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Foundations- Block 1 > Biochem: Dr. Blazyk Lectures > Flashcards

Biochem: Dr. Blazyk Lectures Flashcards

1
Q

What are the monomers of starch, sucrose, and lactose?

A

Glucose; glucose + fructose; glucose+galactose

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2
Q

What are most fats stored as?

A

Triacylglycerols (TAG)

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3
Q

What two macronutrients have essential components?

A

Fat and protein

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4
Q

What percentage of each macronutrient compose the energy reserves in the body?

A

Fat=80 (triglycerides in adipose), protein=15 (contractile proteins), carbs=<1% (glycogen)

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5
Q

What is the process of O2 reacting with macros to produce water, carbon dioxide, and ammonium (and energy)?

A

Oxidation reactions

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6
Q

How much energy is released as heat from oxidation reactions in cells? How much is conserved?

A

60% lost as heat, 40% conserved to produce energy and store energy

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7
Q

What are the three main precursors for anabolic pathways?

A

UDP-glucose, fatty acyl-CoA, Aminoacyl-tRNA

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8
Q

What macronutrients contribute to the citric acid cycle?

A

All three!

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9
Q

What are the intermediates for the Kreb’s cycle in order?

A

Acetyl-CoA, Citrate, Isocitrate, alpha-Ketoglutarate, Succinyl-CoA, Succinate, Fumarate, Malate, OAA

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10
Q

What are the enzymes of the CAC in order?

A

Citrate synthase, Aconitase, Isocitrate dehydrogenase, a-Ketoglutarate dehydrogenase, Succinyl-CoA synthetase, Succinate Dehydrogenase, Malate Dehydrogenase

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11
Q

What are the end products of the TCA Cycle?

A

2 CO2, 3 NADH, 1 FADH2, 1 GTP

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12
Q

Where are the products of the CAC used? Where is the CAC performed?

A

Oxidative Phosphorylation; inside the mitochondria inner membrane

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13
Q

If the ETC stops, what happens to the CAC? Why?

A

It stops; electron carriers (NADH/FADH2) stop being oxidized and cannot accept hydrogen/electrons from the CAC and the intermediate steps stop

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14
Q

What is the chain of electron movement in the ETC?

A

Com 1, Com 2, CoQ, Com 3, Cytochrome C, Complex 4

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15
Q

What complexes in the ETC pumps proteins into the cytoplasm to create a proton gradient?

A

Complex 1,2,4

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16
Q

What is complex 5? How does it work?

A

ATP Synthase; energy from proton gradient (4 protons) creates a conformational change and energy to phosphorylate ADP with Pi

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17
Q

What groups are involved in electron transport within the cytochromes?

A

Heme groups (Fe2+ to Fe3+)

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18
Q

What is the difference between heme of hemoglobin and cytochromes?

A

Iron stays in +2 state in hemoglobin and transfers between +2 and +3 in cytochromes

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19
Q

How many ATP is produced from 1 acetyl-CoA?

A

~10 ATP (3.5 from NADH, 1.5 from FADH2, 1 from GTP)

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20
Q

Where does glycolysis occur?

A

Cytoplasm

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21
Q

What does glycolysis generally produce?

A

Important intermediates for aerobic production

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22
Q

How can glycolysis produce ATP, anaerobic or aerobic?

A

Both

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23
Q

How many irreversible reactions and reversible reactions occur in glycolysis? Which regulate the entire process?

A

3 irreversible, 7 reversible;

Irreversible reactions bottleneck glycolysis

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24
Q

what are the three enzymes of the irreversible glycolysis?

A

Hexokinase, phosphofructo kinase 1, pyruvate kinase

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25
Q

What is the end product of glycolysis? 1 glucose=…

A

2 ATP, 2 pyruvate, 2 NADH

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26
Q

What enzyme is used in the anaerobic stage of glycolysis?

A

Lactate dehydrogenase (pyruvate -> lactate)

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27
Q

How is pyruvate used after aerobic glycolysis?

A

Pyruvate moves into matrix, binds with pyruvate dehydrogenase, and results in 2 Acetyl-CoA (links CAC)

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28
Q

How much ATP is produced aerobically with 1 glucose?

A

30-32 ATP

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29
Q

What causes the variation in the amount of ATP produced from glycolysis/CAC?

A

Which shuttle system transfers NADH into the mitochondria

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30
Q

Where does gluconeogenesis happen?

A

Kidney and Liver (80-90% in the liver)

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31
Q

Where do most of the precursors for gluconeogenesis come from?

A

Proteins via amino acids

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32
Q

What do gluconeogenesis and glycolysis share?

A

Reversible reactions enzymes of glycolysis

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33
Q

What are the irreversible reaction enzymes of gluconeogenesis?

