6. Endocrine - Hormones Flashcards
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
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
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
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
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
Insulin
51aa hormone
B cell islet langehans panc
major anabolic hormone
carb lip pro metab
Two peptide chain disuplh bridge
Rem cpept precursor proinsulin
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
Does insulin act AVw/ CAMP
No
Insul - cell membran rece - autophos TK intrcell part B sub
affect activtyy intracell enxyme - meidate activated intracell pro kinase - protein cascde - probable third messenger
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
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
Regulation of blood glucose
4-7 ref range
fal 3-3.5 fasting
neo lower
2.2 min
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
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
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
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
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