endocrine Flashcards
autocrine cell
prods substance that binds to specific receptor on own cell surface/receptors inside cell
local mediator
paracrine cell
prods substance that binds specific receptor on nearby target cell, e.g. NMJ
local mediator
endocrine cell
prods substance transported in blood, bind to specific receptors on distant target cells
sys to circulate hormones
endocrine glands
collection glands that secr hormones directly into circulatory sys to carry to distant target
cell types in islet of langerhans
- alpha secr glucagon
- beta secr insulin
- delta secr somatostatin
- F secr pancreatic polypeptide
production of insulin
beta cells synth pro-hormone proinsulin -> active insulin by removal water soluble polypep
half life 5-8mins
what does insulin bind to
specific tyrosine kinase mem receptor
how do beta cells cause prod insulin
- glucose enters via GLUT2
- raised intracellular gluc = incr ATP
- ATP sensitive potassium channs blocked
- K+ accumulates in cyt => depol cell mem
- causes V-gated Ca2+ channs open
- Ca2+ in => exocytosis vesicles cont insulin
neg feedback mech
further control of insulin
- GI hormones GIP + GLP-1 = anticipatory release to prevent surge in gluc absorp after meal
- parasymp activity incr secr during + after meal
- symp activity inhibit secr
- incr plasma aas after meal incr secr
where is gluc uptake independent of insulin
- brain (GLUT3 transporters)
- mammary gland, GI tract + kidney = 2AT coupled to Na+ transport
overview how insulin cause effects
- binds tyrosine kinase receptor
- receptor phosphorylates insulin-receptor substrates
- 2nd messenger pathways alter prot synth + existing prots
- => cell metab + mem transport changed
insulin in the liver
GLUT2 receptors can work either way
1. fasted = hepatocytes make gluc + transport out -> blood
2. fed = gluc -> hepatocyte + insulin stims hexokinase gluc -> gluc-6-p for low intracellular conc gluc
GLUT2 always present in cell mems
clinical signs insulin deficiency
- hyperglycaemia
- weight loss bc decr prot synth + incr prot breakdown
- PU/PD
- ketoacidosis bc lots B-ox bc needing E from fat metab => krebs = oxaloacetate -> liver for gluconeogenesis = ketone bods => lots
glucose in CNS
metab almost 100% reliant on gluc = steady transport in + can’t incr/decr rate
gluc level in CSF direct proportional to blood sugar
* excess incr osmolarity CSF => water out neurons
* too little = neurons starve
cells not sensitive to insulin
functions of insulin
- incr glucose oxidation
- incr glycogenesis
- incr lipogenesis
- incr prot synth
- inhibit enzs in catabolic processes
- inc cellular uptake of gluc + aas
==> incr stores glycogen, fat + prot
glucagon
- alpha cells secr + store as active
- water soluble polypeptide
- binds specific G-prot coupled mem receptor
half life 4-6 mins
what stims release glucagon
- decr blood gluc
- incr plasma aas after meal = avoid prot induced hyperinsulinemia (=> hypoglycaemia)
- parasymp activity
- symp activity
effects of glucagon
- incr gluconeogenesis
- incr glycogenolysis
- incr ketogenesis
catabolic
somatostatin effects
- decr secr growth hormone
- paracrine inhibition of insulin + glucagon release
diabetes mellitus clinical signs
- hyperglycaemia
- PD + PU
- ketoacidosis
can get a combo of type I + II
type I vs type II diabetes mellitus
1 = due inadequate insulin secr (more common dogs)
2 = due abnormal target cell responsiveness (more common cats)
why does diabetes cause PU/PD
incr gluc in blood => freely filtered into nephron + renal threshold for reabsorp exceeded => glucosuria => incr urine
AND ECF vol decr + plasma osmolarity incr => thirst centre in hypothal stimmed
why does diabetes cause ketoacidosis
‘fasted state’ => adipose tiss broken down => FAs in blood => liver uses beta-ox to break down but not all acetyl CoA can enter citric acid cycle => excess forms ketone bods, e.g. acetone => large amounts cause illness
topographical anatomy pituitary gland
- extends down from brain via thin stalk
- cradled + protected by sphenoid bone