6. Endocrine - Hormones Flashcards by Sean Hartigan

Hormone vs autacoid and NT

Hormones - chem messenger
ductless gland
release circ
travel distant targ cell
act spec protei rec

Autacoid
chem messenger - act target cell close site release
local hormone/ paracrine
Histamine / PG

NT
chem messenger - rel neurones act adjacent cell usually neurones
periph - adjace effect muscle or gland
action rapid - broef durn
NA/ACH

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MOA hormones

Present in blood stream low conc -targ cell need spec/sensitive - recog and resspon

Spec -receptor
all recept are protein nature

Combo - hormone and receptor - signal = specfic response

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Classif hormones

Receptor locn

signal mediates action

Group 1
Lipophilic - receptor intracellu

Steroid - gluc minereal sex

Calctriol - not steroid derived prescuorse
thyroid
retonic acid

Group 2
hydrophilic horm - Rec in membrane

IIa- cAmp as second mssgr
ADH, Beta adreg, tsh

IIB
CGmp
ANP

IIc
Calciu,/pdei - 2nd
Musc recp oxytocin gastrin

IID- second messgr not est
GH Insulin prolactin

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Could you outline major diff grp 1 & Grp 2

Grp1 steroid & thyorid - all lipphilic - carried bound tport prot
long t1/2
rec = intrace;; second mssgr - act hormone rec complex - bind spec part DNA - alter prodctuion mRNA

Grp 2
Hydrophillic - not bound protein blood and short t1.2
Typically not pro bound blood
short half lices
receptor - loc cell membrane - activation w/ receptor - sep second messenger

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Second messenger?

Third mssgr

Chem mssgr -

Formed result spec hormone recptor combination

Acts intrcell - affect metab processes

Second msgr - intermid carry signal horm to site action

Kinase casdes - act cell second messgr - metabolic alterations in cell

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Insulin

51aa hormone
B cell islet langehans panc

major anabolic hormone

carb lip pro metab

Two peptide chain disuplh bridge
Rem cpept precursor proinsulin

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Actions Insulin carbohydrate metabolism

Lower pl gluc - gluc enter cells

Insulin combine spec membrane bound recprot - diff effect diff cells - two types response act rec
Increased act spec gluc tport membrane
act TK on B subunit rec

Cells effect
Mesucle adipose - incrase facil diff gluc into cyto = carrier prote

hepato
Increase entry gluc - conseq change intracell metabolism
cell

activity membrane carrier - not increased insulin - norm permeable
Intracell metabo
increase glucokinase - trap clu in cell
increased glycogenis - inc act gluc sythn - inhib glycogen phosporylase
increase oxidation glucose -
inhib gluc 6 phos -> glycolyis / conversion to starch/glyocgen

All main fav diffusion gradeint gluc hepatocyt e- keep gluc conc low

No diffrect effect inulin gluc entry most other cell
indir chjange occur in blood glucose level - msucel and adipose 80% body - effect inslin improtant over all metabolism

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Does insulin act AVw/ CAMP

Insul - cell membran rece - autophos TK intrcell part B sub
affect activtyy intracell enxyme - meidate activated intracell pro kinase - protein cascde - probable third messenger

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Effect insulin on lipid protein metabolism

Lipid
Increase entry glucose into adipose cell - increase syn fatty acids in cells - insulin receptor

increased activity lipoprot lipas e- blood increased bdown tg in chlyomicron to fa - enter adipose

Act hormonse sensitive lipase adipose inhib
intracell bdown fat adipose inhibited

Protein metab
Increased activity - glyolyic path - hepatocytes - decrease gluconeo from AA
metob protein aa into energy decreased - protein sparing effect insulin
Increase entry AA muscle and adipose

Net result - increased store fat and ptoein
anabolic action insulin

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Does insulin cross bbb or placenta

No -

No direct effect on neuronal glucose uptake
powerful indir effect change in plasma gluc

brain norm gluc almost excluse as substrae - adeq gluc reequired fucntion
brains RQ .99 - total use carb

Maternal insulin increase during preg - almost double by 3rd trimester
Overcome insulin resitsance d/t place hormone esp hum placetn lactogen. oetriol, progest

Ensure adeq mat pro synth

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Regulation of blood glucose

4-7 ref range
fal 3-3.5 fasting

neo lower
2.2 min

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Outline factors involved in control blood gluc

Glucostat fxn liver?

