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Biochemistry 510 > Exam 2: Metabolism > Flashcards

Exam 2: Metabolism Flashcards

1
Q

What are the 9 Essential Amino Acids?

A
  1. Histidine
  2. Isoleucine
  3. Leucine
  4. Lysine
  5. Methionine
  6. Phenylalanine
  7. Threonine
  8. Tryptophan
  9. Valine
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2
Q

What are the 9 Non-essential Amino Acids?

A
  1. Alanine
  2. Arginine
  3. Asparagine
  4. Aspartate
  5. Glutamate
  6. Glutamine
  7. Glycine
  8. Proline
  9. Serine
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3
Q

What are the 2 Conditionally Essential Amino Acids (& their source)?

A
  1. Cysteine (from methionine)
  2. Tyrosine (from phenylalanine)
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4
Q

What are the important Enzymes in the digestion of proteins (and their location of origin):
–Name 6

A
  1. Pepsin (activated in stomach)
  2. Trypsin (1ST! activated in S.I.)
  3. Chymotrypsin (activated in S.I.)
  4. Elastase (activated in S.I., by Trypsin)
  5. Carboxypeptidase A (S.I.)
  6. Carboxypeptidase B (S.I.)

–Free AA’s activate trypsin in SI. Trypsin activates all other enzymes.

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5
Q

Name of the major membrane protein that transports free amino acids into enterocyte cells in the small intestine:

A

PEPT1: accounts for 60%

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6
Q

How are free AA’s transported after absorption into enterocytes

A

Via portal vein to the liver

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7
Q

What happens to proteins in the liver?

A
  1. De-amination (remove Nitrogen): in Mitochondria of hepatocytes. Urea Cycle
  2. Carbon backbone is used for catabolism (breaking down for energy) or anabolism (building up proteins)
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8
Q

What determines whether amino acids will be catabolized or anabolized?

A

Insulin
–High insulin = increased ANABOLISM (protein synthesis)

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9
Q

What are the 2 Ketogenic Amino Acids?

A
  1. Leucine
  2. Lysine
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10
Q

What are the 5 Amphibolic Amino Acids?

A
  1. Phenylalanine
  2. Isoleucine
  3. Threonine
  4. Tryptophan
  5. Tyrosine
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11
Q

What is a peptide?

A

Molecule composed of between 2-50 amino acids… linked by peptide bonds
-ex: oligopeptides: 3-50
-polypeptides: 50-100

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12
Q

Summarize the TCA cycle

A

-Pyruvate
-Acetyl Co A
(combines with Oxaloacetate to form…)
-Citrate
-Isocitrate
-Alpha Ketoglutarate
-Succinyl-CoA
-Succinate
-Fumarate
-Malate
-Oxaloacetate

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13
Q

What amino acids are most abundant in serum?
Function?

A

-Glutamine
-Glycine
-Alanine

  1. These amino acids are used to transport Nitrogen through blood, so that blood PH does not change
  2. Their C-skeleton is used by non-liver cells for energy
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14
Q

What are the 2 major fates of Amino Acids? Why?

A
  1. Protein
  2. Energy

… because they are not readily able to be stored in our bodies

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15
Q

What is the anabolic state?

A

Amino acids are largely converted into serum proteins by the liver OR skeletal muscle protein (due to exercise or healing)

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16
Q

What is the catabolic state?

A

Amino acids are immediately metabolized for energy and the reminder (stripped Nitrogen) is excreted
-N stripped via urea cycle and excreted
-C skeleton converted into forms that can enter TCA cycle or gluconeogenesis

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17
Q

Aspartate and Asparagine are readily converted into which intermediate of the TCA cycle (via removal of N)

A

Oxaloacetate

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18
Q

Glutamate and Glutamine are readily converted into which intermediate of the TCA cycle (via removal of N)?

A

Alpha-Keo-glutarate

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19
Q

Alanine is readily converted into which intermediate of the TCA cycle (via addition of N)?

A

Pyruvate

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20
Q

What enzyme converts glutamine into glutamate?

A

Glutaminase

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21
Q

What enzyme converts glutamate into alpha keto glutarate?

