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Biochem > Exam 3 - Learning Objectives > Flashcards

Exam 3 - Learning Objectives Flashcards

1
Q

(22/23) what are the two parts of photosynthesis?

A

light and dark reactions

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2
Q

(22/23) what are light reactions?

A

Energy from light is used to boost electrons from a low energy state to a high energy state

These electrons are used to reduce NADP+ to NADPH (for biosynthesis)

The electrons through a ETC are also used to generate a proton-motive force which drives the synthesis of ATP

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3
Q

(22/23) what are dark reactions?

A

Understand that the Calvin cycle takes place in the stroma of chloroplasts

Carbon dioxide gas is trapped as an organic molecule, 3-phosphoglycerate

3-phosphoglycerate undergoes reduction reactions (using NADPH and ATP) to synthesize hexose sugars

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4
Q

(24) Understand the structure of glycogen and why, relative to stored fatty acids, glucose is a more versatile energy source

A

Highly branched homopolymer of glucose (a-14 with branching a1,6 every 12 units or so)

It can be used in glycolysis which is anaerobic

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5
Q

(24) Consider the distinction between muscle and the liver in terms of glycogen synthesis and degradation (Energy needs of each organ)

A

The liver breaks down (degrades) glycogen to glucose during fasting states to regulate blood glucose levels

The muscle stores glycogen (synthesis) then breaks it based on release of glucagon and epinephrine

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6
Q

(24) Understand what the enzymes glycogen phosphorylase, transferase and a-1,6 glucosidase do.

A
  • *Glycogen phosphorylase** – cleaves a-14 bonds
  • *Transferase** – takes three glucose molecules off of the a16 branch and puts them on the main a14 chain
  • *A-16 glucosidase** cuts the branch chain off
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7
Q

(24) Know what organ and why this organ has the enzyme glucose-6-phosphotase

A

The liver has glucose-6-phosphotase because it can release free glucose into the blood to be used by the brain
The livers role is to maintain blood-glucose levels

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8
Q

(24) Understand the regulation of glycogen phosphorylase in the liver versus muscle

A

Glucose molecules are negative allosteric regulators in the liver
AMP and glucose-6-phosphate are allosteric regulators in the muscles
Liver phosphorylase b is not sensitive to glucose
Energy charge of liver is constant
Glycogen phosphorylase has to be phosphorylated by PKA as well as have Ca binding (epinephrine)
Mainly phosphorylated (active) in liver
Mainly dephosphorylated in the muscle until hormone induces signal transduction
Muscle fibers
Slow twitch – Type 1: endurance; low glycogen phosphorylase
Fast twitch - Type IIb: Sprint; increased glycolysis
Intermediate – Type IIa: Trainable

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9
Q

(25)Understand the components of glycogen synthesis and the use of UDP-glucose as a driver of this reaction

A

UDP is the glucose donor in glycogen synthesis
Need UDP to make the glucose bond reactive enough to cleave phosphate bond
Hydrolysis of pyrophosphate drives reaction to create more UDP
Glucose 1 phosphate combining with UTP is a high energy phosphoryl transfer

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10
Q

(25) Know the roles of glycogen synthase and the branching enzyme in the construction of glycogen

A

Glycogen synthase catalyzes the transfer of glucose from UDP-glucose to the growing chain
Transfers to the C4 terminal residue of the glycogen chain (a14 bond)
Primer synthesized by glycogenin
Branching enzyme takes 7 glucoses off chain and forms a 16 bond

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11
Q

(25) Understand how glycogen synthesis and glycogen breakdown are reciprocally regulated

A
  • *- Glycogen synthase is inactive when in phosphorylated b form**
  • Glycogen synthase is active when in unphosphorylated a form
  • B goes to A through the binding of glucose 6-phosphate
  • *- Glucose phosphatase is active when phosphorylated**
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12
Q

(25) Understand the roles of insulin, glucagon, and epinephrine in glycogen metabolism

A
  • Insulin: activates synthesis, stops degradation
    o Inhibits GSK which phosphorylates glycogen synthase (making it inactive)
  • Glucagon and epinephrine: Activates degradation; stops synthesis
    o Phosphorylation of synthase by PKA inhibits synthesis
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13
Q

(25) Be aware of the differences in glycogen metabolism between the liver and the muscle

A
  • PP1 activates synthesis
    - Muscle
    o PKA phosphorylates phosphatase I
    o Phosphorylation of glycogen binding region dissociates catalytic subunit and substrate
    o Phosphorylation of inhibitor inactivates PP1
    - Liver
    o Glucose binds to glycogen phosphorylase a (inhibits) makes transfer to b
    o B does not bind to PP1leading to dissociation and activation
    o PP1 dephosphorylates phosphatase (inactivates) and synthase (activates)
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14
Q

