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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
What is the end product of glycolysis? 1 glucose=...
2 ATP, 2 pyruvate, 2 NADH
26
What enzyme is used in the anaerobic stage of glycolysis?
Lactate dehydrogenase (pyruvate -> lactate)
27
How is pyruvate used after aerobic glycolysis?
Pyruvate moves into matrix, binds with pyruvate dehydrogenase, and results in 2 Acetyl-CoA (links CAC)
28
How much ATP is produced aerobically with 1 glucose?
30-32 ATP
29
What causes the variation in the amount of ATP produced from glycolysis/CAC?
Which shuttle system transfers NADH into the mitochondria
30
Where does gluconeogenesis happen?
Kidney and Liver (80-90% in the liver)
31
Where do most of the precursors for gluconeogenesis come from?
Proteins via amino acids
32
What do gluconeogenesis and glycolysis share?
Reversible reactions enzymes of glycolysis
33
What are the irreversible reaction enzymes of gluconeogenesis?
Glucose-6-phosphatase, fructose 1,6-bisphosphatase, Pyruvate Carboxylase and PEP carboxykinase
34
What are the energy requirements of the irreversible reactions of gluconeogenesis?
2 ATP and 2 GTP (to convert pyruvate to PEP since this is very energetically unfavorable)
35
What pathway generates five-carbon sugars?
Pentose Phosphate Pathway (pentose shunt/ hexose monophosphate pathway)
36
What are the two segments of the pentose shunt? Which are reversible and irreversible?
Oxidation segment (irrevers) and carbon-shuffling reactions (reversible)
37
What are the oxidative reactions of the pentose shunt?
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+
38
How is glycogen used in the liver? Skeletal muscles?
Liver: used to correct low BG Skeletal: used as energy in the absence of usable glucose
39
What is the activating step of glycogenesis?
Glucose 1-P to UDP-Glucose via UDP-glucose pyrophosphorylase (using UTP->PPi)
40
What enzyme makes glycogen “branching”?
Branching Enzyme via cleavages between monomers (1,4 links) and reconnecting them, forming a-1,6 bond
41
What enzyme converts G6P to glucose?
Glucose 6-phosphatase (hydrolysis)
42
What responds to low blood sugar?
Liver (gluconeogenesis/glycogen breakdown)
43
What do muscle cells do with G6P?
Insert it into glycolysis
44
What can remove glucose a1-6 branch where phosphatase can’t?
Glucan transferase (glycogenolysis) and debranching enzyme
45
What is the ratio of G1P and free glucose in glycogen breakdown?
~90% glucose from glycogen breakdown is G1P
46
Where does fatty acid oxidation occur?
In the mitochondrial matrix
47
What does FA oxidation produce?
Acetyl-CoA, NADH, FADH2
48
What processes does FA oxidation depend on to get its intermediates?
CAC and Oxidative Phosphorylation (and ETC) for ATP
49
T or F: FA odxidation can happen without O2 presence
False
50
What protein binds to FA’s and transports them to cells via blood flow?
Albumin
51
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?
Acyl-CoA Synthase; carnitine shuttle; CoA-S side chain
52
What cannot cross the inner membrane of mitochondria? How are FA’s transported then?
CoA; transferring CoA off/back on FA chain with carnitine shuttle in the mitochondrial membrane
53
What are the four steps of FA oxidation?
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
How many acetyl CoA molecules are produced from a 16-carbon Fatty Acid?
8 Acetyl-CoA
55
How many ATP molecules can 8 Acetyl CoA molecules produce? 7 NADH? 7 FADH2?
80 17. 5 10. 5
56
Why is energy stored as fat?
It can result in more ATP per unit weight than glucose (almost 3 times as many ATP units)
57
Where are ketone bodies synthesized?
Liver
58
What are ketone bodies exported for?
Fuel source for peripheral tissues
59
What are the physiological ketone bodies?
Acetoacetate; beta-Hydroxybutarate
60
What are the non-physiological ketone bodies?
Acetone (from acetoacetate)= BAD
61
Where does ketogenesis happen?
Mitochondrial matrix in the liver
62
What are the four steps of ketogenesis?