A

Glucose-6-phosphatase, fructose 1,6-bisphosphatase, Pyruvate Carboxylase and PEP carboxykinase

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34
Q

What are the energy requirements of the irreversible reactions of gluconeogenesis?

A

2 ATP and 2 GTP (to convert pyruvate to PEP since this is very energetically unfavorable)

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35
Q

What pathway generates five-carbon sugars?

A

Pentose Phosphate Pathway (pentose shunt/ hexose monophosphate pathway)

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36
Q

What are the two segments of the pentose shunt? Which are reversible and irreversible?

A

Oxidation segment (irrevers) and carbon-shuffling reactions (reversible)

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37
Q

What are the oxidative reactions of the pentose shunt?

A

G-6-P to 6-P Gluconoacetone (via Glucose 6-P Dehydrogenase)

6-P gluconate to ribulose 5-P (via 6-P Gluconate Dehydrogenase)

Both produce NADH + one other H+

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38
Q

How is glycogen used in the liver? Skeletal muscles?

A

Liver: used to correct low BG

Skeletal: used as energy in the absence of usable glucose

39
Q

What is the activating step of glycogenesis?

A

Glucose 1-P to UDP-Glucose via UDP-glucose pyrophosphorylase (using UTP->PPi)

40
Q

What enzyme makes glycogen “branching”?

A

Branching Enzyme via cleavages between monomers (1,4 links) and reconnecting them, forming a-1,6 bond

41
Q

What enzyme converts G6P to glucose?

A

Glucose 6-phosphatase (hydrolysis)

42
Q

What responds to low blood sugar?

A

Liver (gluconeogenesis/glycogen breakdown)

43
Q

What do muscle cells do with G6P?

A

Insert it into glycolysis

44
Q

What can remove glucose a1-6 branch where phosphatase can’t?

A

Glucan transferase (glycogenolysis) and debranching enzyme

45
Q

What is the ratio of G1P and free glucose in glycogen breakdown?

A

~90% glucose from glycogen breakdown is G1P

46
Q

Where does fatty acid oxidation occur?

A

In the mitochondrial matrix

47
Q

What does FA oxidation produce?

A

Acetyl-CoA, NADH, FADH2

48
Q

What processes does FA oxidation depend on to get its intermediates?

A

CAC and Oxidative Phosphorylation (and ETC) for ATP

49
Q

T or F: FA odxidation can happen without O2 presence

A

False

50
Q

What protein binds to FA’s and transports them to cells via blood flow?

A

Albumin

51
Q

What reacts with a FA in the cytosol to allow it to pass into the mitochondrial matrix? What protein transports it across? What side chain is absolutely necessary?

A

Acyl-CoA Synthase; carnitine shuttle; CoA-S side chain

52
Q

What cannot cross the inner membrane of mitochondria? How are FA’s transported then?

A

CoA; transferring CoA off/back on FA chain with carnitine shuttle in the mitochondrial membrane

53
Q

What are the four steps of FA oxidation?

A

1) First dehydrogenation- AcylCoA Dehydrogen.
2) Hydration- Enoyl-CoA Hydratase
3) second dehydrogenation- 3-hydroxyacyl-CoA DH
4) Formation of Acetyl-CoA - Ketoacyl-CoA Thiolase

54
Q

How many acetyl CoA molecules are produced from a 16-carbon Fatty Acid?

A

8 Acetyl-CoA

55
Q

How many ATP molecules can 8 Acetyl CoA molecules produce? 7 NADH? 7 FADH2?

A

80

  1. 5
  2. 5
56
Q

Why is energy stored as fat?

A

It can result in more ATP per unit weight than glucose (almost 3 times as many ATP units)

57
Q

Where are ketone bodies synthesized?

A

Liver

58
Q

What are ketone bodies exported for?

A

Fuel source for peripheral tissues

59
Q

What are the physiological ketone bodies?

A

Acetoacetate; beta-Hydroxybutarate

60
Q

What are the non-physiological ketone bodies?

A

Acetone (from acetoacetate)= BAD

61
Q

Where does ketogenesis happen?

A

Mitochondrial matrix in the liver

62
Q

What are the four steps of ketogenesis?

A

1) Acetoacetyl-CoA Formation
2) HMG-CoA formation
3) Acetoacetate Formation
4) Ketone body interchange

63
Q

What are the four enzymes in ketogenesis?

A

1) 3-Ketoacyl-CoA thiolase
2) HMG-CoA synthase
3) HMG-CoA Lyase (

64
Q

What are the advantages of ketone bodies compared to FAs?

A

More water soluble, easier vascular transport and cell contact

65
Q

How are ketone bodies used by the cells to produce energy?

A

Generates Acetyl-CoA via breakdown and introduces it into CAC and ETC

66
Q

1 ketone body = _____ Acetyl-CoA

A

2

67
Q

In what cell types does FA biosynthesis occur? Where in the cell?

