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

314 views24 pages
Published on 26 Jan 2013
Page 1 of 24
PSL300 Midterm Overview
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:
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 +
Unlock document

This preview shows pages 1-3 of the document.
Unlock all 24 pages and 3 million more documents.

Already have an account? Log in
Page 2 of 24
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)
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
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)
Unlock document

This preview shows pages 1-3 of the document.
Unlock all 24 pages and 3 million more documents.

Already have an account? Log in
Page 3 of 24
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
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
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.
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
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)
Unlock document

This preview shows pages 1-3 of the document.
Unlock all 24 pages and 3 million more documents.

Already have an account? Log in

Get OneClass Grade+

Unlimited access to all notes and study guides.

Grade+All Inclusive
$10 USD/m
You will be charged $120 USD upfront and auto renewed at the end of each cycle. You may cancel anytime under Payment Settings. For more information, see our Terms and Privacy.
Payments are encrypted using 256-bit SSL. Powered by Stripe.