EXAM 3: BIO&252 (Chapter 18: Part 1)

  1. Hormone Receptors
    • Protein/glycoprotein
    • Located in cell membrane or within cytoplasm, nucleus, or mitochondrion
    • Target = cell with specific receptors/hormones
    • No recpetor, no effect on hormone
  2. Hormone Effects
    1. Cause synthesis of new proteins (ex. make new enzymes

    2. Modify transcription/translation rate of existing proteins (make more/less)

    3. Modify activity/function of existing enzymes (increase/decrease enzyme activity)
  3. Local vs. Circulating Hormones
    • 1. Ciruclating Hormones: "endocrines = "typical hormone" (most abundant)
    •    *Transported in blood; affect target cells all over the body

    • 2. Paracrine Hormones: act only on nearby cells (do not go through the body)
    •    *E.g. somatostatin from delta cells in pancreatic islets inhibits secretion of insulin by beta cells

    • 3. Autocrine Hormones: Act on cell that secretes it
    •    *E.g. Helper T cells release interleukin 2 which stimulates the proliferation of cell that secretes it
  4. Amino Acid Derivatives (biogenic amines)
    • A. Derivatives of tyrosine
    •    *Catecholamines (Epi and Norepi)
    •    *Thyroid Hormones (T3 and T4 thyroxine)

    • B. Derivative of tryptophan
    •    *Melatonin from pineal
  5. Peptide (and protein) Hormones
    • Usually produced as prohormones
    • Prohormone = enzyme = active hormone

    • A. All hypothalamic hormones (releasing hormones, and ADH and OT)
    • B. All anterior pituitary hormones
    • C. All pancreatic hormones
    • D. Calcium-regulating hormones (PTH, Calcitonin)
    • E. Digestive hormones
    • F. Erythropoietin (kidneys)
  6. Lipid Derivatives
    • A. Derivatives of cholesterol = steroid hormones
    •    *From gonads (androgens, estrogens, progestins)
    •    *From adrenal cortex (mineralcorticoids [aldosterone], glucocorticoids [cortisol], gonadocorticoids [androgens])
    •    *From kidneys (calcitrol [Vit D])

    • B. Derivatives of arachadonic acid
    •    *Eicosanoids
    •       Prostoglandins (many tissues)
    •       Leukotrienes (white blood cells)
  7. Water-soluble hormone transport
    • Hormone NOT bound to carrier molecule
    • E.g. Catecholamines, peptides, proteins
  8. Lipid-soluble hormone transport
    • Transport requires a carrier molecule (e.g. steroids, thyroid hormones)
    • Functions of the carrier
    •    a. Increases solubility in plasma and ECF
    •    b. Decreases hormone loss at kidney
    •    c. Forms a hormone reserve

    • Hormone reserve
    • *Equilibrium exists between "bound" and "free" form
    • *Free fraction usually a very small % of total
    • *More of the bound form is released as free form is used up.
  9. Removal of Hormones from Circulation
    • Bind to receptors (some inside of cells)
    • Broken down by enzymes in liver, kidneys
    • Broken down by enzymes in plasma or ECF
  10. Mechanisms of Action
    • Depend upon lipid vs. water solubility
    •    a. Water-soluble hormone: act on membrane receptors
    •    b. Lipid-soluble hormone: act intracelluarly
  11. First and Second Messengers
    • First Messenger (hormone)
    • Bind to receptor (usually a G-protein)

    • Second Messenger
    • E.g. cAMP, cGMP, Ca2+
    • Functions:
    •    *Enzyme activator
    •    *Enzyme inhibitor
    •    *Enzyme cofactor (facilitates function)
  12. Amplification
    • Mechanism of action
    • Many 2nd messengers of the same type are formed
  13. Receptor Cascade
    • Mechanism of action
    • Different 2nd messengers activated, sequence of biochemical reactions
  14. Downregulation and Upregulation
    • Downregulation
    • Hormone levels high
    • Number of receptors and sensitivity to hormones went DOWN

    • Upregulation
    • Hormone levels low
    • Opposite effects
  15. Membrane Receptors
    • G Proteins and cAMP
    •    *Hormone binds receptor, G protein activated
    •       a. Activate adenylate cyclase, which will INCREASE cAMP, or...
    •       b. Activate PDE, which will LOWER cAMP
  16. Increased cAMP Levels
    • cAMP (2nd messenger) activates kinases
    • Kinases phosphorylate proteins which...
    •    *Open membrane channels and alter enzyme acitivity
    • (PDE inactivates cAMP)

    • E.g. Hormones
    • β receptors for E and NE
    • PTH and calcitonin ([Ca2+])
    • FSH and LH (ovaries and testis)

    • E.g. Disease = Cholera - altered G protein function
    • Toxin activates G proteins
    • G proteins can't be turned off
    • Causes increased cAMP levels in gut
    • Increased pumping of Cl- out of cells
    • Na+ and water follow = diarrhea, dehydration, death
  17. Decreased cAMP Levels
    • E.g. E and NE at α2 recpetors
    • G protein activates PDE; adenylate cyclase is not activated
    •    *PDE breaks down cAMP to AMP causing: 
    •       -Decrease cAMP
    •       -Decrease of kinase activation
    •       -Decrease enzyme activity
  18. Intracellular Receptors
    • Hormone must be lipid soluble
    •    *Binds receptors in cytoplasm
    •    *Hormone receptor complex enters nucleus
    •    *Alters gene expression
  19. Cytoplasmic Receptors
    • E.g. testosterone
    • Binds receptor in cytoplasm
    • Hormone receptor complex enters nucleus
    • Alters gene expression

  20. Binding to nuclear and/or mitochondrial receptors
    • E.g. thyroid hormone
    •       a. binds receptors on mitochondria
    •          *increase ATP production and use(NA/K pump)
    •       b. Bind receptors in nucleus
    •            * Alters gene expression
  21. Endocrine reflexes triggered by:
    • 1. Humoral stimuli (concentration in CSF)
    •   e.g. parathyroid gland
    •        .↓ [CA²] in CSF → release PTH
    • 2. Hormonal Stimuli (Tropic hormones)
    •   e.g. adrenal cortex
    •        . Release cortisol in respond to ACTH
    • 3. Neural Stimuli (action potential)
    •   e.g. posterior pituitary 
    •        . Action potentials cause ADH and OT release
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EXAM 3: BIO&252 (Chapter 18: Part 1)