Blood gluc - main narrow - despite vary intrake

Body mech - prevent hyperhlyc - fater meal

Input glucose into blood
Gut- small bowel
episdoic vary

Liver - gluc fall - releases gluc into blood
hormonal reg

Output
muslce and adipose - take up
uptake dep need
Urine 
gluc high - lost in urine

Gucodtat liver - buffer increase and decrease

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How factor min flux in blood gluc after meal fasting

carb meal

Blod gluc rise - absorebed
senosre b cell det increase and relase insulin
Liver - insulin entry - by enz effect
muscle and adipose - two thrid taken up liver
major store - glycogen - some oxidose to Co2 - some util in FA synth

Muslce and adpose - increase entry - convereted stor carbn glycogen muscle cell gyler fat cell
glyerol util synth TG

Blood gluc return normal

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Fasting

Gluc level fall -

Insulin
sens panc det dcerease - insulin falls

Result reer effect hep enzy - glycogenlysis, gluconeogen increase G6Phos
more gluc release liver

Glucagon
Acell - sense decrease+ gluc sec increase

Gluc bind - rec hepatocyte - rises cAMP

Spec enz activated – glycogenolysis + gluconeo
requires cortisol

Resul synergistic falling inmsulin rising gluca - increase rel gluc liver into blood

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Why is sugar control so important

Main reason gypoglc - only energy sub in CN -retina

Uptake depend adeq blood gluc level - not affect insulin

Hypergly:
osmotic effect - dehydrate
lost urine - wawste
osmotic diures loss fluid and electo

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Glucose stores

Glyocgen live rand muscle
branched polymer - con a1,4 a1,6 link

Glycogen broken down - rel cell blood main pl guc

Glyco - muscle broken gluc reside - meatb muscle - gluc not relase muscel
No g6 phosp in muslce

Sto glucose - glycogen osmotic effect smaller than glucose molecule

Max total size glyco store 100 liver 400g muslce
500 gr - 2000kclas energy 24h supply

Gluc store circ small
blood gluc 1g/L
5g gluc whole circ

Total gluc ecf - 10g
Equv 40kclas
proveides site - cells recieve supply

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Other insulin glucagon - what hormones effect gluc level

Corticosteroid
Permsisve glucagon exert effect liver - increase gluconeo
Hypo - increase secretion
inhib utilatsion gluc - favour fat util body cell
Increase blood blucose level -
diabetes occurs excess cortico

Catechol - adren
Increase blood gluc - hpeatic glycogen output liver
lrise

GH 
sec increase hypogly
inhib gluc uptake musl cell
inc rel gluc liver
rise

Thyrpod
Increase GIt abs gluc
may decr - hep glycogen-increase blood gluc level

Oestro - insulin restiance mil

Progest - insulin resitance

HPL - insulin resitsance
increase

Soatostatin

inhib relase insulin glucagon indir effect bgl

Plasma glucose levels in baby after birth

Pl gluc fall min 2.8 by 6h birth

Main foetal supply mother
transpalcetan
birth source suddenyl lost
low or no carb intake

Hep glyco - maj source inital period birth
falling insulin increased glucagon
symp stim contrib increased glycogen - main gluc

Glyocgen depleted newborn - mob tg - ffa rise - alternative energy source
incrased level catechol - import causing change fat metab - catechol effective rasing FFA than raising glucose

Introduction provide gluc - stabil plasma days aftrer birth

Net atp prod

Glcolysis
cytopalsm
1gluc -> 2 pyruvate - 2 atp +2nadh
pyruvate oxidse to acetyl CoA 2NADH/pyruvate
then enter krebs - citric acid cycle

Krebs
Mitochonddia - 2atp 8nadh 2fadh2

ETP mitochon 32 atp

Synth thyroid hormones

Where in the bowel is dietary iodide absorbed

Diet iodine con to idodie abosrbed upper SB
typical west diet contrain more than min amt idoide reqd

Idodide in BS taken thryroid or excreted in urine

Synthesis throyid hormones

T4 T3 syhtn gland

1 Uptake Iodewdi in folluc cell
active tpor
tport against elec grad and conc grad
carrier subj competitive inhib other anion 0 similar size to idodie
anion r/f iodide uptake inhib

Iodide iodine diffuse folluc lumen - reacts tyr to prod MIT
cat thy perox

Thyrosine AA reside - held peptide link - thyroglobulin - reaction cell coloid interface

Further Iodination MIT - prod DIT

TWO DIT oxida couple throytix - remin aa backobne thryoglob
MIT and DIT - reside T2 reside

How are hormone secreted

Stored colloid part thyroglob - secrretion
glob undergo endocyto into cyto of follic cell
Join lyossymes and thryoglob digested release free thryorix t2 mit dit

t3 + t4 secreted but t4 higher
both high protein bound carrier prote and blumin

mIT AND DIT brokken down and iodied recycle

How is secretion cotrlled

Hypothol prod TRH
reach ant pit - hpyohseal prot circ - release TSH fyhrotrope ant pit

TSH bind GPCR in membrane follicular cell
AC Activate - result increase Iodide uptake increased synthesis - relase thyroid hormones

Free T3 + T4 provide neg feedback - inhib release TRH hypothal - inhib TSH rel ant pit

Pituitary

Post - ADH and Oxytocin

Struc sim nonapept

Struct ant pit
pars tubertalise intermidus distalis

Ant develop thakes pouch

Ant most pars dstalis - all trophic
Proteins
GH
Prolaction

Glycoprote -
FSH
LH
TSH

Polypept
ACTH
MSH

Which cells prod hormones

acidophil - HG Prlaction Basopl glycoprote and polypept

Control calcium Ref range what {ca icf] [Ca in bag blood]

