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Membrane Transport And Cell Signalling > Insulin Action And Signalling > Flashcards

Insulin Action And Signalling Flashcards

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1
Q

What is the purpose of blood glucose homeostasis

A

To maintain blood glucose at approx 90mg/dl

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2
Q

What are the 2 main functions of the pancreas

A

Exocrine function
Endocrine function

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3
Q

Describe the exocrine function of the pancreas

A

Release digestive enzymes through ducal structures directly into the gut to help digestion

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4
Q

What is the endocrine function of the pancreas

A

Maintain blood glucose levels via the pancreatic islets

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5
Q

What are the 3 type of cells in the islets

A

Beta cells; release insulin
Alpha cells; release glucagon
Delta cells; release somatostatin

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6
Q

Why is important that the pancreatic islets have a good capillary network

A

So that they can sense changes in blood glucose rapidly and can release hormones directly into the blood stream

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7
Q

What inhibits insulin release

A

Adrenaline and somatostatin

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8
Q

What stimulates the release of insulin

A

Glucose (major regulator)
Gut hormones
Amino acids

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9
Q

What inhibits glucagon release

A

Insulin
Gut hormones
Glucose

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10
Q

What stimulates the release of glucagon

A

Cortisol
Adrenaline
Amino acids

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11
Q

Describe the process that insulin is formed

A

Pre-pro insulin -> pro insulin -> insulin + c peptide

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12
Q

How is insulin stored prior to release

A

Within secretory granules and stored as a hexatrimeric complex

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13
Q

Describe the structure of pro insulin

A

Folded in the ER to form the A chain and D chain
Disulphide binds between the A and D chains and within the A chain

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14
Q

Describe the cleavage of pro insulin to insulin

A

Cleaved at position 31 and 65 to end up with insulin (A and B chain connected via disulphide bonds) and C peptide

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15
Q

Why is C peptide a better diagnostic tool than insulin

A

Is a stable molecule with a longer half life than insulin
Will indicate if a patient can produce their own insulin

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16
Q

What happens when glucose enters a beta cell

A

Glucose converted to glucose-6-phosphate via glucokinase
Glucose 6-p undergo glycolysis -> pyruvate
Pyruvate undergoes Krebs cycle
= Production of ATP

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17
Q

What happens if the blood glucose is at a normal level

A

Not much glucose 6-p = low ATP levels
K-ATP channels channel remain open = no depolarisation = no release of insulin

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18
Q

What happens if there’s an increase in blood glucose levels

A

More glucose enters cell = more glucose 6-p
More pyruvate = higher ATP:ADP
K-ATP channel closes to the membrane potential depolarises
Ca2+ channel opens allowing an influx of Ca+ into cell
= release of insulin

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19
Q

Describe the structure of glycogen

A

Branched polymer of glucose w 14 and 1-6 glycosidic bonds

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20
Q

What is the first line of defence for declining blood glucose levels

A

Hepatic glycogen is degraded between meals

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21
Q

Why can’t muscle cells maintain blood glucose levels

A

It can’t release glucose back into the bloodstream
Only acts a store for its own tissue

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22
Q

How does the brain respond to glucose and insulin in the post prandial state

A

Doesn’t respond to insulin but has a high demand for glucose

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23
Q

How do muscle cells respond to insulin and glucose in the post prandial state

A

Wont respond to glucose unless insulin present
Will then take glucose -> glycogen via glycolysis and oxidation

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24
Q

How do adipose tissues respond to insulin and glucose in the post prandial state

A

Take in glucose and convert into triglycerides and it also signals for the tissue to take any fat in from circulation