A

Glutamate dehydrogenase

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22
Q

What enzyme converts Alanine into Pyruvate?

A

Alanine transaminase

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23
Q

What enzyme converts Asparagine into Aspartate?

A

Asparaginase

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24
Q

What enzyme converts Aspartate into Oxaloacetate?

A

Aspartate Transaminase

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25
Q

What are the Steps of the Urea Cycle?

A
  1. Glutamine–>Glutamate
    **brings ammonia into mitochondria
  2. Carbomyl-Phosphate
  3. Citrilline
    (Add Arginine–>Aspartate. 2nd N)
  4. Argino-succinate
    (Fumarate prod. Recycled into TCA)
  5. Arginine
    (Urea)
  6. Ornithine
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26
Q

Which substrates of urea cycle occur in the mitochondrial matrix of hepatocytes (vs cytosol)?

A

Mitochondria:

-Carbomyl-Phosphate
-Citrilline (transported into cytosol)
-Ornithin (transported into cytosol)

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27
Q

How long after a meal is the fed state?

A

0-3 hours

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28
Q

How long after a meal is the Post-absorptive state?

A

3-12/18 ish hours

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29
Q

How long after a meal is the fasting state?

A

18 hours - 2 days

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30
Q

How long after a meal is the starvation state?

A

Fully adapted state lasting 2+ weeks

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31
Q

Predominant Energy Substrate in Dif. phases:

BRAIN

A

Fed: Glucose
Post -Absorptive: Glucose
Fasting: Glucose
Starvation: Ketones

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32
Q

Predominant Energy Substrate in Dif. phases:

Liver

A

Fed: Glucose
Post -Abs.: Glycogen –> Glucose/ FA’s
Fasting: Fatty Acids
Starvation: Fatty Acids

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33
Q

Predominant Energy Substrate in Dif. phases:

Adipose

A

Fed: Glucose
Post -Absorptive: Fatty Acids
Fasting: Fatty Acids
Starvation: Fatty Acids

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34
Q

Predominant Energy Substrate in Dif. phases:

Muscle

A

Fed: Glucose
Post -Abs. : Glycogen –> Glucose
Fasting: Fatty Acids
Starvation: Ketones/ Fatty Acids

35
Q

What is a Ketone?

A

An alternative fuel for the body that is made when glucose is in short supply. Made in the mitochondria of the Liver (as a result of FA degradation)

–ketones are used for energy during fasting, long periods of exercise, or when you don’t have as many carbohydrates

36
Q

What promotes Ketogenesis?

A

During prolonged starvation/fasting/diabetes, oxaloacetate is depleted in the liver due to its use in gluconeogenesis. So it cannot combine with Acetyl-coA to become Citrate for TCA cycle…

so:
ACoA build up in the Liver mitochondria!

37
Q

Name 3 examples of Ketone bodies:

A
  1. Acetone
  2. Acetoacetate
  3. Beta-hydroxybutyrate
38
Q

Why can’t the liver use ketones for energy?

A

The SCOT (succinyl-coA 3 ketoacid coA) is not expressed in the liver…

and this is the enzyme that attaches the coA factor onto the ketone bodies…

so that they can be utilized as energy in liver
**most other tissues express SCOT

39
Q

Where is insulin produced?

A

Beta cells… in the pancreas. Specifically in the islet of Langerhans

40
Q

Is insulin conserved in the body?

A

YES!

41
Q

What is produced in the islet of Langerhans?

A
  1. Glucagon (Alpha cells)
  2. Insulin (Beta cells)
  3. Somatostatin
42
Q

What allows for the rapid release of insulin in the presence of glucose in the bloodstream?

A

Insulin is packaged into granules that sit at the plasma membrane, which leads to rapid (nearly instant) release during glucose-spike from food!

43
Q

What is Incretin?

A

Hormone that stimulates the Beta Cells to secrete more Insulin

44
Q

What is the Incretin effect?

A

If you orally ingest glucose your insulin levels will spike up much more than if you injected insulin into the bloodstream.

this suggests that the stomach/SI secretes incretins which have an additive effect, which produces a larger insulin response.

