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Biochem > Lecture 16+17: Glycolysis, PDH, TCA > Flashcards

Lecture 16+17: Glycolysis, PDH, TCA Flashcards

1
Q

Possible fuel sources for ATP and their storage forms

A

Glucose (glycogen), fatty acids (triglycerides), amino acids (proteins)

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2
Q

How does alcohol inhibit gluconeogenesis (clinical case)? How can it be treated?

A

Treatment with thiamine, glucose infusion

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3
Q

Key regulated steps in glycolysis

A

Hexokinase, PFK, pyruvate kinase

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4
Q

ATP investment and return steps in glycolysis

A

Net = 2 ATP (2 in, 4 out)

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5
Q

High energy phosphate donors in glycolysis

A

1,3-bisphosphoglycerate and phosphoenolpyruvate (PEP)

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6
Q

What does iodoacetate inhibit?

A

Generation of NADH by G3P DH in glycolysis

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7
Q

How is NADH re-oxidized to NAD in aerobic conditions?

A

Reducing equivalents from NADH are transported by shuttles to the ETC and finally to O2

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8
Q

How is NADH re-oxidized to NAD to anaerobic conditions?

A

NADH reduces pyruvate to lactate via lactate DH

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9
Q

Pasteur effect

A

Anaerobic fermentation of pyruvate into acetaldehyde then reduction by alcohol DH and NADH into EtOH in yeast. Inhibited by oxygen.

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10
Q

How is glucokinase different from hexokinase?

A
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11
Q

What roles does glucokinase play compared to hexokinase?

A

Because glucokinase is most sensitive to changes in [gluc.] at physiological ranges, it acts as a glucose sensor for the liver and pancreas. Hexokinase instead wants to bring in glucose as quickly as possible, especially with high energy demand (e.g. working muscle).

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12
Q

How does glucokinase play a role in glucose dysregulation in diabetes?

A

Liver glucokinase is positively controlled by insulin, and so is low in diabetes -> impaired blood glucose response.

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13
Q

Mature Onset Diabetes of the Young (MODY2)

A

Inhibitory mutation in beta cell glucokinase resulting in insufficient insulin release despite high blood glucose.

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14
Q

Persistent Hyperinsulinemic Hypoglycemia of Infancy (PHHI)

A

Activating mutation in beta cell glucokinase leading to insulin production even with low blood glucose.

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15
Q

GLUT2 vs GLUT4

A

GLUT4 is found in muscle and fat and is activated by insulin and anoxia.

GLUT2 acts independent of insulin and is part of glucose sensing in the liver/pancreas by achieving rapid equilibrium with blood glucose.

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16
Q

How is PFK regulated?

A

Activation: ADP, AMP, F-2,6-bisPi
Inhibition: ATP (feedback), citrate

17
Q

Why are AMP and ADP more sensitive indicators of changes in [ATP]?

A

ADP is generally at a lower concentration -> larger percent changes
[AMP] is 2nd order to [ADP] by myokinase (adenylate kinase), so a 3x increase in ADP leads to a 9x increase in AMP

18
Q

Why does citrate inhibit PFK?

A

Citrate buildup is an indicator of available alternate fuel, i.e. fatty acid oxidation produces acetyl-CoA. Acetyl-CoA can’t be transported out of the mitochondria, so it is instead converted to citrate which can be transported to the cytosol where PFK is located.

19
Q

What role does fructose-2,6-bisphosphate play? How is it regulated?

A

F26BP is important in signaling for control of glycolysis/gluconeogenesis in the liver. Glucagon (low blood gluc.) activates Protein Kinase A, inhibiting PFK2 and activating F26BPase -> decreased PFK activity in liver

20
Q

How is fructose-2,6-bisphosphate regulated in muscle?

A

PFK2/F26BPase don’t have the PKA phosphorylation site in muscle, and so are not affected by glucagon.

21
Q

Role of the liver in glucose levels

A

The body mainly uses the glycogen stores in the liver to regulate blood glucose in close coordination with the pancreas via insulin/glucagon.

22
Q

Why is PFK the primary regulated step in glycolysis and not hexokinase?

A

Glucose-6-P can go to glycolysis, glycogen, or the PPP. Inhibition of hexokinase by G6P means, with little flux to glycogen/PPP, hexokinase activity follows PFK. When PFK activity increases/decreases, so does hexokinase activity.

23
Q

How is pyruvate kinase regulated in muscle?

A

Weak competitive inhibition by ATP

24
Q

How is pyruvate kinase regulated in the liver?

A

Strong allosteric inhibition by ATP; also inhibited by Ala and PKA phosphorylation. Depends on high F16bP levels.

25
Q

What is PKM2?

A

PKM2 is the fetal form of pyruvate kinase

26
Q

What’s bad about high fructose in food?

A

Fructose bypasses early regulated steps of glycolysis in the liver via aldolase B, which can lead to obesity.

27
Q

Aldolase B deficiency

A

Aldolase B deficiency in the liver leads to fructose intolerance due to as phosphate groups get tied up in F1P from fructose/fructokinase.

28
Q

Glucokinase Inhibitory Protein (liver)

A

Binds glucokinase for nuclear retention. Inhibited by F1P, which stimulates glucokinase.

29
Q

Galactosemia

A

Deficiency in galactose-1-P uridyl transferase, trapping P in galactose-1-P

30
Q

PDH Complex enzymes

A
  1. Pyruvate DH
  2. Dihydrolipoyl transacetylase
  3. Dihydrolipoyl DH
31
Q

How is PDH allosterically regulated?

A

Activated by CoA, NAD
Inhibited by acetyl-CoA, NADH
(ratios)

32
Q

Why is PDH complex regulation important?

A

Pyruvate can be converted back into glucose, but acetyl-CoA creation is irreversible.

33
Q

How is PDH complex covalently regulated?

A

PDH can be inactivated by phosphorylation via PDH kinase; reversed by PDH phosphatase

34
Q

How is PDH kinase regulated?

A

Acetyl-CoA:CoA, NADH:NAD, ATP:ADP ratios

35
Q

How is PDH phosphatase regulated?

A

Activated by insulin, pyruvate, and calcium

36
Q

PDH deficiency

A

X-linked E1-alpha gene, inefficient E1 import to mitochondria leads to elevated lactate, pyruvate, and Ala due to low pyruvate -> acetyl-CoA. Can be treated sometimes with thiamine or a ketogenic diet (PDH cofactor or bypassing PDH)

37
Q

PDH cofactors and their vitamin precursors

A

Thiamine (B1) -> TPP
Riboflavin (B2) -> FAD
Nicotinate (Niacin) -> NAD
Pantothenate -> CoA

38
Q

How does arsenic impact glucose metabolism?

A

Arsenic interacts with lipoic acid, inhibiting aKG DH, PDH, and branched chain AA DH

Biochem (24 decks)

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