(25) Understand the metabolic fates of individuals suffering from Type I and Type II diabetes

A
  • Excessive glucose is excreted in the urine
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15
Q

(26) Understand that the pentose phosphate pathway consists of two phases

A
  • The oxidative generation of NADPH
    o Uses biosynthetic pathways
    o NADPH is generated when glucose 6-phosphate is oxidized to ribulose 5-phosphate
  • The non-oxidative interconversion of sugars
    o Ribulose 5-phosphate is then converted into ribose 5-phosphate which is a precursor to RNA, DNA, ATP, NADH, FAD, and coenzyme A
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16
Q

(26) Be familiar with the four modes of the pentose phosphate pathway

A
  • Ribose-5-phosphate needs exceed the needs for NADPH
    o Rapidly dividing cells require precursors for DNA and RNA
  • Ribose5-phosphate and NADPH needs are balanced
    o Biosynthetic reducing power and nucleotide precursors are needed
  • More NADPH is needed then ribose-5-phosphate
    o NADPH is needed for fatty acids and cholesterol synthesis in the liver
  • NADPH and ribose-5-phosphate are both required
    o Reducing power and ATP (through pyruvate) are both needed
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17
Q

(27) Understand the nature of lipolysis

A
  • Degradation of TAG to release fatty acids and glycerol into the blood for transport to energy-requiring tissues
  • Activation of the fatty acids and transport into the mt for oxidation
  • Degradation of fatty acids to acetyl CoA for processing by the TCA cycle
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18
Q

(27)Know the roles of glucagon and epinephrine in the catabolism of TAGs

A
  • Stimulate lipid breakdown through 7G proteins
  • Perilipin and is phosphorylated by PKA; ATGL activated by coactivator (DAG)
  • Perilipin phosphorylates HS lipase (MAG)
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19
Q

(27) Understand the fates of free fatty acids and glycerol in lipid metabolism

A

- Free fatty acids
o Fatty acid oxidation
§ Fatty acid activation
§ Shuttled to mt
§ Acyl moiety degraded two carbons at a time
o Acetyl CoA
o CAC
o CO2 and water
- Glycerol
o Glycolysis
§ Pyruvate
o Gluconeogensis
§ Glucose

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20
Q

(27) Be familiar with the role carnitine plays in the transport of fatty acids

A
  • Allows transport into the mt
  • Translocase
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21
Q

(27) Understand the steps of B-oxidation

A
  • Oxidation (FAD)
  • Hydration (H2O)
  • Oxidation (NAD+)
  • Thiolysis (CoA)
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22
Q

(27) Understand the additional steps needed for the degradation of unsaturated and odd numbered fatty acids

A
  • Odd numbers require just the isomerase
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23
Q

(27) What is the product of the final round of odd-chain fatty acid degradation?

A
  • Propionyl CoA
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24
Q

(27) What are the three forms of ketone bodies?

A
  • Acetoacetate,
  • acetone
    o Formed spontaneous
  • 3-hydroxybutyrate
    o Reduction of acetoacetate
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25
Q

(27) Understand liver ketogenesis

A
  • Fatty acids fed into TCA cycle if oxaloacetate is present
  • If no oxaloacetate, then they become ketone bodies
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26
Q

(27) Have an appreciation for why animals cannot convert fatty acids into glucose

A
  • Two carbons enter when acetyl CoA condenses with oxaloacetate, but two carbons are lost when two molecules of CO2 are given off
27
Q

(27) Understand the role of insulin in fatty acid metabolism

A
  • Insulin curtails fatty acid metabolism in adipose tissues. Absense causes fatty acid release producing large amounts of acetyl CoA
28
Q

(27) What mechanisms are faulty in diabetics?

A
  • Glucose cannot enter cells?
  • All energy has to be derived from fatty acids, leading to production of acetyl CoA
29
Q

(27) Understand how the body handles starvation

A
  • Protein degradation (if let continue leads to tissue failure)
  • Ketone bodies after several days
  • Ketone bodies are the largest source of fuel for the body
30
Q

(28) Understand the three stages of fatty acid synthesis

A
  • Transfer of acetyl CoA out of the mt into the cytoplasm
  • Activation of acetyl CoA to form malonyl CoA
  • Repetitive addition and reduction of two carbon units
31
Q

(28) Recall the roles citrate and oxaloacetate play in glycolysis, gluconeogenesis, and fatty acid synthesis

A
  • Citrate: Oxaloacetate + Acetyl CoA
    o TCA
    o Reverse TCA for FA synthesis
    § Fa synthesis: NADH to NADPH
  • Oxaloacetate:
32
Q

(28) Understand the different sources of NADPH. What pathways generate NADPH?

