PSL300H1 Study Guide - Midterm Guide: Semen Analysis, Zona Glomerulosa, Y Chromosome

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PSL300 Midterm Overview
Introduction
1. Physiology
Definition = the science of how the body f’ns
spans from molecules to organisms (bridges the gap b/w cell & molec bio and ecology)
divided into organ systems (in PSL300: integumentary, muscular, skeletal, nervous, endocrine, reproductive systems)
key aspect = homeostasis: the process of maintaining a constant internal env’t despite changing conditions
o perturbations can be (1) internal or (2) external homeostasis thrown off organisms attempts to compensate
if compensation fails, illness/disease; if succeeds, wellness
o negative feedback (response opposes direction caused by initial stimulus)
e.g. regulation of bp
o positive feedback (response reinforces direction caused by initial stimulus; requires some outside factor to put brake)
e.g. oxytocin and control of uterine contractions
o biological rhythms result from changes in a setpoint (e.g. circadian)
o maintaining homeostasis (and other f’ns) requires intercellular communication
local: GAP JUNCTIONS (channels for ion flow b/w cells), CONTACT-DEPENDENT SIGNALS (membrane-bound
ligand and receptor), AUTOCRINE SIGNALS (signal acts on receptors of same cell types)
long distance: endocrine system (hormones) & nervous system (neurotransmitters and neurohormones)
Endocrine system
o hormones are produced in (i) primary or (ii) secondary endocrine glands
o glands secrete hormones into the bloodstream (vs. duct in exocrine)
o How were many hormones identified?
remove gland/replace gland or extract/implant gland or extract to produce excess and see effects
purify extract and test for effect in biological assays
Case Study: Maintenance of Blood Pressure
o knowledge of the physiology of b.p. control allows treatments:
drugs
direct baroreceptor stimulation
Classification of Hormones and Control of Release
2. Features of Hormones
can be made in diff places in body; made by cells in specific endocrine glands or other tissues
transported in blood to DISTANT TARGETS & bind to specific receptors
may act on multiple tissues
alter activity of target cells
action must be terminated
maintain homeostasis or cause change in many physio processes
3. Case Study: Man with Hyperglycemia
hyperglycemic, too much insulin in blood
Cause: only makes proinsulin insulin f’n decline, overproduction due to stimulus of high [gluc]
o can check by testing for C-peptides in blood
4. Types of Hormones
Peptide/Protein Hormones (3+ AAs)
o most of the hormones
o made in advance & stored in secretory vesicles (like secreted proteins)
release by exocytosis upon signal
goes through same sequence of protein synthesis starting in rough ER
preprohormone fed thru RER signal sequence cleaved = prohormone Golgi processing hormone
a single PREPROHORMONE can contain: (i) just one copy of the hormone, (ii) several copies of the same
hormone, or (iii) 2+ types of hormones
examples of processing
insulin DISULFIDE BONDS are formed in proinsulin protein is cleaved at two sites, producing insulin +
C-peptide
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FSH glycosylated
o water soluble (dissolved in plasma) i.e., don’t need carrier
SHORT half-life in plasma (b/c unprotected)
o bind to membrane receptors
final products cleaved during processing
Steroid (cholesterol derivatives)
o synthesized only from cholesterol (complex pathways making many intermediates as distinct hormones)
in (i) mitochondria and (ii) smooth ER
the various complements of enzymes are characteristic of specific steroid-producing cells
o made ON DEMAND (no storage; just diffuse out)
released by SIMPLE DIFFUSION
o bound to carrier proteins in plasma longer half-life
o bind to cytoplasmic or nuclear receptors (slow mechanism)
but SOME act on PM receptors, producing fast action like peptides!
