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

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Hae- Young Kee

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 Page 1 of 16  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 2+ o ↑ free cytosolic [Ca ] 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 (liver)  ↑ glycolysis  ↑ ATP/ADP  ATP blocks ATP- sensitive K channel  K builds up on inside of cell and becomes positive  DEPOLARIZATION  voltage-gated Ca 2+ channels open up and cytosolic [Ca ] ↑  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) Page 2 of 16 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 cle2ves PIP into I3 and diacylglycerol  (3) IP goes to ER membrane and opens Ca channels, ↑ cytosolic Ca ; (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) Page 3 of 16 o acts on LIVER CELL via β2 receptors  cAMP produced by adenylate cyclase  PKA (i) activates phosphorylase b kinase which activates phosphorylase a; inactivates glycogen synthase kinase (so it can’t phosphorylate & activate glycogen synthase)  more glycogen breakdown, less polymerization 12. Signal Modulation  hormone can be degraded  receptor down- or up-regulation (receptors internalized or added)  receptor DESENSITIZATION (e.g., by phosphorylation)  breakdown of 2nd messengers  biological effect  FEEDBACK to reduce hormone secretion o e.g., ↓ plasma [glucose]  ↓ insulin secretion Calcium Balance 13. Physiological Roles of Calcium  intracellular signal2+g (e.g., hormone secretion) o e.g., surge in [Ca ] inside oocyte upon fertilization  blood clotting  neural excitability & muscle contraction  building & maintaining BONE 14. Distribution of Calcium  ECF – 0.1% o exchanges calcium w/ bone and cells (analogous to a “buffer”)  Bone – 99.0%  Intracellular – 0.9%  input through small intestine = output through excretion = 4 mmoles/day 15. Maintenance of Bone  bone = constantly formed/resorbed  Structure overview o osteon = unit of bone that runs the “length” of bone and has ring structures ‒ contains blood vessel and nerve o spongy bone (lateral shock absorbance) & compact bone (strongest; withstand a lot of force) o calcium in bone mainly hydroxyapatite C10(PO4 6OH2(small amt. ionized and exchangeable)  Bone dynamics o resting phase  resorption  cavity made by osteoclasts  formation/repair  Cell Types Involved o osteoclasts – removes Ca from bone and puts into plasma (osteoclast for “cleave”) + ‒ has microenv’t of low pH (H pumped) with seals on either side o osteoblasts (osteoblast for “build”) promote osteoclast formation via RANKL/RANK interaction ‒ osteoclast precursors express RANK (receptor activator of nuclear factor kappa B) on cell surface ‒ osteoblasts express RANKL (RANK ligand) on surface  bind to RANK differentiation & fusion of osteoclast precursors  multi-nucleate osteoclast ‒ osteoprotegerin (OPG) secreted by osteoblast blocks RANKL/RANK interaction  a way to modulate s.t. signal is not too strong (i.e. modulation of osteoclast formation – a control point)  OPG analogs = can be drug therapy for osteoporosis (by reducing osteoclast formation) o osteocytes = required osteoblasts  Hormones Involved o hormones work hard together to maintain critical plasma Ca levels, even to the detriment of bone! ‒ act on 3 targets: bones, kidney (excretion), dige2+ive tract (nutrient absorption) o parathyroid hormone (PTH) – main effect to ↑ plasma [Ca ] ‒ release from chief cells of parathyroid glands (essential for life, unlike thyroid)  has calcium-sensing receptor (G protein-coupled 2+inhibition of adenylyl cyclase  PLC activated  PTH synthesis/secretion inhibited in response to high Ca in ECM)  exact intracellular pathway not all worked out yet 2+ ‒ super sensitive to changes in EC [Ca ] 2+  steep increase in response to falling levels of blood Ca ‒ ↑ plasma [Ca ] by acting directly on bone and kidney  on OSTEOBLASTS: ↑ RANKL, ↓ OPG  overall ↑ osteoclast formation  bone resorption Page 4 of 16  ↑ reabsorption @ DISTAL TUBULE, ↓ phosphate reabsorption @ PROXIMAL TUBULE  ↑ calcitriol synthesis (see Calcitriol) o calcitriol – main effect: ↑ plasma [Ca ] but also spare bone; help deposition in bone over the long-term (s.t. no huge amts. of bone resorption) ‒ synthetic pathway: 7-dehydroxycholesterol  skin: cholecalciferol (vitam3n D )  liver: 25- hydroxycholecalciferol  PTH on kidney: 1,25-dihydroxycholecalciferol (CALCITRIOL) ‒ intracellular action:  binds to vitamin D nuclear receptor  ↑ exp. of channels/binding proteins/transporters in KIDNEY & 2+ INTESTINE; ↑ RANKL & OPG in osteoblasts  ↑ plasma [Ca ]  thus, brings more [Ca ] into plasma, w/o resorbing much from bone 2+ o calcitonin – main effect: ↓ plasma [Ca ] and inhibit bone resorption 2+ ‒ secreted from C cells (aka parafollicular cells) of thyroid – C cells have [Ca ]-sensing receptors  when Ca binds, stimulates release of calcitonin ‒ actions: 2+  protect skeleton from Ca loss during pregnancy and lactation  ↓ activity of osteoclasts  inhibit bone resorption (s.t. overall, osteoblast activity is greater and bone is formed)  inhibits calcium reabsorption in kidneys  Control of Plasma Phosphate Levels 2+ o PTH: ↑ P release from bone (b/c they follow Ca ) and ↓ reabsorption from kidney  so aims to raise plasma P levels but also increases its excretion (modulating effect?) o calcitriol: ↑ P absorption in intestine, ↑ reabsorption by kidney  get P in: over long term, need both calcium + P to form bone 16. Case Study: Boy with Rickets  symptoms: slowed postnatal growth, motor retardation, lower limb deformities, rickets, and alopecia (baldness)  lab: hypocalcemic & hypophosphatemic (i.e., low Ca and P4 ) o 25-hydroxycholecalciferol levels normal o CALCITRIOL levels >> normal  PTH levels HIGH (causing high calcitriol levels); calcitonin levels LOW  Cause: resistant to calcitriol (mutation in VitD receptor)  Treatments: give super-physiological doses of calcitriol; supplement Ca ; use analog of calcitriol Water and Ion Balance 17. Distribution of Water in the body  Cells – 2/3  ECF – 1/3 o interstitial 75% (1/4 of total) o plasma 25% (1/12 of total)  Balance o intake (2.2 L/day) + metabolic production (0.3 L/day) = output (urine, sweat, breath, feces; 2.5 L/day total) 18. Kidney  osmotic gradient in kidney from cortex (low) to medulla (high) o excretory pathway: blood enters Bowman’s capsule of a nephron and filtrate gets into GLOMERULUS  proximal convoluted tubule  Loop of Henle  distal tubule  collecting duct  ureter  bladder ‒ filtrate ≠ excreted urine… a lot is added/removed along this pathway ‒ due to osmotic gradient, as filtrate travels down proximal tubule, water leaves (concentrating filtrate) ‒ in the DISTAL tubule, ions are reabsorbed, but not water 19. Hormones in Regulating Water Balance  vasopressin (= anti-diuretic hormone, ADH) – main effect: 2 H O reabsorption o synthesized in hypothalamus, and secreted from posterior pituitary o stimulus = REDUCED STRETCH of atria, aortic and carotid arteries + osmoreceptors in hypothalamus ‒ osmolarity = most potent stimulus for ADH release o ADH works on the COLLECTING DUCT to increase H 2 permeability and absorption (“Always Digging Holes”)  water goes back into blood ‒ inserts aquaporin-2 water pores through a signal cascade through a G protein pathway (cAMP asmessenger) which ultimately causes fusion of vesicles containing these porins Page 5 of 16  AP-2 put into apical membrane (adjacent to collecting duct lumen) ‒ vasopressin allows water to leave since the interstitial osmolarity becomes progressively higher down the collecting duct (w/o vasopressin, water won’t leave, and urine will be in high volume and dilute) + +  aldosterone – main effect: ↑ Na reabsorption, ↑ K secretion o synth. in cortex  acts on DISTAL TUBULE & COLLECTING DUCT (on principal cells) + + + + + ‒ prevents degrada+ion of apical Na channe+ + ↑ expression of Na and K channels and Na /K ATPase (basal membrane)  K will leave the cell and Na will enter the cell from apical membrane due to electrochemical gradient; ATPase pumps K from blood and puts Na back in blood + o negative feedback: simple (K , osmolarity) & complex (renin-angiotensin II) ‒ renin-angiotensin-aldosterone pathway: JUXTAGLOMERULAR cells detect changes in blood volume/b.p. in afferent arteriole  secretes RENIN if drop in b.p.  renin converts angiotensinogen to angiotensin I  converted into angiotensin II by angiotensin-converting enzyme (ACE)  effects  hypothalamus – thirst and behavioural responses; ↑ b.p.