacological effects.
Classic example furnished later: hyperthyroidism (excess TH) leading to growth stunting, menstrual‐cycle disruption, energy imbalance, etc.
Conversely, hyposecretion can impair normal physiology (e.g., type 1 diabetes – absence of insulin).

Three broad inputs decide whether an endocrine gland releases (or withholds) hormone:
1. Other hormones (tropic/trophic control).
2. Nervous input (neurotransmitters from CNS or ANS).
3. Ion or nutrient levels in the bloodstream bathing the gland.
Integration of these signals obeys the same summation principle seen in neurons – nothing happens “in a vacuum.”