1) Acetoacetyl-CoA Formation 2) HMG-CoA formation 3) Acetoacetate Formation 4) Ketone body interchange
63
What are the four enzymes in ketogenesis?
1) 3-Ketoacyl-CoA thiolase 2) HMG-CoA synthase 3) HMG-CoA Lyase (
64
What are the advantages of ketone bodies compared to FAs?
More water soluble, easier vascular transport and cell contact
65
How are ketone bodies used by the cells to produce energy?
Generates Acetyl-CoA via breakdown and introduces it into CAC and ETC
66
1 ketone body = _____ Acetyl-CoA
2
67
In what cell types does FA biosynthesis occur? Where in the cell?
Mainly LIVER, lesser so adipocytes Cytoplasm
68
What is the key regulatory enzyme of FA biosynth?
Acetyl-CoA Carboxylase (to make Malate CoA)
69
What kind of effector is ADP/AMP on PFK1?
Positive effector allosterically bound
70
What kind of effector is ATP on PFK1?
Negative effector allosterically bound
71
How can consistently high ATP levels in the liver affect PFK1? What is the molecule that bypasses this issue?
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
What hormone is released in hypoglycemic conditions? Hyperglycemia?
Glucagon; Insulin
73
What spurs release of F2-6BP in the liver? Why?
Insulin; to increase rate of glycolysis and slow rate of glycogenesis
74
What enzymes participate in covalent modification via phosphorylation?
Phosphatase and Kinases
75
What is a free form protein? (In relation to covalent modifications via phosphorylation)
The one with the -OH group unbound by Pi
76
What is the effect of insulin on intracellular phosphatase?
Insulin activates them during hyperglycemia to activate glycogenesis
77
What is the effect of glucagon on intracellular kinases?
Activates kinases, phosphorylates enzymes, glycogenesis activated
78
How does genetic regulation differ from allosteric or covalent regulation?
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
What does is stimulated in the liver in well-fed conditions? What stimulates this?
Glycolysis, glucogenesis, Pentose Shunt, FA Synth, Cholesterol synth, Lipogenesis Insulin
80
What is stimulated in adipose cells when the body is well-fed? What stimulates this?
Glycolysis, Pent Shunt, FA Synth, Cholesterol Synth, Lipogenesis Insulin
81
What is stimulated in muscle cells when the body is well-fed? What stimulates this?
Glycogenesis (insulin)
82
Why is glycolysis activated/not activated in myocytes and liver/adipose cells under hyperglycemic conditions?
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
What general type of hormone is insulin? Release of this molecule usually results in anabolism or catabolism?
Insulin is an anabolic hormone Release favors the biosynthetic pathways to increase energy reserves (glycogen, ATP production via glycolysis, and FA Synthesis)
84
What is stimulated in adipocytes in a fasting state? What stimulates this?
Lipolysis to mobilize TAG reserves (MOSTLY EXPORTED) Glucagon
85
What is stimulated in hepatocytes in a fasting state? What stimulates this?
Glycogenolysis, gluconeogenesis, B-oxidation, ketogenesis Glucagon
86
What is the liver’s primary responsibility under fasting conditions?
Maintain glucose homeostasis
87
What is the primary source of glucose under fasting conditions in the liver?
Breakdown of glycogen If no glycogen, gluconeogenesis takes over (not as good/fast)
88
What is the most abundant source of precursors for gluconeogenesis?
Proteins (amino acids) from muscle fibers
89
What is the liver’s primary source of glucose production in fasting? What is the primary energy source during fasting?
Glycogenolysis (and gluconeogenesis if this isnt available) Fatty Acid Oxidation for energy (from adipose TAGs)
90
What is the role of Acetyl-CoA in fasting conditions?
1) generate only as much ATP as NEEDED for the body | 2) use all excess A-CoA to generate ketones
91
What is stimulated in myocytes in a fasting state? What stimulates this?
Glycogenolysis ONLY VIA epinepherine and AMP/Ca2+ Glucagon does not mobilize glycogen in muscle cells
92
What is the main energy source for muscle cells in fasting state?
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
What hormones are counterregulatory to insulin? What are their relationship?
Glucagon, epinephrine, cortisol, and growth hormone They work together collectively against insulin action
94
Why is it important to have a variety of hormones to collectively work against insulin?
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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