Amine (derived from single AAs)
o Tryptophan derivative = MELATONIN
secreted at night (sleep); made in pineal gland
has diverse effects (see Chart)
o Tyrosine (Tyr) derivatives = CATECHOLAMINES + THYROID HORMONES
catecholamines = epinephrine + NE
synthesized in adrenal medulla
stored in vesicles prior to release
5. Hypothalamus & Anterior Pituitary
regulate release of several hormones
o hypothalamus secretes NEUROHORMONES (= trophic hormones; released at axon terminals that act on ant. pit. cells)
anterior pituitary in response releases HORMONES
ant. pit. hormones = prolactin, GH, TSH, ACTH, LH & FSH
6. Stimulus-Action Mechanisms
Endocrine CELLS directly sense stimuli, then secrete hormone
o e.g., parasympathetic stimulation of insulin release
stimuli act through intracellular pathways to:
o change membrane potential
o free cytosolic [Ca2+]
o alter enzyme activity (e.g., through phosphorylation)
o transport of hormone substrates into cell (and thus ↑ hormone synthesis)
o alter gene regulation (genes that code for hormones/enzymes needed for hormone synthesis)
o promote survival (and sometimes GROWTH) of the endocrine cell
Example: Glucose Stimulation of Insulin Release
o high plasma [glucose] binding to GLUT2 receptors on β-cells ↑ glycolysis ↑ ATP/ADP ATP blocks ATP-
sensitive K+ channel K+ builds up on inside of cell and becomes positive DEPOLARIZATION voltage-gated Ca2+
channels open up and cytosolic [Ca2+] fusion of insulin-containing vesicles with PM and release
o overall: glucose triggers insulin release
7. Factors Determining Hormone Action
hormone action depends on: (i) QUANTITY of hormone released, (ii) carrier proteins, (iii) amount of RECEPTORS on target
cell
o the target cell elicits a physiological response that may up- or down-regulate the # receptors on PM
o hormones can be metabolized in liver, kidney, then excreted in urine
8. Detecting Hormones
hormones = POTENT (need concentrations in the nano- or picomolars)
measurements (sensitive method):
o immunoassay: tagged ANTIBODY for hormone detection in blood/urine
e.g., pregnancy test
o immunohistochemistry: detection in tissue
o (both use antibodies)
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Receptors & Signaling
9. How do hormones signal?
bind to receptor conformational change and altered activity of RECEPTOR alter activity of intracellular signaling
pathways change in synthesis of target proteins and/or modification of existing proteins
10. Receptors
Features
o large proteins
o in families bind to similar hormones (e.g., adrenergic receptors)
o multiple receptors can bind a single ligand the same hormone can elicit diff responses in diff tissues
e.g., epinephrine on cardiac vs. skeletal muscles
o variable numbers on/in target cell
either on PM, cytosol, nucleus
o can be activated/inhibited
Properties
o very high affinity for specific hormone
e.g., androgen receptors bind more strongly to androgens than to estrogens (even though very similar structure)
o saturable (like any enzyme)
e.g., bound labeled testosterone as a f’n of concentration: peaks & plateaus = saturation
o reversible (i.e., non-covalent binding)
e.g., cold hormones get “kicked off” androgen receptors more easily by other androgens; but if enough estrogen
is added, can also compete with cold androgens
Two main types
o intracellular receptors bind lipid-soluble hormones (i.e., steroid and some amines)
cytosolic and/or nuclear
DIRECTLY alter gene transcription = genomic effects
the hormone-receptor complex (HRC) binds to hormone-responsive elements (HREs) on DNA (specific
sequences) the proteins produced thru gene regulation has a biological effect
only the genes with HREs will be activated/repressed
e.g., estrogen
sometimes the receptors recruit co-repressors to inhibit transcription
SLOW process
o plasma membrane receptors
G protein-coupled receptors
most common signaling pathway in our body
many diff types of G proteins s, i, q, etc.
targets: ADENYLYL CYCLASE, PHOSPHOLIPASE C, GUANYLYL CYCLASE, ion channels
Pathway 1: hormone binds α-subunit exchanges GDP for GTP (GTPase) = active activated adenylyl
cyclase (AC) AC catalyzes conversion of ATP into cAMP cAMP activated protein kinase A (PKA)
phosphorylates many downstream proteins, activating or inhibiting cellular response
cAMP is broken down by cAMP phosphodiesterase (caffeine inhibits this enzyme, prolonging action of
cAMP)
Pathway 2: Hormone binds activated G protein then activates phospholipase C (PLC) PLC cleaves PIP2
into IP3 and diacylglycerol (i) IP3 goes to ER membrane and opens Ca2+ channels, cytosolic Ca2+; (ii)
DAG activates phosphokinase C (PKC), which acts on downstream enzymes/proteins cellular response
receptor-enzyme receptors (the receptor has enzyme f’n)
e.g., INSULIN receptor = has cytosolic tyrosine kinase which undergoes autophosphorylation
insulin activates 2 signaling pathways: Ras-MAP kinase and PI-3 kinase/PKB
Ras Raf MEK Erk = transcription factor proteins
PI-3 kinase/PKB glycogen synthesis, glucose transport, apoptosis suppression
11. Fight-or-Flight Responses
Liver glucose release; fat FA release; heart muscle contraction; skeletal muscle blood vessels LESS vasoconstriction;
intestine, skin, kidney vasoconstriction
epinephrine + NE diverse physiological effects via diff receptors/effectors
o adrenergic receptors β1, β2, α2, α1
β1, β2 activate AC
α2, α1 activate PLC
Epinephrine ↑ glycogenolysis, ↓ glycogenesis (i.e., more break-down, less synthesis)
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