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FDN Week 5 (Block 2) > Dr. Kilberg - Glucose > Flashcards

Dr. Kilberg - Glucose Flashcards

1
Q

What is the difference between a steroid and a hormone signaling system?

A

Steroids diffuse across the nuclear membrane directly.

Hormones enter nucleus via transport proteins.

**They both bind nuclear DNA and alter transcription***

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2
Q

What are some of the characteristics of a tyrosine kinase?

A
  1. Hormone / Growth (insulin) factor binds to membrane bound receptor
  2. Self phosphorylation on tyrosine residue
  3. Kinase cascade follows
  4. GLUT 4 mobilized into cell membrane
  5. Uptake of glucose
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3
Q

Describe the inisitol of G-Protein activity.

A

Inisitol Phosphate Signaling

  1. Binding to surface receptor
  2. Activation of G protein relay GDP–>GTP
  3. Release of secondary messenger
  4. Increases Ca+
  5. Ca+ activates protein kinase
  6. Kinase activity increases intracellular effects
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4
Q

Describe the G-Protein cAMP signaling process?

A
  1. Hormone binds (Glucagon)
  2. Receptor changes shape and interacts
  3. Gs subunit binds to receptor
  4. GDP –> GTP swap
  5. Adenlylate Cylase activated
  6. Reverse process to inactivate on Gi subunit (except hydrolysis)
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5
Q

What pancreatic cells release insulin?

A

Beta cells

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6
Q

Where does GLUT 4 exist?

A

In muscle and adipose tissue.

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7
Q

How is the stimulatory subunit of the g-protein complex used to regulate adenylate cyclase production?

A

Activation is on the Ga-Subunit and includes a GDP->GTP replacement.

Deactivation of the Gs-subunit is by loss of the stimulatory ligand and the subsequent hydrolysis of GTP to GDP.

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8
Q

What does adenylate cyclase make?

A

It makes cAMP (cyclic AMP)

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9
Q

What does cAMP activate?

A

It activates PKA (protein kinase A)

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10
Q

Once PKA is activate by cAMP what happens?

A

PKA phosphorylation of cellular protein on serine and threonine residues activates intracellullar response to the original ligand binding.

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11
Q

What enzyme breaks down cAMP?

A

cyclic nucleotide phosphodiesterase

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12
Q

If you inhibit the breakdown of cAMP what happens?

A

We sustain the cellular response to the original ligand.

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13
Q

What inhibits the breakdown of cyclic nucleotide phosphodiesterase?

A

Caffeine

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14
Q

PKA structure?

A
  • 4 subunits
  • 2 regulatory / 2 catalytic
  • 4 binding sites for cAMP on regulatory subunits
  • Release of catalytic subunits
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15
Q

Where and on what subunit does pertussis act?

A

It acts on the G-inhibitory subunit in the lungs

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16
Q

How does the pertussis toxin work?

A

It blocks the activation of the inhibitory subunit by blocking the GDP –> GTP transfer. This is by ADP-Ribosylation (the addition of the ADP-Ribose to the inhibitory subunit blocks GDP –> GTP transfer)

With this always inactivet the stimulatory subunit runs away affecting Na+/ H2O balance / tranfer in the lung.

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17
Q

Where and on what subunit does the cholera toxin work?

A

Cholera works on the G-stimulatory subunit by ADP-ribosylation of the stimulatory subunit when it is active. This means it can’t be deactivated. This is present in the GI tract.

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18
Q

What is the difference between pertussis and cholera toxin activity?

A

Pertussis - ADP-rybosylation of the inhibitory subunit in the GDP state so that it can’t be activated via GDP –> GTP transfer.

Cholera - ADP-Ribosylation of the stimulatory subunit in the active state blocking the ATP–> ADP hyrdrolysis process and leaving the stimulatory subunit active.

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19
Q

Where does insulin bind on what?

A

It bind on the alphaunit of the membrane bound tyrosine kinase.

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20
Q

Step 2 of insulin pathway?

A

Autophosphrylation of the beta-subunit of the tyrosine kinase. This is on a tyrosine residue.

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21
Q

Step 3 of insulin pathway?

A

Phosphorylation of a tyrosine residue on IRS-1 (insulin receptor substrate) this activates IRS-1 and a kinase cascade that activates cellular proteins and effects.

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22
Q

What transporter is affected by insulin?

A

GLUT4 (the only one)

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23
Q

Where does GLUT 4 exist?

