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PSL300 Midterm Review - French_s section Lec 1-12.pdf

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Michelle French

PSL300 Midterm Overview Introduction 1. Physiology Denon = the science of how the body fns 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, reproduve systems) key aspect = homeostasis: the process of maintaining a constant internal envt despite changing condons o perturbans can be (1) internal or (2) external homeostasis thrown o organisms ampts to compensate if compensa n fails, illness/disease; if succeeds, wellness o negave feedback (response opposes direon caused by inal sus) e.g. regulan of bp o posve feedback (response reinforces direon caused by inal sus; requires some outside factor to put brake) e.g. oxytocin and control of uterine contraons o biological rhythmsresult from changes in a setpoint (e.g. circadian) o maintaining homeostasis (and other fns) requires intercellular communication local: GAP JUNCTIONS (channels foron 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 (neurotransmiers 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 idend? remove gland/replace gland or extract/implant gland or extract to produce excess and see eects purify extract and test for eect in biological assays Case Study: Maintenance of Blood Pressure o knowledge of the physiology of b.p. control allows treatments: drugs direct baroreceptor saon Classication of Hormon es and Control of Release 2. Features of Hormones can be made in di places in body; made by cells in specic endocrineor other ssues transported in bloodto DISTANT TARGETS & bind to specic receptors may act on multiple tissues alter acvity of target cells acn 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 fn decline, overproduon due tomulus of high [gluc] o can check by tesng for C-pepdes in blood 4. Types of Hormones Pepde/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 starng 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 Page 1 of 16 FSH glycosylated o water soluble (dissolved in plasma) i.e., dont need carrier SHORT half-life in plasma (b/c unprotected) o bind to membrane receptors nal products cleaved during processing Steroid (cholesterol derivaves) o synthesized only from cholesterol (complex pathways making many intermediates as disnct hormones) in (i) mitochondria and (ii) smooth ER the various complements of enzymesare characterisof speci steroid-producing cells o made ON DEMAND (no storage; just diuse 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 aon like pepdes! Amine (derived from single AAs) o Tryptophan derivative = MELATONIN secreted at night (sleep); made iineal gland has diverse eects (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 = pron, GH, TSH, ACTH, LH & FSH 6. mulus-n Mechanisms Endocrine CELLS directly sensestimuli, then secrete hormone o e.g., parasympathemulaon of insulin release stimuli act through intracellular pathwaysto: o change membrane potenal 2+ o free cytosolic [Ca] o alter enzyme acvity (e.g., through phosphorylan) o transport of hormone substrates into cell (and thus hormone synthesis) o alter gene regulan (genes that code for hormones/enzymes needed for hormone synthesis) o promote survival (and somemes GROWTH) of the endocrine cell Example: Glucose Smulan of Insulin Release o high plasma [glucose] binding to GLUT2receptors (liver) ycolysis ATP/ADP ATP blocks ATP- sensitive K+channel K builds up on inside of cell and becomes posive DEPOLARIZATION voltage-gated Ca 2+ 2+ channelsopen up and cytosolic [Ca ] fusion of insulin-containing vesicles with PM and release o overall: glucose triggers insulin release 7. Factors Determining Hormone Ac hormone aon 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. Deng Hormones hormones = POTENT (need concentraons in the na no- or picomolars) measurements (sensive method): o immunoassay: tagged ANTIBODY for hormone deteon in blood/urine e.g., pregnancy test o immunohistochemistry: den in ssue o (both use anbodies) Page 2 of 16 Receptors & Signaling 9. How do hormones signal? bind to receptor conformational changeand altered avity of RECEPTOR alter acvity of intracellular signaling pathways change in synthesis of target proteins and/or modion of exisng proteins 10. Receptors Features o large proteins o in families bind to similar hormones (e.g., adrenergic receptors) o muple receptors can bind a single ligand the same hormone can elicit di responses in di ssues e.g., epinephrine on cardiac vs. skeletal muscles o variable numbers on/in target cell either on PM, cytosol, nucleus o can be avated/inhibited Prope o very high anity for specihormone 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 testostere as a fn of concentraon: peaks & plateaus = saturaon o reversible (i.e., non-covalent binding) e.g., cold hormones get kicked o 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 transcripon = genomic eects the hormone-receptor complex(HRC) binds to hormone-responsive elements (HREs) on DNA (speci sequences) the proteins produced thru gene regulaon has a biological eect only the genes with HREs will be avated/repressed e.g., estrogen somemes the receptors recruit co-repressors to inhibit transcripon SLOW process o plasma membrane receptors G protein-coupled receptors most common signaling pathway in our body many di types of G proteins s, i, qc. targets: ADENYLYL CYCLASE, PHOSPHOLIPASE C, GUANYLYL CYCLASE, ion channels Pathway 1: hormone binds -subunit exchanges GDP for GTP (GTPase) = acve acvated adenylyl cyclase (AC) AC catalyzes conversion of ATP into cAMP cAMP acvated protein kinase A (PKA) phosphorylates many downstre
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