*  vasoconstriction (to ↑ b.p.*)  aldosterone secretion (salt, and thus water, retention  ↑ b.p.*)  atrial natriuretic hormone (ANH) – main effect: ↓ Na and H O reabsorption, ↑ K reabsorption (antagonist of 2 aldosterone & ADH) o Discovery: atria of hearts had granules  dissected and performed biological assay  rats showed drop in b.p. upon injection of atrial extract, but not ventricular o family: ANP (expressed in atria and brain), BNP (ventricles and brain), CNP (brain, pit, vessels, kidneys; main effect vasodilation) o Mechanism: ↑ blood volume  atrial/ventricular stretch  ANP/BNP release, respectively  acts on various organs ‒ hypothalamus – inhibits release of VP ‒ kidney – dilates afferent arteriole (to ↑ glomerular filtrate release) & ↓ renin secretion; acts on DISTAL TUBULE + to ↓ Na reabsorption ‒ adrenal cortex – ↓ aldosterone secretion ‒ medulla oblongata – ↓ sympathetic output ‒ all of these ultimately ↓ b.p.* 20. Case Study: The thirsty woman  extreme thirst and frequent urination  appears normal  Diagnosis: diabetes insipidus o ADH secretion inhibited or is non-functional  so no water reabsorption (all lost to urine) o test – ADH levels, check ADH gene or its receptor gene  Key point: ADH is important Pancreatic Hormones 21. Metabolism = anabolism (building molecules) + catabolism (breaking molecules down to get E) = sum of all chemical body rxns  basal metabolic rate (BMR): an individual’s E expenditure while resting @ comfortable temperature, fasted (i.e., not digesting)  energy balance  fed vs. fasted state o fed: glycogenesis, lipogenesis, protein synthesis ‒ dominant hormone = INSULIN o unfed/fasted: glycogenolysis, lipolysis, protein degradation, gluconeogenesis ‒ dominant hormone = GLUCAGON 22. Endocrine Pancreas  α cells  glucagon  β cells  insulin  δ cells  somatostatin (GHIH) 23. Feeding vs. Fasting Metabolism  RATIO of glucagon vs. insulin  overall effect (ultimately, homeostasis) 24. Insulin  Effects o ↑ glucose transport into insulin-sensitive cells ‒ by ↑ GLUT4 transporters to the PM (fat, muscle cells)  facilitated diffusion of glucose into cells Page 6 of 16  if no insulin, GLUT4 are internalized ‒ in LIVER: insulin activates hexokinase to maintain glucose conc. grad. (by phosphorylating the glucose that comes into cell to glucose 6-P, s.t. [ginsidealways low)  thus, indirectly increase glucose uptake by liver o activate enzymes for glycolysis, glycogenesis, lipogenesis ‒ inhibits enzymes for glycogenolysis, gluconeogenesis, and lipolysis o promotes lipogenesis and inhibits beta-oxidation (breakdown of fat) o enhances cell proliferation  Stimulus for Insulin Release o GLUT2 transporter is 2+ways on β cells of 2+ncrease  glucose enters  glycolysis  ATP  *ATP blATPchannel  depolarization  Ca channel opens  Ca influx triggers exocytosis of insulin-containing vesicles o Intravenous vs. Intrajejunal GLUCOSE Injections ‒ intrajejunal (small intestine) injection of glucose causes more rapid drop in blood [glucose] & plasma insulin peaks higher than intravenous ‒ explanation: cells in small intestine detect rising [glucose] and release GASTROINTESTINAL HORMONES  gastric inhibitory peptide (GIP) – main effect to ↑ insulin release, ↓ gastric emptying/acid (slowing down for more thorough digestion)  glucagon-like peptide-1 (GLP-1) – main effect to ↑ insulin, ↓ glucagon, ↑ β cell growth, ↓ gastric emptying/acid, feeling of satiety ‒ these gastrointestinal hormones serve as feed-forward regulation, b/c anticipate high blood [glucose] and preparing for it (insulin) o Summary of Stimuli ‒ ↑ plasma [glucose] ‒ gastrointestinal hormones ‒ ↑ plasma [AAs] ‒ parasympathetic NS o INHIBITOR = sympathetic NS 25. Glucagon  antagonist of insulin o ↑ glycogenolysis, gluconeogenesis, ketogenesis o main goal = prevent hypoglycemia  Pathway o G protein-coupled amplification of signal (same pathway as epinephrine!)  