Final: Homeostasis Flashcards
(20 cards)
How does GLUT2 contribute to b islet cells to respond to elevated glucose levels?
facilitates passive glucose uptake into beta cells when blood glucose is high
How does glycolysis contribute to b islet cells to respond to elevated glucose levels?
Glycolysis metabolizes glucose leading to increased ATP production which is a metabolic signal for high glucose
How do ligand gates K+ channels contribute to b islet cells to respond to elevated glucose levels?
CLOSING IT
high intracellular ATP binds to and closes the K+ channels, reducing K+ efflux causing membrane depolarization
How do voltage gated Ca2+ channels contribute to b islet cells to respond to elevated glucose levels?
OPENS
depolarization opens these channels allowing for calcium influx which is the trigger for insulin secretion
How does insulin containing secretory vesicles contribute to b islet cells to respond to elevated glucose levels?
elevated calcium causes vesicles to FUSE WITH PLASMA MEMBRANE and release insulin into the bloodstream
How do insulin receptors tell fat cells to increase glucose in response to insulin?
RTK on fat cell binds insulin and autophosphorylates and activates downstream signaling cascades
How do proteins with SH2 domains tell fat cells to increase glucose in response to insulin?
phosphotyrosine residues bind to insulin receptor via SH2 domains to help recruit signaling molesules like PIK3
How does protein kinase B tell fat cells to increase glucose in response to insulin?
phosphorylates targets to promote GLUT4 translocation and glucose uptake
How does TUG tell fat cells to increase glucose in response to insulin?
anchors GLUT4 vesicles in cytoplasm under basal (no insulin) conditions
What leads to proteolytic cleavage of TUG and what happens after?
PBK signaling
GLUT4-containing vesicles are released
How does protease tell fat cells to increase glucose in response to insulin?
cleaves TUG when signaled by insulin via PKB
releases GLUT4 vesicles for trafficking into the membrane
How does Rab GTPase tell fat cells to increase glucose in response to insulin?
when bound to GTP it promotes vesicle trafficking of GLUT4 towards the plasma membrane
How does Rab GAP tell fat cells to increase glucose in response to insulin?
inactivates Rab by stimulating GTP hydrolysis
prevents GLUT4 vesicle trafficking under non-insulin conditions
What inactivates Rab GAPs to allow GLUT4 movement?
PKB
How does kinesin tell fat cells to increase glucose in response to insulin?
moves GLUT4 vesicles along MTs towards the plasma membrane once Rab is active
How does GLUT4 tell fat cells to increase glucose in response to insulin?
translocates to plasma membrane and facilitates glucose uptake into the fat cell
How does a prolyl hydroxylase keep HIF-1 in check under normal oxygen levels? What is it a ‘tag’ for?
hydroxylates specific proline residues on HIF-1a
only functions when oxygen is available
acts as a tag for recognition by the VHL protein
How does VHL (E3 Ub ligase) keep HIF-1 in check under normal oxygen levels?
recognizes hydroxylated HIF-1a and targets it for ubiquination
What does upregulation of HIF-1 do?
improve oxygen supply (VEGF and Epo)
reduces dependence on oxygen (glycolysis)
optimizes blood flow and local responses (iNOS)
What is the cause of increased number of capillaries?
excessive production of VEGF because of the mutated or non functional VHL protein being unable to degrade HIF-1