A
  • Pentose-phosphate pathway
  • Fatty acid synthesis
33
Q

(28) What reaction does acetyl CoA carboxylase 1 catalyze? What step is this considered in fatty acid synthesis?

A
  • Acetyl CoA to malonyl CoA (step 2??)
34
Q

(28) Fatty acid synthesis is composed of a series of reactions catalyzed by the enzyme complex fatty acid synthase. Know the general steps that occur.

A
  • Condensation
  • Reduction
  • Dehydration
  • Reduction
35
Q

(28) What is the end product of these reactions?

A
  • Reduced product that stores energy in electrons
  • Palmitate
36
Q

(28) How does the cell produce fatty acid chains longer than C16? And unsaturated fatty acids?

A
  • By proteins attached to the ER
  • Extend palmitate by adding two carbons using malonyl CoA
37
Q

(28) Understand what eicosanoids are and how they act.

A
  • Derived from polyunsaturated fatty acids
  • 20 carbon long signal molecules
  • Local mediators (short lived)
  • Bind to membrane receptors
38
Q

(28) What are the factors that regulate acetyl CoA carboxylase I?

A
  • Phosphorylation = off
  • Allosterically stimulated by citrate
  • Insulin stimulates
  • Glucagon and epinephrine inhibit
39
Q

(28) Understand the cellular consequences of heavy ethanol consumption. (Has to do with NADH)

A
  • Increase in NADH inhibits, gluconeogenesis and fatty acid oxidation. Inhibits TCA due to the enzymes isomerase dehydrogenase and a-ketoglutarate dehydrogenase
40
Q

(29) Have a basic understanding of how TAGs are formed

A
  • Synthesized from a phosphatidate and acetyl CoA
  • Triacylglycerol synthase is bound to the ER and synthesizes TAG in two steps
41
Q

(29) What is phosphatidylcholine? What does it do?

A
  • Most common phospholipid in mammals
  • Membrane lipid? 50% of membrane
  • Synthesized through two paths
42
Q

(29) What role do sphingolipids play in the cell?

A
  • Membrane lipids
43
Q

(29) Understand the causes of respiratory distress syndrome and Tay-Sacs disease

A
  • Respiratory distress is caused by failure in the biosynthesis of dipalmitoyl phosphatidylcholine
  • Tay-Sacs is a failure of lipid degradation, specifically, gangliosides, leading to neuronal swelling
44
Q

(29) Understand how cholesterol synthesis is regulated

A
  • Liver is the major site of synthesis
  • HMG CoA reductase controls the synthesis and catalyzes the synthesis of mevalonate
  • First step is committed (acetyl CoA + Acetoactyl CoA )
  • Reductase regulated by gene expression, rate of mRNA translation, degradation of the protein, and phosphorylation which decreases activity
45
Q

(29) Understand in a general sense how cholesterol and TAGs are transported throughout the body

A
  • Lipoproteins
46
Q

(29) Understand the different form of lipoproteins

A
  • Pro-atherogenic properties – increases their risk of atherosclerosis (buildup of plack)
  • Greater the protien and lower fat = high density
  • Chylomicrons and their remnants
    o Exogenous lipoprotein pathway
    § Dietary fats to the peripheral body
  • Very low-density lipoproteins
    o Endogenous lipoprotein pathway
  • Low-density lipoproteins
    o Major cholesterol carrier
    o End of VLDL process (uptake by liver or placks)
  • High-density lipoproteins (anti-atherogenic)
    o Good cholesterol (anti-inflammatory)
    o A1 and LCAT
47
Q

(29) What are the consequences of aberrant LDL receptors

A
  • Increase risk of atherosclerosis and heart attack
48
Q

(29) What is the evidence for the protective effects of HDLs

A
  • They can take up the cholesterol and return it to the liver
49
Q

(29) Understand the functions of the various steroid hormones

A
  • Progestogens – prepares lining or uterus (essential for pregnancy)
  • Androgens – male secondary sex characteristics
  • Estrogens - female secondary sex characteristics
  • Glucocorticoids – promote gluconeogenesis and the formation of glycogen, enhance the degradation of fat and protein, and inhibit the inflammatory response
  • Mineralocorticoids – Regulate salt balance, volume, and pressure of blood
50
Q

(30) Understand how aa are degraded

A
  • Removal of amino group and conservation of the carbon skeleton
51
Q

(30) Be aware of the fact that liver cannot deaminate branched chain aa. What organ utilizes these aa as an energy source?

A
  • Muscle uses branched-chains aa as fuel
52
Q

(30) Understand how nitrogen is transported from muscle to liver. What are the two principle transport mechanisms?