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25
How does the liver respond to insulin and glucose in the post prandial state
Converts glucose -> glycogen and convert surplus glucose/mono acids to lipids Fat translocates out in lipoproteins which are taken up by adipocytes
26
What happens to excess glucose after the glycogen stores have been used up during the postprandial state
Glucose > pyruvate -> Krebs cycle -> citrate -> fatty acids Modulated by insulin and is dependent on excess glucose conc
27
Why does insulin modulate the conversion of glucose -> fatty acids
Increases the activity of pyruvate dehydrogenase and increases the txn of a fatty acid synthase and acetyl CoA carboxylase Drives the pathway to fatty acids
28
How does the muscles respond to insulin and glucose in the post absorptive state
Convert proteins into amino acids and release them into the blood stream
29
How does adipose tissues respond to insulin and glucose in the post absorptive state
Convert triglycerides -> fatty acids and glycerol and release fatty acids are released into the blood Muscle cells take up fatty acids and metabolise them for fuel instead of glucose
30
How does the liver respond to insulin and glucose in the post absorptive state
Converts glycogen -> glucose and releases into blood Amino acids -> glucose via gluconeogenesis Fatty acids -> energy for its own metabolism Fatty acids -> ketone bodies for the brain
31
Why can glucose not be taken into the cell in the absence cells of insulin
GLUT4 is associated w vesicles in the cytoplasm not at the plasma membrane in the absence of insulin
32
Describe what happens when insulin binds to the membrane of a muscle cell
GLUT4 translocation to the plasma membrane to bring glucose into the cel
33
How does insulin increase the formation of glycogen
Activating glycogen synthase = dephosphorylation
34
Why do muscle cells express hexakinase 1/2
Rapid metabolism of glucose in the cell
35
Why does high glucose levels activate pyruvate dehydrogenase
More conversion of pyruvate -> acetyl CoA
36
How does the glucose -> triglycerides in the adipose tissues
Glucose metabolised to pyruvate Insulin increases the txn of fatty acids cid synthase and acetyl CoA carboxylase Forms triglycerides
37
Why do the adipose tissues convert glucose -> triglycerides
There is no glycogen storage only fat
38
Why does insulin switch of hormone sensitive lip abase when glucose levels are high
Inhibit the degradation of triglycerides -> fatty acids acids that could be converted into energy
39
What do the adipose tissues do with triglycerides when glucose is high
Lipoprotein lipase converts triglycerides -> monacylglycerol hitch Cana be taken up into adipose tissues Can be converted into triglycerides when needed
40
Why does the liver express GLUT2 instead of GLUT4
Has a higher affinity for glucose
41
Why does the liver express glucokinase
Conversion of glucose -> glucose 6-P when glucose levels are high
42
What effects does insulin have on the liver
Increases translation on glucokinase Stimulates activity of glycogen synthase Decreases activity of glycogen phosphorylase Increases the txn of acetyl CoA carboxylase
43
What is property of RTK receptors
Has tyrosine kinase activity -> it can phosphorylate tyrosine residues to evoke a cascade of effects
44
Describe the PH domain
Pleckstrin homologous domain Binds to phosphorylated inositol phospholipid in the plasma membrane
45
Why is the PH domain important
Locates signal proteins to the plasma membrane
46
Describe the PTB domain
Binds to phosphotyrosine P-Y residues
47
Describe the SH2 domain
SRC homologous 2 domains binds P-Y readies surrounded by unique protein sequences
48
Describe the SH3 domain
Src homology 3 domain Binds specifically to proline rich regions
49
Describe the insulin receptor
Tyrosine kinase receptor and part of the insulin-IGF1R Has 2xalpha and 2xbeta subunits
50
Describe the function of the IR alpha subunits
Sit on the membrane and bind insulin
51
Describe the function of IR beta subunits
Transmembrane and has tyrosine kinase activity
52
How do the 2 isoforms of IR happen
Alternative splicing
53
What happens when insulin binds to the alpha subunit of IR
Causes transphosphorylation and activation of beta subunits and its tyrosine activity
