Energy Metabolism I

Question 1

Catabolism

Answer 1

degradation of molecules

Question 2

Anabolism

Answer 2

biosynthesis of molecules

Question 3

Are living organisms at equilibrium?

Answer 3

No

Question 4

Types of enzyme regulation in metabolic pathways and their speeds

Answer 4

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

Question 5

futile cycle

Answer 5

what would happen if catabolic and anabolic pathways were not regulated

Question 6

Goals of energy metabolism

Answer 6

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

Question 7

Niacin

Answer 7

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

Question 8

Reduction of NAD+

Answer 8

-can park 2 electrons on it to become NADH

Question 9

Difference between NAD+/NADP+

Answer 9

• NADP just has an additional phosphate

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

Question 10

B Vitamins

Answer 10

Very important building blocks for cofactors/coenzymes

Question 11

Beriberi (deficiency in what vitamin)

Answer 11

Thiamine (B1)

Question 12

Pernicious anemia (deficiency in what vitamin)

Answer 12

Cobalamin (B12)

Question 13

glucose transporters/transport

Answer 13

• 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

Question 14

Tissues where glucose transport is not insulin-dependent

Answer 14

liver, brain, cornea, erythrocytes

Question 15

GLUT 1

Answer 15

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

Question 16

GLUT 2

Answer 16

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

Question 17

GLUT 3

Answer 17

Km=2mM

-primarily in neurons

Question 18

GLUT 4

Answer 18

Km=5mM

• in muscle and adipose
• regulated by insulin

Question 19

GLUT 5

Answer 19

fructose transporter

Question 20

what increases/decreases GLUT 4 translocation to membrane

Answer 20

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

Question 21

type I diabetes

Answer 21

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

Question 22

Two ways to measure blood glucose

Answer 22

• instantaneous blood glucose level

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

Question 23

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

Answer 23

• 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)

Question 24

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

Answer 24

hexokinase phosphorylating glucose to to glucose 6-phosphate

Question 25

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

Answer 25

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

Question 26

one molecule of glucose becomes what in glycolysis?

Answer 26

2 molecules of pyruvate

Question 27

Pyruvate

Answer 27

- can be completely oxidized (requiring oxygen and mitochondria) - can become lactate (anaerobic glycolysis)

Question 28

where in the cell does glycolysis occur

Answer 28

cytosol

Question 29

Phosphofructo-1-kinase (PFK-1)

Answer 29

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

Question 30

what is the first *committed* step of glycolysis?

Answer 30

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

Question 31

regulation of PFK-1

Answer 31

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

Question 32

fructose 2,6-bisphosphate mechanism of action

Answer 32

activates PFK-1

Question 33

pyruvate kinase deficiency

Answer 33

- 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)

Question 34

lactate dehydrogenase

Answer 34

- 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

Question 35

What is the problem with NADH in anaerobic glycolysis?

Answer 35

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

Question 36

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

Answer 36

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

Question 37

oxidative path of PPP

Answer 37

generates NADPH--> for biosynthetic reactions

Question 38

non-oxidative path of PPP

Answer 38

generates ribose 5-phosphate-->for nucleotide biosynthesis

Question 39

NADPH roles

Answer 39

- reductive biosynthesis - maintains reduced glutathione in cytosol - detoxifies reactive oxygen species

Question 40

glucose 6-phosphate dehydrogenase (G6PD)

Answer 40

-generates the first NADPH in PPP

Question 41

G6PD deficiency (fauvism)

Answer 41

- X-linked | - causes hemolytic anemia due to inability to detoxify oxidizing agents

Question 42

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

Answer 42

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