A
  • Glucose-alanine cycle
    o Glutamate to alanine
  • Urea cycle
53
Q

(30) Be familiar with the steps of the urea cycle

A
  • Cabamoyal phosphate synthase
    o Bicarb to Carbomoyal phosphate – requires N-acetyl glutamate to be active
    o Ornithine transcarbomoylase catalzyes transfer of carbomoyal group
    o Arginosuccinal synthase (apartate +Citrulline) to arginosuccinate
    o Arginosuccinase catalyzes (arginosuccinate to arginine + fumarate)
    o Arginase catalyzes (arginine to ornithine and urea)
54
Q

(30) Understand the difference between ketogenic aa and glucogenic aa

A
  • Ketogenic aa
    o Produce Acetyl CoA (for the TCA) or fats
    o Only leucine and lysine are solely ketogenic
  • Glucogenic aa
    o Produce glucose
55
Q

(31) Understand what nitrogen fixation is. Know how this is done

A
  • Nitrogen gas to ammonia to glutamate and other aa
  • Nitrogen-fixing bacteria
  • The reductase provides high-energy electrons in the form of ferredoxin for reducing
  • The nitrogenase uses the electrons to reduce NH2 to NH3 (in water will use proton and go to NH4)
56
Q

(31) Understand how nitrogen is incorporated into building blocks of aa

A
  • Glutamate dehydrogenase ammonia and a-ketoglutarate to generate glutamate
57
Q

(31) Where do carbon skeletons come from to generate the aa

A
  • Intermediates of the glycolytic pathway, TCA, and the pentose phosphate pathway
58
Q

(31) Understand the biosynthetic families of aa

A

- TCA
o Oxaloacetate
§ Aspartate goes to Asparagine, M, Threonine, and Lysine
· Threonine can go to isoleucine
o A-ketoglutarate
§ Glutamate goes to glutamine, pro, and arginine
- Glycolysis
o Pyruvate
§ Goes to alanine, valine and leucine
o 3-phosphoglycerate
§ Serine goes to Cystine and glycine
- Pentose phosphate pathway
o Ribose 5 phosphate
§ Goes to histidine
- Glycolysis and pentose phosphate pathway
o Phosphoenolpyruvate with erythrose 4 phosphate
§ Goes to Phenylalanine, tyrosine and W
§ Phenylalanine can also go to tyrosine

59
Q

(31) Understand the difference between essential and non-essential aa

A
  • Essential – cannot synthesize ourselves / need to get in diet
60
Q

(31) What do the co-factors tetrahydrofolate and S-adenosyl methionine (SAM) do?

A
  • Activated methyl donor
  • Tetrahydrofolate is a has a lower transfer potential so is used less
61
Q

(32) Understand the difference between the de novo and salvage pathways of nucleotide biosynthesis

A
  • De novo: Nucleotides synthesized from simple precursors (requires ATP and CO2 as well as activated ribose and aa)
  • Salvage pathway: preformed bases are recovered and attached to an activated ribose (activated ribose and base)
62
Q

(32) How are ribonucleotides converted into deoxyribonucleotides?

A
  • The 2’ hydroxyl group of ribose is replaced by a h atom in a reaction catalyzed by ribonucleotide reductase which acts on all four ribonucleotides
63
Q

(32) Focus on figures 32.2, .3, .4, .8, and .11

A

- 32.2: - De novo versus salvage
- 32.3: De novo pathway for pyrimidine nucleotide synthesis
o The C2 and N3 atoms in the pyrimidine ring come from carbamoyl phosphate, whereas the other atoms of the ring come from aspartate
o Bicarbonate + NH3 with 2 ATP makes carbamoyl phosphate
o Carbamoyl phosphate and Aspartate make pyrimidine ring
o Pyrimidine ring with PRPP (a ribose phosphate) make UTP to CTP to RNA
o UTP to TTP to dCTP to DNA
- 32.4: PRPP to 5-Phosphoribosyl-1-amine
o Use ammonia, Glu, Gln and removes two P
- 32.4: De novo pathway for purine nucleotide synthesis
o Requires 9 additional steps from pyrimidine synthesis
o Purine ring to IMP to GTP to RNA (GTP to dGTP to DNA)
o IMP to ATP to dATP
- 32.8
o RNA bases with ribonucleotide reductase go to base diphosphate then further processing yields dNTP
- 33.11b
o ATP positive regulator of ribonucleotide reductase
o dATP is neg regulator of ribonucleotide reductase
o Regulation of substrate specificity
§ dGTP pos reg of RR to dADP
§ TTP pos reg of RR to dGDP
· Neg reg of RR to dUDP and dCDP
§ ATP pos reg of dUDP and dCDP

Biochem (12 decks)

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