2.2-2.55 free Ca ++ 50% Ca bound alb 45% Ca complexes 5-10% Low 100nm grad free ca - 10000 ecf 1mM ICF 100nM 0 calcium bound citrate - mech ensure not clot

Type coagulip caused hypocal

None ca- low enough affect coag not compat life | Hypocalc massive tfusion depress contractily

Mech maintain ca blood level stable

ECF [Ca] fairly tight hormnaol control - predom PTH, calcitonin, 1 25 dihtdo - caltriol calcitrol act vit d Plasma [ca] control sign PTH release pth gland response hypoCa act bone kidney - indirect gut calcitriol - rise plasma Ca ``` Calcitriol Formed kidney act bone and gut intest abosrp ca increased osteclast act increased Actions rise plasma ca ``` Calcitonin parafollic thyroid cell effective lower Ca - phys role not est

Renal actions PTH

Reabs Ca dist tube Decrease reab Phos prox tube Increase Calcitriol - prox tub cell Net reslts - plus act PTH on bone - increa ca mobil and act calcitriol bowel = net increased plasma [Ca]

How do hormones interact w/ cells

Hormones attach spec recportop on or in cells Most recport in cell memnbrae some locate nucleus or cytoplasm Brin biolog change - occupatin ligand alter effector mech 1 Intermed couplin gmech to effector receptor connect effector mech thru intermed coupling mech gpor - result second messenger ion channel 2 Ligan gated Ion channel Ligan bind direct ion chanell and affect open / closing gaba receprot cl chanell nic rec Na 3 Bind intracell rec affter tcipt mRNA bind intracell rec affect cpsepc mrna bind DNA Receptor both ligand bind and enzymatic fxn Rec - enzym activty which act conform change ligand bind tk act gf Gcycl anp

What are gpro

Cell embrane assoc pro - import signal tduction Hetertrimer 3 sub unit a b y diff gene subunit cominbed - diff gpor a - def effect usual interact effector mech bind gdp and gtp nuceoltide - guanosine analoge adp and atp resepct inactive state GDP bound grpo gdp dissoc + gtp bind = grpo act

Diff gpro

Gs - stim effect ac act Gi inhib AC inhib Gt involve photorecp eye Gq inbolbe Plc reg

How gpro involved signal transduction mech

Coupling between activation spec receptor cell membrane and activation effector mech - affect intracell process Activation of effector - AC Plc - production second messenger Ion channel - affect directly or by second messnger (Ca IP3) signal carried accross membrane by process Signall mech provides amplication signal Amplification signal: Intric gtpase activity of activated gpo important sev reasons 1 Rate hyrdol gtp slow - assists sustain signal allow greater amplication 2 Slef reg gpro - terminate own activty certain time 3 Directionalaity - reaction propagates 1 direct

What are fts of receptors couple gpro

Signif struct sim gpcr - superfamily all consits single polypept chain - 7 transmembrane a helical segment specific ligand binds in pocket between transmembrane signal

How does GPro signal transduction signal work Seq event

Modules work sequence - cary excell signal - across cell embrane and activate specific second messenger in cell Ligand bind spec gpcr - membrane confomrational change - result spec assoc gpro activate a subunit gpro - release gdp and binds gtp gpro sep gtpa + gtpby gtpa - interact effector protein (enz/íchan) results activation or inhib of enzyme - or open / close channel GTP hydro to GDP - gtpase act a subunit and gdp aby inactive form and gpro - reconsitiude ``` Ex - nind norad to beta act SA Act GS AC act Camp prod Gs act hydro gtp ->gdp ```

Name sone non gpro horomones / nt

ACH- nic rec GABA at gaba Steroid + thyroid - bind intracell rec Insulin + insulin rec ANP + guanylate cyclate act

Metabolic rate

Rate energy production body all energy apperas heat - form w/ highest entropy Thermal equil - all heat must be lost

WHAT is the BMR

Metabolic rate - standard cond rest room temp 12h after meal result repot as % above or below age adjust standard value

How is it determind

Calorimetry direct - Total amt heat energy prod body ody subject -atwater benedict chamber met rate - amt heat energyt in 1 hr Indirrect est - measure o2 consump as its proportional o2 consumo 250ml min - 15l hr mult 4.8 72.3 kcal hr divide by body surf area - standrd result typical 70kg - 40kcals m2

How is o2 consumption measured

Subjects breath oxy from wet spiurometer exp co2 absorbed circ close and co2 abs rate decrease equal to oxy cosnump cona be connected rotating ddrum - circu vvol v time slope proportioal o2 consump

why is oxygen consumption to bmr

Vast maj energy derived aerobic metab prod atp via ox phos mito obligatory a/w fixed o2 consump final rx etpc cyto ox - irrev 2H 1/2 O2 => H20