Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Metabolism > Review - II > Flashcards

Review - II Flashcards

1
Q

Where does glycogenolysis occur?

A

Liver and skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is beta oxidation?

A

Conversion of FAs to AcCoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why is lypolysis?

A

Hydrolyzing triglycerides into FAs and glycerol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Can AAs become AcCoA?

A
  • Yes

- Can be deaminated and oxidized to acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What can happen to AcCoA?

A

Enter TCA cycle
Produce ketone bodies
Produce fatty acids and sterols

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can cause chronic lactic acidosis?

A

PDH deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Genetics of PDH deficiency?

A
  • Predominantly an X-linked dominant

- Caused by mutation in E1 alpha gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How to treat PDH deficiency?

A
  • Dietary supplementation with thiamine, carnitine, and lipoic acids
  • Dichloroacetate – inhibitor of protein kinase subunit of PDH complex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How much ATP does 1 CAC generate?

A

10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is generated in CAC and ATP conversion?

A
  • 3 NADH @ 2.5 ATP each = 7.5 ATP
  • 1 FADH2 @ 1.5 ATP each = 1.5 ATP
  • 1 GTP @ 1 ATP each = 1 ATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 Key enzymes in CAC?

A
  1. Isocitrate dehydrogenase
  2. Alpha-ketoglutarate dehydrogenase
    - Both can be regulated allosterically and under fine and coarse control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Modulation of Isocitrate dehydrogenase?

A
  • Inhibition - High concentration of ATP

- Activation- High ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Modulation of Alpha-ketoglutarate dehydrogenase?

A
  • Activation - High concentration of Ca

- Inhibition - High amount of NADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does Succinyl CoA Feedback?

A
  • High concentrations inhibit conversion of Acetyl-CoA to citrate
  • Also inhibits formation of additional succinyl CoA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What usually provides Oxaloacetate in CAC?

A

Fumarate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can provide OAA in lieu of fumarate?

A

Asparate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What usually provides alphaketoglutarate in CAC?

A

Citrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What can procide alphaketoglutarate if shortage of citrate?

A

Glutamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What can provide propinyl coA in CAC?

A

Valine

Isoleucine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is performed first during starvation?

A

Glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sources for gluconeogenesis?

A

Pyruvate
Lactate
Glycerol
Glucogenic amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does gluconeogenesis occur?

A

Liver

Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does muscle release from stored glycogen?

A

Lactate

Alanine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Does gluconeogenesis require ATP?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where does ATP for gluconeogenesis come from?

A
  • Overnight metabolism of fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is PEP?

A
  • Activated form of pyruvate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is intermediate between PEP and pyruvate?

A

OAA

28
Q

What else is required for pyruvate to PEP conversion?

A
  • Bicarb
  • Biotin
  • Expenditure of ATP
29
Q

Gluconeogenic precursors?

A
  • Fructose
  • Galactose
  • Glycerol
  • Propionate
  • Aspartate
  • Alanine
  • Lactate
30
Q

What is Cori Cycle?

A
  • Generation of glucose from lactate
  • Lactate gets into the liver and generates a glucose molecule
  • Utilizes 6 ATP in the process
31
Q

Where does cori cycle happen?

A

Lactate comes from RBCs & skeletal muscle

Then moves to liver

32
Q

What is alanine cycle?

A

Gluce from alalanine

33
Q

Where does alanine come from?

A

Skeletal muscle in exercise

34
Q

Byproduct of alanine cycle?

A

Ammonia which is turned into urea

35
Q

4 key enzymes in glycogenolysis?

A
  1. Pyruvate carboxylase - mitochondrial
  2. PEP carboxykinase
  3. Fructose 1,6 biphosphatase
  4. Glucose 6 phosphatase
36
Q

What happens in Pyruvate carboxylase deficiency?

A
  • Cannot convert pyruvate to oxaloacetate
  • Increased alanine, lactate, and pyruvate
  • Lack of enzyme reduces gluconeogenesis process and reduces the urea cycle
  • Recurrent seizures
  • Developmental Delay
  • Metabolic acidosis
37
Q

What happens in Glucose 6 phosphatase deficiency?