A

Adipose and Muscle (primary site of insulin reaction and GLUT 4 mobilization)

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24
Q

Other than glucose regulation in the blood what does insulin do?

A

It acts as a growth factor

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25
Q

What are the two dietary sugars?

A

Lactose and Sucrose

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26
Q

What are the dietary sugars broken into?

A

Glucose and Fructose

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27
Q

What happens to glucose in the cytoplasm?

A

Glucose –> Pyruvate via glycolysis

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28
Q

How many ATP come out of glycoysis?

A

2 NADH + 4ATP

Each NADH = 3 ATP

It costs 2 ATP

NET ATP = 8 ATP

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29
Q

What is the end result of glycolysis?

A

Pyruvate + 8 ATP

30
Q

What does pyruvate dehydrogenase complex do?

A

It breaks up pyruvate into acetyl-CoA and releases CO2 in the process.

31
Q

What is stage 2 of Acetyl-CoA oxidation?

A

The TCA / Citric Acid Cycle which produces reduced electron carriers. NADH and FADH2. This is via citrate and OAA

32
Q

What is stage 3 of the Acetyl-CoA oxidation?

A

ETC and oxidative phosphorylation. This is the oxidation of electron carriers and making ATP.

33
Q

Total ATP in aerobic respiration?

A

36ATP

8 from glycolysis (2 NADH and 2ATP)

6 from PDC (2NADH)

24 from ETC / Ox Phos (6 NADH + 2FADH2 +2ATP)

34
Q

How may ATP out of anaerobic glucose metabolism.

A

2 ATP

35
Q

What is the cost to convert pyruvate to lactate using LDH

A

6 ATP - this is the use of the NADH that would normally be generated.

36
Q

What is the process of making glucose called?

A

Gluconeogenesis

37
Q

Where does gluconeogensis occur?

A

Excess glucose on the liver is absorbed and stored as glycogen for mobilization into the blood.

Excess blood sugar in the muscle gets stored in the muscle as glycogen - it is only used for muscle energy.

38
Q

What is the intermediate product when converting excess glucose to glycogen?

A

Glucose-6-Phosphate

39
Q

What are the precursors that are fed into the TCA that can make glycogen?

A

Lactate –> Pyruvate

Glucogenic Amino Acids

40
Q

What does it cost to create Glucose from Pyruvate?

A

12 ATP

41
Q

How does ATP affect glycolysis?

A

Glycolysis = Glucose –> Pyruvate (need energy)

So, ATP inhibits glycolysis.

42
Q

How does AMP affect glycolysis?

A

Low AMP = need energy

If we need energy then AMP stimulates glycolysis.

43
Q

How does AMP affect gluconeogenesis?

A

Gluconeogenisis is done when energy is high and glucose needs to be stored.

This means that AMP inhibits gluconeogenesis so ensures that glucose remains available for glycolysis and ATP production.

44
Q

How does glucagon and insulin affect gluconeogenesis and glycolysis?

A

Glucagon = low energy = stimulates glycolysis

Insulin = high energy / high glucose = stimulates gluconeogenesis

45
Q

What joins acetyl-Coa with pyruvate to form OAA?

A

Pyruvate Carboxylase

46
Q

Without what is pyruvate carboxylase useless?

A

Acetyl-CoA

47
Q

Pyruvate Kinase is phosphorylated for activation, what stimulates this?

A

Glucagon turns it on and insulin turns it off.

48
Q

What turns lactate back into glucose for use?

A

The liver

49
Q

The liver creates what using lactate, pyruvate and AA’s

A

Glucose but it is an energetically costly process but required for the organs that use glucose as the primary fuel.

50
Q

Pyruvate + CoA + ? = ?

A

(1) Pyruvate Dehydrogenase Complex
(2) Acetyl-CoA

51
Q

When you have CoA, Pyruvate and PDC what is made?

A

You make Acetyl-Coa, 2 NADH, and CO2

2 NAHD = 6 ATP

52
Q

How is pyruvate dehydrogenase complex regulated?

A

Pyruvate Dehydrogenase Complex is responsible for catalyzing the formation of Acetyl-CoA and NADH from pyruvate and NAD+. Products inhibit activity and substrates increase activity. Kinase adds a Pi and turns it off phosphatase removes a Pi and turns is on.

53
Q

How does PDC (pyruvate dehydrogenous complex) get regulated in adipose tissue?