in target – LIVER: makes [glucinsidegh by glycogenolysis/gluconeogenesis  glucose transported outward by GLUT2 transporters  Stimuli for Release o ↓ plasma [glucose] o ↑ plasma [AAs] (*this is also a stimulus for insulin release) o sympathetic NS  Inhibitor of Release o GLP-1 (think: “glucagon-like peptide is jealous of glucagon b/c he can’t be quite like him… so antagonizes him”)  Proglucagon: 3 (distinct) active hormones o expressed in α cells, L cells of intestine, and brain o glucagon + GLP-1 + GLP-2 ‒ in α cells: main product = glucagon ‒ in L cells of intestine, and brain: main products GLP-1, GLP-2 o differential processing depends on complement of enzymes present in each cell type 26. Somatostatin  inhibits endocrine & exocrine secretions (“Negative Nancy”)  Stimulus = high [glucose] & [AAs] 27. Diabetes Mellitus  type 1 diabetes (insulin-dependent diabetes, juvenile diabetes) o endogenous insulin secretion reduced/absent o treated by insulin injections/pumps o GLUT4 doesn’t reach PM o results in polyphagia  constantly eating, b/c “satiety center” in brain is never stimulated by insulin Page 7 of 16 ‒ and polydipsia  constantly drinking, b/c dehydration due to water loss caused by high filtrate osmolarity (glucose)  type 2 diabetes (non-insulin-dependent diabetes, mature onset diabetes) o majority of diabetics o DEFECT in insulin secretion, and ↓ responsiveness of target cells to insulin o treated by diet, exercise, oral hypoglycemic (which stimulates secretion of insulin), and sometimes insulin injections  both types  HIGH blood [glucose] when uncontrolled Adrenal Gland 28. Structure  adrenal medulla = modified sympathetic ganglia (inner core) o catecholamines  adrenal cortex = steroid factory (outer layer) o sex steroids, mineralocorticoids, glucocorticoids 29. Catecholamines  Regulation o SYMPATHETIC STIMULATION (NT = ACh)  chromaffin cells release epinephrine/NE/DA into blood  to target tissues  main hormone = epinephrine b/c secreted in large quantities  Role of Epinephrine o LIVER – glycogenolysis  glucose release o FAT – FA release o HEART - ↑ force of contraction o INTESTINE – muscle relaxation (i.e., no digesting) o INTESTINE, SKIN, KIDNEY – arteriole constriction (i.e. diverting blood away from digestive, excretory systems and from the peripheries of body, skin) ‒ intestine has α receptors, so only vasoconstriction o MUSCLE – arteriole contraction (α adrenergic receptors); arteriole relaxation (β2) ‒ b/c both α, β2  LESS vasoconstriction (not more vasodilation)  also, metabolite accumulation (e.g.2 CO )  vasodilation o BRAIN - ↑ alertness  Adrenergic Receptors o β1, β2 – activatesG  adenylate cyclase  cAMP and PKA pathway o α1, α2 – activateqG and Gi, respectively  PLC 3 IP + DAG pathway 30. Adrenal Cortex: Specific Steroids synthesized in Specific Zones  horizontal layers: each with specific set of enzymes and their concentrations to make these steroids 31. DHEA and Androstenedione  = weak androgens (< 20% activity of testosterone, but converted to more potent androgens & estrogens in peripheral tissues)  in MEN: no physiological role  in WOMEN: maintain pubic & axillary hair, source of estrogens after menopause  CHILDREN: contribute to andrenarche (onset of puberty)  pubic hair, body odour, skin oiliness, and acne  Regulation o synthesis stimulated by adrenocorticotrophic hormone (ACTH) – activates an enzyme at an early step in STEROIDOGENESIS o over lifespan – intrinsic changes in enzyme activity ‒ e.g., DHEA surges at birth then falls  surges again @ puberty  gradual decline over lifetime 32. Aldosterone & Cortisol  both bind to mineralocorticoid receptors o 100x more cortisol than aldosterone in blood  Why does cortisol not activate receptors in principal cells (kidney)?
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