54
What happens when the beta subunit on the IR becomes phosphorylates
Phosphorylation of other tyrosine residues on the subunit Exposes binding site for proteins w PTB and SH domains
55
What site is phosphorylated on the beta subunit in the IR
Activation loop
56
What happens at the juxtamembrane domain in the beta subunit on the IR
Phosphorylation of tyrosine residues creates binding site for PTB domain
57
What happens at the C-terminal domain in the beta subunit on the IR
Phosphorylation of tyrosine residues creates binding site for SH2 domain
58
What happens at the Ser/Thr sites on the beta subunit on the IR
Inhibition of receptor kinase activity when the sites have been phosphorylated
59
What are the 2 adapter proteins that sit below the IR
She and IRS1-4
60
Describe Shc
SH2 containing adapter proteins Has 3 different domains; PTB, SH2 and CH1 domains Binds to IR via PTB and SH2 domains
61
What is the purpose of CH1 domain on Shc
Phosphorylation of tyrosine kinase uncovers binding site for proteins w an SH3 domain e.g Grb2
62
What happens once Grb2 is bound to CH1
Conveys signal to sos which links to the MAP-kinase signalling pathway
63
What is the purpose of the insulin receptor substrate IRS
Essential for most of insulins biological actions in the liver muscles at adipose tissues
64
Describe the structure of IRS and their functions
PH domain; binds to a phospholipid in the plasma membrane PTB; binds directly to PTB binding site on IR
65
Why doe the IRS have a lot of tyrosine residues
Leads to phosphorylation of many downstream sites once bound to IR
66
What sites act as positive regulators on the IRS
Y - phosphorylation sites Docking protein w SH2 domain Can bind GRB2, PI3K and SHP2
67
What sites act as negative regulators on IRS
S/T phosphorylation sits Phosphorylated by stress kinases activated by lipids, inflammation or components of insulin signalling a
68
What happens after the IRS binds to the IR
Becomes phosphorylated by IR tyrosine kinase activity
69
Describe the insulin signalling pathways that lead to MAP-kinase pathway activation
IR -> IRS -> Grb2 -> SOS -> MAPK IR -> Shc -> Grb2 -> SOS -> MAPK
70
How does Grb2 interact w SOS
Activated by binding to IRS or Shc allowing it to bind to SOS via SH3 domain
71
How does SOS act as a GDP/GTP exchange factor (GEE)
Exchanges GDP for GTP on RAS to activate it
72
Describe how RAS is activated and then activates ERK
RAS activated when its bound GTP is exchanged for GDP RAS-GTP activates Raf Raf activates MEK MEK activates ERK
73
How does PI-3 kinase pathway lead to activation of AKT
Recruitment of IRS to IR beta Recruitment of PI3K to IRS via SH2 domains and formation of PIP3 Recruitment of AKT and PDK1 by PIP3 to plasma membrane Phosphorylation of AKT
74
How is PIP3 formed by recruitment of PIK3K
Activation of catalytic activity of PIP3K adds aa phosphate to inositol phospholipid in the plasma membrane
75
Describe the structure of PI3K
Regulatory subunit p85 Catalytic subunit p110
76
Describe the regulatory unit p85 on PI3K
Contains; 2 SH2 domains allowing it to bind to IRS 1 SH3 domain that allows it to bind to p110 subunit
77
Describe the catalytic subunit p110 on the PI3K
Activated by interaction w the p85 subunit When active it allows the addition of the phosphate group to the inositol rings Allows it to localise to the plasma membrane
78
What mediates the degradation of PIP3 signal
Phosphate and tension homologous deleted on chromosome 10 (PTEN) Removes phosphate group from position 10
79
How does PIP3 dual phosphorylate AKT
PIP3 activates mTORC2 and PDK1 PDK1 phosphorylates AKT on Thr308 mTORC1 phosphorylates AKT on Ser473
80
What is the function of AKT once it has ben phosphorylated
Regulates proteins and and glycogen synthesis as well as GLUT4 translocation
81
What regulates the movement of storage vesicles containing GLUT4
AS160
82
How does AS160 regulate GLUT4 translocation
Maintains Rab in its GDP form Rab requires to be bound to GTP to facilitate movement
83
How does the AS160 complex become inactive
Phosphorylation ok AKT -> phosphorylation of AS160 complex

Membrane Transport And Cell Signalling (4 decks)

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