A

Adipose tissue stores excess glucose. If there is excess glucose you don’t need PDC still needs to be activated so that we can create Acetyl-Coa and send that into fat synthesis. So this means that insulin stimulates the phosphatase that takes off the Pi and activates the PDC.

54
Q

ATP Accounting for Glycoysis, phase 1 of respiration, phase 2 respiration.

A

Glucose –> Pyruvate (aerobic) = 8 ATP

Pyruvate –> Acetyl-CoA = 6 ATP

TCA = 24 ATP

All of these are harvested via the ETC and OxPhos

55
Q

Why is vitamin B important?

A

It is used in the syntesis of NAD and FAD. Vitamin deficiency causes issues in ETC and OxPhos

56
Q

If we oxidize fatty acids why does blood sugar still drop in with low glucose diets?

A

The oxydation of FA’s feeds Acetyl-CoA into the TCA. The TCA releases 2 carbons and so all of the carbons that are fed in are lost in CO2. This means that neither acetyl-coa or FA’s oxidation can maintain blood glucose levels.

57
Q

When blood sugar is low and we don’t have the needed glucose –> pyruvate conversion to power the TCA what happens?

A

The TCA is not running and creating OAA so we need some to condense with Acetyl-CoA. We do this via the pyruvate carboxylase which makes OAA from pyruvate. This allows powering of the TCA.

58
Q

How is pyruvate carboxylase regulated?

A

We turn on pyruvate carboxylase to transform Acetyl-CoA to citrate. To turn up the production requires increased OAA concentration. Therefore - [OAA] is the single biggest regulator. It turns out that high levels of Acetyl-CoA that need to enter the TCA and become citrate acts as a positive allosteric affector of pyruvate carboxylase.

59
Q

Why do we store glucose as glycogen?

A

It is not hydrated

It packs more tightly

It is a concentrated form of energy storage

It is structured to allow access to many places to oxidize it.

60
Q

Insulin stimulates:

A

The mobilization of GLUT4 to membrane

Stimulization of Glycogen Synthase to produce glycogen from excess glucose.

61
Q

How much glucose is available at any given time?

A

~327g (brain uses 100g per day)

62
Q

What are the phases of starvation and what is the objective?

A

Phase 1: 1st day - maintain blood glucose

Phase 2: day 1 thru 3 - maintain blood glucose

Phase 3: Up to 300 days - survival

63
Q

Excess glucose that enters the liver has what fates?

A

Glucose –> Glycogen (glyconeogenesis)

Glucose –> Pyruvate –> Acetyl-CoA - Fat (glycolysis / PDC / FA’s synth)

64
Q

How is glucose used in the brain?

A

It is the primary fuel and produces CO2 and H2O

65
Q

How is excess glucose used in the adipose tissue?

A

FA’s synthesis into TAG’s for fat storage.

66
Q

How is excess glucose used in muscle?

A

It goes through glycogen synthesis.

67
Q

When you are out of glucose what happens during early starvation?

A
  1. Glycogen signals for low blood sugar
  2. Glucose is used primarily for brain
  3. Muscle exhausted glycogen starts using glucose produced by liver
  4. Glycogen stores are available but running out?
68
Q

When the body is out of glycogen? (phase II of starvation)

A

Protein, AA, and lactate all get converted to pyruvate and into gluconeogenesis. This is critical to keep glucose available for brain.

69
Q

Third phase of starvation?

A
  1. Glucose, Glycogen and AA usage is low
  2. Fat mobilized and this creates ketone bodies
  3. The production of Acetyl-CoA from FA’s
  4. No OAA to make Citrate with Acetyl-CoA
  5. Low glucose means low pyruvate
  6. This leads to ketoacidosis
70
Q

What happens when the I/G ratio is off in an insulin dependent diabetes patient?

A
  1. Glucose in muscle and adipose goes down
  2. Pyruvate will be reduced
  3. No insulin to drive glycolysis
  4. Therefore no OAA coming from the TCA
  5. Glucagon is elevated, cAMP is elevated
  6. Lipid mobilization occurs
  7. Protein mobilization
  8. Making glucose from protein and lipids
  9. PEPCK is pulling malate and carbons out of the TCA cycle.
  10. Lack of OAA in presence of Acetyl-CoA
  11. Malate is pulled off so no OAA
  12. Severe ketoacidosis, pH drops, Coma, Death

FDN Week 5 (Block 2) (10 decks)

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