Summary: Physiology: Endocrine

Read the summary and the most important questions on Physiology: Endocrine

• 1 Lecture 1: Homeostasis

• 1.1 What is it?

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• What happens when there is homeostatic imbalance?

  Disturbance resulting in stress/disease

• 1.2 How is it controlled?

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• How is the internal environment controlled?

  Sensory: monitoring of blood composition
  Response: responding to changes in blood composition

• What are the internal communication methods for homeostasis?

  1. Nervous system: synaptic transmission, rapid
  2. Endocrine system: chemical transmission, rapid or slow

• 1.3 Classes of hormones

• What makes a chemical a hormone?

  Hormones exert their effects on specific target cells (TC) by interacting with receptor proteins

• 1.3.1 Nature

• What are the different classes of hormones?

  1. Amino acid derivatives (epinephrine, melatonin, thyroxine)
  2. Peptides (hypothalamic hormones, insulin)
  3. Proteins (growth hormone, prolactin)
  4. Steroids (glucocorticoids, mineralocorticoids, gonadal steroids)

• 1.4 Hormone receptors

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• Where are the receptors for steroid/thyroid hormones found?

  Cytoplasm/nucleus of target cells

• 1.4.1 G-protein

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• How does adenylate cyclase cAMP work as a second messenger?

  1. Hormone binds to a receptor
  2. Alpha subunit dissociates from G-protein complex
  3. Alpha subunit activates adenylate cyclase (AC)
  4. AC catalyzes the production of cAMP
  5. CAMP activates protein kinase
  6. Protein kinase phosphorylates other enzymes in the cell

• How does phospholipase C work as a second messenger?

  1. Hormone binds to a receptor
  2. Alpha subunit dissociates from G-protein complex 
  3. Alpha subunit activates phospholipase C
  4. DAG and IP3 are formed
  5. IP3 binds receptors on ER
  6. Stored Ca2+ diffuses into cytoplasm

• Which hormones use two different G-protein messenger mechanisms?

  Epinephrine/norepinephrine (a1 and beta adrenergic)

• 1.4.2 Tyrosine kinase

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• How does the tyrosine kinase second messenger work?

  1. 2 half receptors form dimer
  2. Insulin binding to dimer causes autophosphorylation of receptor
  3. Active tyrosine kinase receptor phosphorylates insulin receptor substrate
  4. Active signaling molecule causes cascade of effects (glucose uptake/anabolism)