Review Cards Flashcards

1
Q

Name differences in Hexokinase and Glucokinase (location, affinity, regulators)

A

Rxn: Glucose –> G-6-P

Glucokinase: in liver, low affinity, high Km for glucose

  • Glucose –> cytosol
  • F-6-P –> nucleus
  • Insulin –> increase expression (inducible)

Hexokinase: outside liver, high affinity, low Km for glucose

  • G-6-P negative feedback
  • Non-inducible, constitutive
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2
Q

What is the main activator of PFK-1?

A

F-2,6-bisP allosteric activator

Reaction: PFK-1: F-6-P –> F-1,6,-P

Other activators: AMP, ADP
Inhibitors: ATP, Citrate

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3
Q

How is PFK-2 differentially regulated in liver and muscle under fasting?

A

Liver: PFK-2 kinase domain is phosphorylated by glucagon/Epi –> inhibited –> no F-2,6-bisP –> inhibit hepatic glycolysis

Muscle: PFK-2 phosphatase domain is phosphorylated by Epi, so kinase is active –> increased F-2,6-bisP –> activate PFK-1 –> glycolysis active

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4
Q

What are the regulators of Pyruvate Kinase?

A

[Reaction: PEP –> Pyruvate]

Activated by insulin (de-phosphorylation) and F-1,6-bisP (feed forward)

Inhibited by glucago/Epi (phosphorylation), ATP, Alanine

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5
Q

What are the 4 fates of Pyruvate?

A
  1. Transamination –> Alanine
  2. Pyruvate Carboxylase –> Oxaloacetate
  3. LDH –> Lactate
  4. PDH –> Acetyl CoA
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6
Q

What are the names of the 2 shuttles that regenerate NAD+?

A
  1. Malate-Aspartate
  2. Glycerol-Phosphate

Use them to regenerate NAD+ in the mitochondria because NADH can’t cross the membrane; they can be reoxidized by ETC, so get a lot more ATP from this than making lactate

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7
Q

What is the reaction catalyzed by LDH? What is the point? How is it different in skeletal and heart muscle?

A

Pyruvate + NADH+ –> Lactate + NAD+

  • To regenerate NAD+
  • Skeletal m. will convert Pyruvate –> Lactate (2 ATP)
  • Heart m. will convert Lactate –> Pyruvate for TCA
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8
Q

What is catalyzed by PDH? How is it regulated?

A

Pyruvate + CoASH + NAD+ –> Acetyl CoA + NADH

  • Needs vitamin cofactors
  • Acetyl CoA, NADH are feedback inhibitors
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9
Q

What is Galactosemia?

A

Deficiency of Galactose-1-P-Uridyltransferase –> accumulation of galactose –> increase of galactitol –> cataracts, jaundice, enlarged liver, kidney damage, brain damage

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10
Q

What are the 3 sources of Acetyl CoA?

A
  1. Glycogen –> Glucose –> Pyruvate –> Acetyl CoA
  2. TAGs –> FFA –> Acetyl CoA
  3. Proteins –> a.a. –> Acetyl CoA
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11
Q

What are the 3 fates of Acetyl CoA?

A
  1. TCA
  2. Ketone bodies
  3. Sterols, FAs
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12
Q

How many ATP are made with each cycle of TCA?

A

9 ATP + 1 GTP = 10 ATP

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13
Q

What does isocitrate dehydrogenase control? How is it regulated?

A

Fine control of TCA
Reaction: [isocitrate –> a-ketoglutarate]
Activated by: ADP
Inhibited by: ATP, NADH

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14
Q

What does a-ketoglutarate dehydrogenase control? How is it regulated?

A

Fine control of TCA
Reaction: [a-ketoglutarate –> succinyl coA]
Activated by: ADP, Ca2+
Inhibited by: ATP, GTP, NADH, Succinyl coA

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15
Q

What are the non-carbohydrate precursors used to make glucose in Gng?

A

Pyruvate, Lactate, Glycerol, Glucogenic a.a.

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16
Q

What is the first step of gluconeogenesis? Enzyme? Reaction? Regulation?

A

Pyruvate –> Oxaloacetate

  • Enzyme: Pyruvate Carboxylase
  • Requires ATP, Biotin cofactor
  • Activated by Acetyl CoA
17
Q

Where are GLUT-2 and GLUT-4 receptors located? What are their differences?

A

GLUT-2 is insulin-independent ([glucose]-mediated) and is on hepatocytes

GLUT-4 is insulin-dependent and is in skeletal muscle

18
Q

How is Glycogen Phosphorylase regulated?

A

(draw)

19
Q

How is Glycogen Synthase regulated?

A

(draw)

20
Q

What is the rate limiting enzyme of the PPP? What is the effect of its deficiency?

A

Glucose-6-Phosphate Dehydrogenase

  • Hemolytic Anemia (oxidative stress on RBCs)
  • Protective against Malaria (b/c pathogen needs NADPH)
21
Q

What is the rate limiting enzyme of FA biosynthesis? How is it regulated?

A

[Acetyl CoA –> Malonyl CoA]
Catalyzed by Acetyl CoA Carboxylase

Activated by: low fat diet, insulin, citrate
Inhibited by: Palmitoyl-CoA, Glucagon/Epi

22
Q

What does HSTL do? How is it regulated?

A

HSTL: [TAGs –> FA + Glycerol]

Activated by Epi/Glucagon, ACTH
Inhibited by Insulin

23
Q

What is the rate-limiting enzyme of Fatty Acid B-oxidation? What is its regulator?

A

CPT-1: brings FA into mitochondrial matrix
[FA –> Acetyl CoA] via [Carnitine –> acylcarnitine]

  • Inhibited by Malonyl-CoA (product of Acetyl-CoA Carboxylase), so you don’t want to make ketone bodies if you are making FA (don’t use what you’re making)
24
Q

What pathway is HMG-CoA Synthase involved in? Where is it located?

A

Ketone body formation [Acetoacetate –> HMG CoA]

Liver mitochondria