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Week 4/5 FMM > Energy Metabolism I > Flashcards

Energy Metabolism I Flashcards

1
Q

Catabolism

A

degradation of molecules

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2
Q

Anabolism

A

biosynthesis of molecules

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3
Q

Are living organisms at equilibrium?

A

No

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4
Q

Types of enzyme regulation in metabolic pathways and their speeds

A
  • allosteric regulation; instantaneous
  • covalent modification; fast
  • rate of protein synthesis and turnover; over hours
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5
Q

futile cycle

A

what would happen if catabolic and anabolic pathways were not regulated

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6
Q

Goals of energy metabolism

A

maintain pools of energy storage units (ATP or NADH/NADPH)

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7
Q

Niacin

A
  • essential to get in diet
  • building block of NAD
  • derived from Vitamin B3
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8
Q

Reduction of NAD+

A

-can park 2 electrons on it to become NADH

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9
Q

Difference between NAD+/NADP+

A
  • NADP just has an additional phosphate

- important for certain enzyme interactions but in terms of reducing potential, it is the same

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10
Q

B Vitamins

A

Very important building blocks for cofactors/coenzymes

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11
Q

Beriberi (deficiency in what vitamin)

A

Thiamine (B1)

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12
Q

Pernicious anemia (deficiency in what vitamin)

A

Cobalamin (B12)

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13
Q

glucose transporters/transport

A
  • bring glucose into the cell by facilitated passive diffusion
  • activated by insulin
  • stored in the cells and come to the plasma membrane when signaled by insulin (except in cells where glucose transport is not dependent on insulin)
  • saturable: they have a specific Km and can be saturated if there is enough glucose
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14
Q

Tissues where glucose transport is not insulin-dependent

A

liver, brain, cornea, erythrocytes

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15
Q

GLUT 1

A

Km=1-2mM
-present in CNS and RBCs because you want them to use glucose at a constant rate so even when blood glucose is low, glucose can still bind

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16
Q

GLUT 2

A

Km= 15-20mM

  • liver, intestine, kidney, Beta cells
  • want to be able to sense the rate at which glucose is coming in so want a higher Km so that you can respond proportionally to amount of glucose (if you have a lot of glucose, you will respond even with a high Km
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17
Q

GLUT 3

A

Km=2mM

-primarily in neurons

18
Q

GLUT 4

A

Km=5mM

  • in muscle and adipose
  • regulated by insulin
19
Q

GLUT 5

A

fructose transporter

20
Q

what increases/decreases GLUT 4 translocation to membrane

A

Increases: exercise (HIF-1 involved)
Decreases: diabetes type 2 (body stops responding properly to insulin)

21
Q

type I diabetes

A

inability to produce insulin (Beta cell destruction in pancreas–immune system attacks beta cells)

22
Q

Two ways to measure blood glucose

A
  • instantaneous blood glucose level

- HbA1c levels (over a couple months)–works because RBCs live for about that long

23
Q

hexokinase I (what does it do, km, what inhibits it)

A
  • phosphorylates glucose to trap it in the cell; first step of glycolysis
  • low Km (so it is always saturated)
  • inhibited by glucose-6-phosphate (feedback regulation)
24
Q

what is the first step of glycolysis (irreversible but not committed)

A

hexokinase phosphorylating glucose to to glucose 6-phosphate

25
Q

Hexokinase IV (where do you find it, km, inhibition)

A
  • abundant in liver
  • high Km
  • not inhibited by glucose 6 phosphate because liver wants to be able to take in massive amounts of glucose
26
Q

one molecule of glucose becomes what in glycolysis?

A

2 molecules of pyruvate

27
Q

Pyruvate

A
  • can be completely oxidized (requiring oxygen and mitochondria)
  • can become lactate (anaerobic glycolysis)
28
Q

where in the cell does glycolysis occur

A

cytosol

29
Q

Phosphofructo-1-kinase (PFK-1)

A
  • catalyzes first committed step of glycolysis of Fructose-6-phosphate to fructose 1,6-bisphosphate
  • allosterically regulated
30
Q

what is the first committed step of glycolysis?

A

PFK-1 conversion of Fructose-6-phosphate to fructose 1,6-bisphosphate

31
Q

regulation of PFK-1

A

-allosterically regulated by ATP (ATP inhibits) and AMP/fructose 2,6-bisphosphate (activate)

32
Q

fructose 2,6-bisphosphate mechanism of action

A

activates PFK-1

33
Q

pyruvate kinase deficiency

A
  • pyruvate kinase is the enzyme that ultimately creates pyruvate
  • deficiency of it can lead to hemolytic anemia (especially damaging to RBCs because they rely solely on glycolysis for ATP)
34
Q

lactate dehydrogenase

A
  • transfers electrons from NADH to pyruvate (generating lactate) so that NAD+ can be recycled in anaerobic conditions
  • can also be used to take lactate and use it as fuel under aerobic conditions
35
Q

What is the problem with NADH in anaerobic glycolysis?

A

it’s a problem if there is no oxygen/mitochondria (because NADH can’t be recycled back to NAD+)

36
Q

which NADH shuttle is more efficient? What is the other shuttle called? Where are they active

A 
more efficient= Malate/aspartate shuttle  (forms 3 ATP per NADH)--heart, liver, kidney 
Glycerophosphate shuttle (forms 2 ATP per NADH)--skeletal muscle and brain
37
Q

oxidative path of PPP

A

generates NADPH–> for biosynthetic reactions

38
Q

non-oxidative path of PPP

A

generates ribose 5-phosphate–>for nucleotide biosynthesis

39
Q

NADPH roles

A
  • reductive biosynthesis
  • maintains reduced glutathione in cytosol
  • detoxifies reactive oxygen species
40
Q

glucose 6-phosphate dehydrogenase (G6PD)

A

-generates the first NADPH in PPP

41
Q

G6PD deficiency (fauvism)

A
  • X-linked

- causes hemolytic anemia due to inability to detoxify oxidizing agents

42
Q

why are anti-malarial drugs dangerous for folks with G6PD deficiency

A

they can cause hemolytic anemia
-usually females that are carriers of G6PD have increased resistance to malaria because RBCs die faster so malaria has harder time staying active

Week 4/5 FMM (8 decks)

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