A
  • Blocks gluconeogenesis and glycogenolysis
  • Cannot generate glucose from glucose-6-phosphate
  • Glycogen storage disease type I (von Gierke disease)
  • Increased liver size and elevated serum uric acid and lactate levels
  • Poor tolerance of fasting
  • Growth retardation
  • Hepatomegaly
38
Q

What does ethanol ingestion cause?

A
  • Hypoglycemia because the high amount of NADH opposes gluconeogenesis
  • Ethanol metabolism raises NADH/NAD ratio
  • Removes pyruvate and OAA from pool of glucogenic precursors
39
Q

What does high NADH cause?

A
  • Conversion of pyruvate and OAA to lactate and malate
40
Q

How does glucose enter hepatocyte?

A

Glut2

41
Q

What does G6P do?

A

Convert G6P to Glucose

42
Q

Transporter on skeletal muscle?

A

GLUT4

43
Q

Muscle or liver store more glycogen?

A

Muscle

44
Q

What stimulates glycogen break down in muscle?

A

Epinephrine or muscle contraction

45
Q

Why cant skeletal muscle synthesize glucose?

A
  • There is no G6Pase in skeletal muscle
46
Q

Summary of steps of glucose storage?

A
  • Glucose can be converted to G6P
  • G6P is converted to G1P
  • From there G1P is converted to UDP glucose
  • Glycogen synthase and branching enzyme converts UDP glucose to glycogen
47
Q

What converts glycogen to G1P?

A

Debranching enzyme and glycogen phosphorylase

48
Q

Which form of glycogen phosphorylase is phosphorylated?

A
  • B is dephosphorylated
  • A is phosphorylated
  • A is Active
49
Q

What leads to conversion of phosphorylase A to B?

A
  • Increased levels of glucose and insulin favor glycogen storage
  • Activates phosphoprotein phosphatase
  • Dephosphorylates active form of phosphorylase a
  • At the same time, glycogen synthase is activated
50
Q

Allosteric regulation of glycogen phosphorylase?

A
  • AMP converts B to A
  • ATP converts A to B
  • High glucose inactivates A
51
Q

Active and inactive forms of glycogen synthase?

A
  • A is dephosphorylated
  • B is phosphorylated
  • A is active
52
Q

Regulation of glycogen synthase?

A
  • Insulin leads to activation
  • Glucagon leads to inhibition
  • G6P binds to B activating it
53
Q

What does G6P dehydrogenase do?

A
  • Catalyzes first step in pentose phosphate pathway

- Converts G6P to 6-phosphogluconate

54
Q

What does pentose phosphate pathway create?

A
  • Penthose phosphate pathway generates lots of NADPH
55
Q

How is o G6P dehydrogenase deficiency inherited?

A

X linked

56
Q

What does G6P dehydrogenase deficiency cause?

A
  • Hemolytic anemia
  • RBCs cannot handle oxidative stress in absence of G6P dehydrogenase
  • Increased bilirubin
  • Decreased hemoglobin
57
Q

What does NADPH doe in RBC?

A
  • Maintains glutathione in reduced state
  • Protect RBCs against oxidative stress
  • If NADPH levels reduced, glutathione can be oxidized
  • Oxidation produces hydrogen peroxide as a byproduct
  • Toxic to RBCs
58
Q

What does glutathione do?

A

Protects RBC from oxidative stress

59
Q

What is drug than can generate oxidative stress?

A

Dapsone, used for malaria

60
Q

What can increase oxidative stress?

A
  • Oxidative drugs (anti-malaria drugs like dapsone)
  • Infection (produces free radicals)
  • Favism
61
Q

Symptoms of PDH deficiency?

A
  • Elevated Serum lacate, pyruvate
  • Microcephally
  • Poor muscle coordination
  • Mental retardation
62
Q

What can succily coA come from?

A

Propionyl coA or alphe ketoglutarate

63
Q

Where does fumarate usually come from?

A

Siccinyl CoA

64
Q

What can also create fumarate?

A

Phenylalanine
Aspartate
Tyrosine

65
Q

How much ATP does alanine cylcle use?

A

10

66
Q

What does cAMP do do glycogen phosphorylase?

A

Increases its activity

Metabolism (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions