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35 Cards in this Set
- Front
- Back
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Endocrine cells of the pancreas
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ISlets of langerhans surrounding a capillary, 1-2% or total wt of pancrease
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list the cells of the pancreas and what they secrete
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beta cells: insulin
alpha cells - glucagon Delta cells - somatostatin F-cells (p-p cells) - pancreatic polypeptide |
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beta cell production of insulin, describe in detail how insulin is made from precursors
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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
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secondary messenger signals that release insulin granules
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Ca (IP3 from ACh and ATP from glucose)
cAMP (beta adrenergic and PKA) PIP3(stim preproinsulin gene, largely unknown) |
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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 |
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Insulin clearance
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insulinase in liver and kidney remove insulin from blood, disappears 20 min after secretion stops, can remove insulin before it joins circulation
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Glucose Tolerance test
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give glucose, if over 200 mg/dl [plasma gluc] after 2 hours, = diabetic
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Normal insulin and gluc levels
after eating meal? |
insulin = 3-8
gluc = 100 peak insulin = 150 peak gluc = 150 |
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Insulin R
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cys rich binding domain grabs insulin, autophos of tyr kinase domain, autophos of IRS,
PIP2--> PIP3 --> aKT PIP2--> IP3 DAG(PKB and Ca) |
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actions of insulin
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+ glut transporters
+ aa uptake and prot syn + lipoprotein lipase(chylomicron)FA syn - HSL, FA catab |
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what increases insulin
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gluc aa ketones
intracellular cAMP stim by BETA adrenergic glucagons and K+ |
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what decreases insulin
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catecholamines
ALPHA adrenergic receptors somatostatin |
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describe/draw gluc transport into beta cells and how it causes insulin release
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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 |
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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) |
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What stimulates insulin release
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Ach
gluc aa ketones glucagons |
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what acts negatively on insulin release
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somatostatin
IGF |
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how does glucose cause insulin release
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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 |
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how does Ach cause insulin release
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ACh -> Gq -> PLC-> PIP2 -> IP3 and DAG -> Ca and PKC
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How does somatostatin inhibit insulin release and what cell is somatostatin made from
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delta pancreatic cells
somatostatin activates G alpha i beta adrenergic stimulates G alpha s (increase cAMP and PKA) |
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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) |
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insulin effect on liver adipose
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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) |
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insulin effects on liver protein
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stimulates synthesis of proteins and reduces protein degradation
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insulin effects in muscle
glycolysis glycogen synthesis |
increases glucose to glycogen conversion - ( + hexokinase, + glycogen synthase)
increases glycolysis (+ PDH + PFK) |
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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 |
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Glucagon effects on liver
glycogenolysis |
G-alpga S = increased PKA
increases glycogenolysis (+ glycogen phosphorylase, + Protein phosphatase Inhibitor) |
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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) |
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Somatostatin
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blood flows from beta (insulin) to delta (somatostatin) so little effect of somatostatin on insulin
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factors which increase glucagon release
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AA's!
beta receptors ACh |
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factors inhibiting glucagon release
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glucose
alpha receptors insulin somatostatin |
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glucagon stimulates insulin release because it binds and increases cAMP
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insulin inhibits glucagon because IT binds and decreases cAMP
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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 |
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why does a high carb meal make you hypoglycemic
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carbs mostly stimulate insulin, glucagon secretion is mostl AA,
w/o glucagon you get hypoglycemic AA meal will stim both glucagon and insulin release |
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GLP
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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 |
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pancreatic polypeptide
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released from F cells in response to exercise, stress, hypoglycemia and starvation
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somatostatin
effects on glucagon and insulin |
paracrine inhibition of both
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