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35 Cards in this Set

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Endocrine cells of the pancreas
ISlets of langerhans surrounding a capillary, 1-2% or total wt of pancrease
list the cells of the pancreas and what they secrete
beta cells: insulin
alpha cells - glucagon
Delta cells - somatostatin
F-cells (p-p cells) - pancreatic polypeptide
beta cell production of insulin, describe in detail how insulin is made from precursors
ribosomes make prepro right in ER, there it is cleaved to proinsulin. Proinsulin goes to golgi, is then cleaved to insulin and C peptide and packaged into vesicles
secondary messenger signals that release insulin granules
Ca (IP3 from ACh and ATP from glucose)
cAMP (beta adrenergic and PKA)
PIP3(stim preproinsulin gene, largely unknown)
Insulin release from beta cells
biphasic:
biphasic

quick - 3-5 min, amt released depends on CHANGE in blood gluc(rate of rise)

gradual: 1 hr, responds to STRENGTH of stimulus
Insulin clearance
insulinase in liver and kidney remove insulin from blood, disappears 20 min after secretion stops, can remove insulin before it joins circulation
Glucose Tolerance test
give glucose, if over 200 mg/dl [plasma gluc] after 2 hours, = diabetic
Normal insulin and gluc levels

after eating meal?
insulin = 3-8
gluc = 100

peak insulin = 150
peak gluc = 150
Insulin R
cys rich binding domain grabs insulin, autophos of tyr kinase domain, autophos of IRS,

PIP2--> PIP3 --> aKT
PIP2--> IP3 DAG(PKB and Ca)
actions of insulin
+ glut transporters
+ aa uptake and prot syn
+ lipoprotein lipase(chylomicron)FA syn
- HSL, FA catab
what increases insulin
gluc aa ketones
intracellular cAMP stim by BETA adrenergic
glucagons and K+
what decreases insulin
catecholamines
ALPHA adrenergic receptors
somatostatin
describe/draw gluc transport into beta cells and how it causes insulin release
GLUT 2 into cell
gets converted to ATP
ATP inhibits K efflux channels
This causes membrane to depol untill it activates the V-gated Ca channels
Causes calcium indiced calcium release from ER

Ca causes granules of insulin to exocytose
Actions of insulin

glut transporters
aa
2 enzy's for FA
increases glut transporters
increases protein synthesis

stim lipoprotein lipase
inhibits HSL(de-P'd)
What stimulates insulin release
Ach
gluc
aa
ketones
glucagons
what acts negatively on insulin release
somatostatin
IGF
how does glucose cause insulin release
glucose is made into ATP via TCA, the extra ATP inhibits potassium eflux channels

this puts membrane closer to depol until eventually V-gated calium channels are opened

calcium causes calcium induced calcium release from ER and that larger increase in cytosolic Ca causes insulin vesicles to exocytose
how does Ach cause insulin release
ACh -> Gq -> PLC-> PIP2 -> IP3 and DAG -> Ca and PKC
How does somatostatin inhibit insulin release and what cell is somatostatin made from
delta pancreatic cells

somatostatin activates G alpha i

beta adrenergic stimulates G alpha s (increase cAMP and PKA)
insulin effect on liver
concerning glycogenolysis and glycolysis
GLUT 2, glucose -> malonyl CoA,

stops glycogenolysis
increases glycolysis( + PFK, Pyruvate kinase, and PDH)
decreases gluconeogenesis (- PEP carboxykinase, F1,6b Phosphatase)
insulin effect on liver adipose
Decreases FA oxidation(+ acetyl CoA carboxylase is de'P'd to active form-> malonyl CoA -> (-) CAT I so no FA oxidation in mito)

Increases lipogenesis (+ fatty acid synthase, which makes FFA, since you have a bunch of FFA's floating around which the cell cant shuttle into mito oxidation, instead they're esterified with glycerol to TG's)
insulin effects on liver protein
stimulates synthesis of proteins and reduces protein degradation
insulin effects in muscle

glycolysis
glycogen synthesis
increases glucose to glycogen conversion - ( + hexokinase, + glycogen synthase)

increases glycolysis (+ PDH + PFK)
insulin effects on adipocytes

GLUT transporters
TG synthesis
FFA synthesis
breakdown of stored TG's
increases glut4

Increases TG synthesis: glucose --> *alpha glycerol-phosphate* -->TG

Increases FFA synthesis from glucose: ( + PDH and +acetyl CoA carboxylase)

decreases TG stored breakdown: (-)HSL
Glucagon effects on liver

glycogenolysis
G-alpga S = increased PKA

increases glycogenolysis (+ glycogen phosphorylase, + Protein phosphatase Inhibitor)
Glucagon effects on liver

FA-> TG export
FA oxidation
Ketones
increases FA -> TG export:

increases FA oxidation: (- acetyl CoA carboxylase so malonyl CoA 'brake' comes off CAT)
Somatostatin
blood flows from beta (insulin) to delta (somatostatin) so little effect of somatostatin on insulin
factors which increase glucagon release
AA's!

beta receptors
ACh
factors inhibiting glucagon release
glucose
alpha receptors
insulin
somatostatin
glucagon stimulates insulin release because it binds and increases cAMP
insulin inhibits glucagon because IT binds and decreases cAMP
glucagon secreteing cells (alpha cells)

do they have more alpha or beta receptors?
have more beta b/c want cAMP

insulin has more alpha adrenergic,

so when epi is released it stops insulin release and starts glucagon release
why does a high carb meal make you hypoglycemic
carbs mostly stimulate insulin, glucagon secretion is mostl AA,

w/o glucagon you get hypoglycemic

AA meal will stim both glucagon and insulin release
GLP
glucagon like polypeptide

pre-proglucagon is secreted in the lower gastro-intestinal tract. here it is turned into GLP-1 and -2

when chyme occurs in GI, GLP's are released into blood and cause early insulin release and signals satiety
pancreatic polypeptide
released from F cells in response to exercise, stress, hypoglycemia and starvation
somatostatin

effects on glucagon and insulin
paracrine inhibition of both