A

Mainly LIVER, lesser so adipocytes

Cytoplasm

68
Q

What is the key regulatory enzyme of FA biosynth?

A

Acetyl-CoA Carboxylase (to make Malate CoA)

69
Q

What kind of effector is ADP/AMP on PFK1?

A

Positive effector allosterically bound

70
Q

What kind of effector is ATP on PFK1?

A

Negative effector allosterically bound

71
Q

How can consistently high ATP levels in the liver affect PFK1? What is the molecule that bypasses this issue?

A

It can keep glycolysis from happening, which can result in both cell and systemic death

F2-6BP binds at the same time, but acts as a positive effector that is more potent than ATP’s action

72
Q

What hormone is released in hypoglycemic conditions? Hyperglycemia?

A

Glucagon; Insulin

73
Q

What spurs release of F2-6BP in the liver? Why?

A

Insulin; to increase rate of glycolysis and slow rate of glycogenesis

74
Q

What enzymes participate in covalent modification via phosphorylation?

A

Phosphatase and Kinases

75
Q

What is a free form protein? (In relation to covalent modifications via phosphorylation)

A

The one with the -OH group unbound by Pi

76
Q

What is the effect of insulin on intracellular phosphatase?

A

Insulin activates them during hyperglycemia to activate glycogenesis

77
Q

What is the effect of glucagon on intracellular kinases?

A

Activates kinases, phosphorylates enzymes, glycogenesis activated

78
Q

How does genetic regulation differ from allosteric or covalent regulation?

A

It increases the physical number of enzymes active via transcription, and its effect is larger; MUCH slower than covalent/allosteric (hours to days vs. seconds to minutes)

(Insulin incr glycolysis enzyme production, glucagon is vise versa on glycogenesis and glycogenolysis)

79
Q

What does is stimulated in the liver in well-fed conditions? What stimulates this?

A

Glycolysis, glucogenesis, Pentose Shunt, FA Synth, Cholesterol synth, Lipogenesis

Insulin

80
Q

What is stimulated in adipose cells when the body is well-fed? What stimulates this?

A

Glycolysis, Pent Shunt, FA Synth, Cholesterol Synth, Lipogenesis

Insulin

81
Q

What is stimulated in muscle cells when the body is well-fed? What stimulates this?

A

Glycogenesis (insulin)

82
Q

Why is glycolysis activated/not activated in myocytes and liver/adipose cells under hyperglycemic conditions?

A

Muscle cells require glycogen reserves to be broken down when transferring from an inactive to an active state.

Liver/adipose use excess blood glucose for breakdown and energy production, whereas the muscle cells are more interested in storing the glucose for later use

83
Q

What general type of hormone is insulin? Release of this molecule usually results in anabolism or catabolism?

A

Insulin is an anabolic hormone

Release favors the biosynthetic pathways to increase energy reserves (glycogen, ATP production via glycolysis, and FA Synthesis)

84
Q

What is stimulated in adipocytes in a fasting state? What stimulates this?

A

Lipolysis to mobilize TAG reserves (MOSTLY EXPORTED)

Glucagon

85
Q

What is stimulated in hepatocytes in a fasting state? What stimulates this?

A

Glycogenolysis, gluconeogenesis, B-oxidation, ketogenesis

Glucagon

86
Q

What is the liver’s primary responsibility under fasting conditions?

A

Maintain glucose homeostasis

87
Q

What is the primary source of glucose under fasting conditions in the liver?

A

Breakdown of glycogen

If no glycogen, gluconeogenesis takes over (not as good/fast)

88
Q

What is the most abundant source of precursors for gluconeogenesis?

A

Proteins (amino acids) from muscle fibers

89
Q

What is the liver’s primary source of glucose production in fasting? What is the primary energy source during fasting?

A

Glycogenolysis (and gluconeogenesis if this isnt available)

Fatty Acid Oxidation for energy (from adipose TAGs)

90
Q

What is the role of Acetyl-CoA in fasting conditions?

A

1) generate only as much ATP as NEEDED for the body

2) use all excess A-CoA to generate ketones

91
Q

What is stimulated in myocytes in a fasting state? What stimulates this?

A

Glycogenolysis ONLY VIA epinepherine and AMP/Ca2+

Glucagon does not mobilize glycogen in muscle cells

92
Q

What is the main energy source for muscle cells in fasting state?

A

Fatty acids from adipocytes and ketones from the liver***

***REQUIRES sufficient oxygen and high mitochondrial density since ONLY aerobic ATP production can be used

93
Q

What hormones are counterregulatory to insulin? What are their relationship?

A

Glucagon, epinephrine, cortisol, and growth hormone

They work together collectively against insulin action

94
Q

Why is it important to have a variety of hormones to collectively work against insulin?

A

Muscle cells cannot use glucagon, so they need other chemical messengers to properly adapt to fasting statesq

Foundations- Block 1 (17 decks)

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