**The gap in the graph is specifically the incretin effect

45
Q

Understand the Insulin Tolerance Test

A

Tests for insulin receptors uptake of glucose.

-measures blood glucose levels over time after insulin has been injected?

46
Q

Effects of increased Insulin in Tissues:

Muscle

A

INCREASE glucose transport (GLUT4)

INCREASE glycogen synthesis

47
Q

Effects of increased Insulin in Tissues:

Liver

A

INCREASE glycogen synthesis

INCREASE lipogenesis (making more)

DECREASE gluconeogenesis

48
Q

Effects of Increased Insulin in Tissues:

Adipose

A

INCREASE glucose transport (GLUT4)

INCREASE lipogenesis (making more)

DECREASE lipolysis (mobilization)

49
Q

Threshold carbohydrate level to achieve Ketosis:

A

< 20-50 CHO per day (<1 banana)

50
Q

What is Ketoacidosis

A

High-levels of ketones that changes PH of blood

51
Q

What is GLP-1?

A

Glucagon-like-peptide-1: Incretin hormone that stimulates insulin secretion or the “incretin effect”.

Like Ozempic. Produces more insulin, which increases rate of glucose uptake and metabolism.

52
Q

What is AMP Kinase?
(like opposite of MTOR)

A

Master intracellular energy sensor and metabolic “switch” regulator

–plays a pivotal role in energy homeostasis & cellular metabolism matching energy demand w/supply (ADP/ATP ratio):

INCREASES ATP PRODUCING PATHWAYS (decreases ATP using processes)

53
Q

Name 4 ATP consuming pathways:
**Inhibited by AMP Kinase

A
  1. Fatty Acid Synthesis
  2. Cholesterol Synthesis
  3. Glycogen Synthesis
  4. Protein Synthesis
54
Q

Name 3 ATP Producing Pathways:
**promoted by AMP Kinase

A
  1. Glycolysis
  2. Beta-oxidation (FA breakdown –> AcoA)
  3. Glucose uptake
55
Q

What does Glucagon do?

A

Stimulates glucose production to increase blood sugar levels (in low-glucose state).

Opposite function of Insulin

56
Q

What causes loss of water weight on ketogenic diet?

A

Depletion of Glycogen stores = loss of water weight, because glycogen traps a lot of water and maintains a lot of water bonds

57
Q

What are 3 fates of glucose after consumption?

A
  1. Storage (glycogen)
  2. Glycolysis (pyruvate –>TCA –>ATP)
  3. Fatty acid synthesis (FA)
58
Q

What are the stem cell origins for
-White
-Beige
-Brown
… adipocytes?

A

White + Beige = Mesenchymal stem cells

Brown = Muscle stem cells

59
Q

What is a GWAS?

A

Genome-Wide Association study

60
Q

What is FTO?

A

Fat Mass + Obesity gene:
-not causal.

A gene the distally encodes (via stimulation of IRX3 gene) for mesenchymal differentiation towards white adipocytes rather than beige adipocytes

61
Q

What gene/s influence mesenchymal stem cell differentiation?

A

FTO distally influences IRX3 gene, which impacts mysenchemal differentiation into more white adipocytes rather than beige.

62
Q

What is the difference between white, beige, and brown adipocytes?

A

White adipocytes have LOW mitochondrial density and largely are storage of excess glucose as fat (triglycerides).

Brown/beige adipocytes have HIGH mitochondrial density and are largely important for thermogenesis, and potentially endocrine functioning.

63
Q

What is Caloric Restriction?

A

Theory that restricting calories can extend life by 20-40% (even up to 50% longer) in rodents.

There is debate in the field currently about this effect in non-human primates

64
Q

What is a HAT? What does it do?

A

Histone Acetyl Transferases. (Epigenetic regulation of the genome)

–Catalyze the transfer of an acetyl group from Acetyl-CoA in nucleus.

HAT= ON = Open for transcription

65
Q

What is a HDAC? What does it do?

A

Histone De-acetylases.

–REMOVE an acetyl group.

HDAC = OFF = Closed for transcription

66
Q

What is a Histone?

A

They act as spools around which DNA winds to create structural units called nucleosomes.

So HATS and HDAC’s wind & unwind “spool” to expose certain genes to be transcribed

67
Q

What are 3 major categories that contribute to obesity?

A
  1. Psychology (will-power)
  2. Environment (lifestyle)
    –snack food industry
  3. Biology (genetics)
68
Q

What are the 3 v’s in the snack food industry?

A
  1. Variety (a lot of flavors)
  2. Value (cheap)
  3. Velocity (consume fast)
69
Q

Do adult humans have brown and white adipocytes?

A

All humans have ALL types of adipocytes.

70
Q

Describe Ob/Ob mouse vs db/db mouse vs +/+ mouse:

A

Ob/Ob: does NOT produce leptin
db/db: no leptin RECEPTOR
+/+ : Wild Type

71
Q

What is AMP Kinase?

A

Promotes ATP generating processes
-glycolysis
-glucose uptake

72
Q

What is MTOR?

A

Serine Threonine-Kinase that is the major ANABOLIC regulator (builds things. Uses ATP)

–active in the presence of glucose

-protein synthesis
-new DNA
- Lipid synthesis… etc. etc. etc.

73
Q

What is the relationship between ATP and AMP/ADP levels?

A

As ATP drops, AMP and ADP levels increase.

74
Q

Treating Obesity:

Type 1:
Type 2:

A

Type 1: Insulin

Type 2: Diet/Exercise/ Lifestyle changes
–also drugs like metformin (acts on hyperglycemia response)
-GLP1’s: increase Incretin effect/release of insulin… but might not respond completely effective if completely resistant

75
Q

What Amino Acids have branched chains?

A

Isoleucine
Leucine
Valine

76
Q

Physiology contributing to hyperglycemia:
2 Reasons

A
  1. Muscle + Adipocytes do NOT respond well to insulin (ie. don’t bring in glucose into cells effectively)
  2. Liver is pumping out more glucose b/c it is running gluconeogenesis
77
Q

What is the function of Acetyl-CoA in the Nucleus?

A

It is transferred onto Histone proteins and opens up DNA…
Epigenetic modification

78
Q

Difference between Glucose Tolerance Test and Insulin Tolerance Test:

A

GTT: Glucose given
–healthy: should see spike and then come back down to regular levels
–T2D: spike, and then stays high for a long time

ITT: Insulin given
–healthy: glucose levels drop, and then slowly moderate to normal over time
–T2D: glucose levels do not drop much at all

79
Q

Healthy Adipose:

A

Increased adipogenesis
Decreased cell volume
Increased insulin sensitivity
Decreased inflammation

**More cells but smaller

80
Q

Unhealthy Adipose:

A

Decreased adipogenesis
Increased hypertrophy
Decreased insulin sensitivity
Increased low-grade inflammation
Increased macrophages infiltration

**Bigger cells. Leads to lipotoxicity (ectopic lipid deposits, and insulin resistance. Type 2 diabetes and inflammation.)

81
Q

Physiology contributing to hyperglycemia in T2D:

A
  1. Muscle and adipocytes do NOT respond as well to insulin (don’t take glucose into the cell very effectively)
  2. Liver is running more gluconeogenesis which produces more glucose in the blood stream
82
Q

What does Metformin do?

A
  1. Increases mobilization of GLUT4 receptors, which increases uptake of glucose into the cell
  2. Decreases the rate of gluconeogenesis in the liver so that there is less glucose released into the bloodstream
83
Q

What is the insulin mechanism?

A

1st and 2nd wave insulin:
1st wave– is packaged into granules stored @ the plasma membrane, so the first spike in the chart is due to the rapid release of insulin

2nd wave: Sustained insulin response, due to reserve/secondary granules that need to move up to the plasma membrane to be release

84
Q

How does the Insulin Receptor work?

A

Insulin Receptor is a TYROSINE-KINASE receptor located throughout the body.
Upon presence of insulin Tyrosine-Kinase is AUTOPHOSPHORYLATED, which causes signaling events… and it allows tyrosine kinase to be recognized and acted upon.

ex: Glut4 is brought to the cell membrane

Biochemistry 510 (2 decks)

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