Summary PSL300 Term Test 1 Review

PSL300
Term Test 1 Review
Endocrine System
Lecture 1: Introducton to PPysiology
 Physiology is tPe study of Pow tPe body works
 Negatie feedbaak㹀 is wPen a cPange in a variable is reduced
 Positie feedbaak㹀 is wPen a cPange in a variable increases

Lecture 2: Hormones
Hormones: cPemical messengers tPat alter actvity of target cells to maintain Pomeostasis; made in
specifc glands wPere tPey bind to receptors; acton must be terminated
 Protein hormones—most Pormones, made in advance, secreted by exocytosis, water soluble,
membrane bound, sPort Palf-life
 Steroid hormones—syntPesized from cPolesterol, difuses out, water insoluble,
cytoplasm/nucleus bound, long Palf-life
 Tyrosine hormones (amine)—catecPolmines (bePave like peptdes, dopamine/norepinepPrine/
epinepPrine, from adrenal medulla, stored in vesicles, SNS), tPyroid Pormones (T3 and T4)
 Insulin release—stmulated by glucose
o Glucose enters cell metabolized ATP goes up  K+ cPannels close cell
depolarized voltage cPannels open insulin released
o Insulin reduces glucose (-ve feedback)
 Anterior pituitary hormones
o FLATPEG = FHS, LH, ACTH, TSH, prolactn, endorpPins, GnRH

Lecture 3: Receptors and Signaling
Rekeptors: important for regulatng processes like metabolism, Pomeostasis, growtP, blood pressure,
temperature
 Drugs work on receptors
 Hormones signal tProugP receptors
o Binds to receptor, cPanges conformaton, alters actvity of intracellular signaling
patPways, and leads to cPange in syntPesis/modifcaton of proteins
 CPanges membrane potental
 Agonist—stmulates a receptor
 Antagonist—inPibits a receptor
 Receptors are large proteins tPat are actvated and inPibited
 Can Pave multple receptors for one ligand or multple ligands for one receptor
 Located in cell membrane, cytoplasm and nucleus
 HigP afnity, saturable, specifc, reversible
 Two types:

Intracellular receptors
 Cytosolic and nuclear
 Directly alter gene transcripton = genomic efects

Plasma membrane receptors

, G-protein coupled receptors
 Sits in inactve state w/ multple G-protein subunits
 AlpPa subunit Pas multple isoforms: G(as), G(ai), G(aq) responsible for signalling
 G(as) = alpPa stmulatory, G(ai) = alpPa inPibitory, G(aq) = two patPways
 G(as)adenylyl kyklasekAMPPKAkell response
 G(as) actvates adenylyl cyclase
 No PKA pPospPorylaton, no efects
 G(aq)PLC(a) DAG PKC/(ba) IP3 Ca2+kellular response
 G(aq) actvates pPospPolipase C, two patPways result
o Actvate DAG  PKC
o Actvate IP3  Ca2+ release

Receptor-enzyme receptors
 Ex. Insulin receptor
 Insulin actvates two signaling patPs: Ras-Map kinase and PI-3 kinase/protein kinase B
 Insulin actvates PI3K/MAPK patPways and translocaton of GLUT4 to allow for glucose uptake

Receptor-channel
Integrin receptor
Take away points
 Hormone response elements are specifc DNA sequences
 Sometmes receptors recruit co-repressors to inPibit transcripton
 Only genes witP tPose elements will be repressed
 FigPt or figPt responses mediated by GPCRs (SNS)
 EpinepPrine and norepinepPrine Pave diverse pPysiological efects via diferent receptors and
efectors
 EpinepPrine increases glycogen breakdown and decreases syntPesis
 EpinepPrine Pas multple receptors, cause multple responses

Hormone modulaton
 Hormone is degraded
 Receptor down-regulated or up-regulated
 Receptor desensitzaton
 Breakdown of secondary messengers
 Biological efect provides feedback to reduce secreton

Lecture 4: Calcium Balance
Ca2+:
 Intracellular signaling
 Hormone secreton
 Blood clotting
 Neural excitability and muscle contracton
 Building and maintaining bone
 TPree locatons of Ca2+: