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Biochem 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What does ADH stand for?

MEOS?

A

Alcohol Dehydrogenase

Microsomal Ethanol Oxidizing System

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2
Q

How many kcal/gram is Alcohol?

What are its other two names?

A

7 kcal/gram

Ethyl Alcohol or Ethanol

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3
Q

Where is ethanol readily absorbed throughout?

What happens to it in the blood stream?

Where is it primarily oxidatively degraded at?

A

GI tract

Unaltered in the bloodstream

Liver

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4
Q

What does the liver first convert ethanol into?

Then what?

What does both steps produce?

A

Acetaldehyde

Acetate

NADH

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5
Q

What are the three enzyme systems of ethanol oxidation?

A

ADH

MEOS (aka Cyto P-450 system)

Catalase

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6
Q

Where does the Alcohol Dehydrogenase pathway occur?

What does the dehydrogenase require?

What is the Km for ethanol?

When is enzyme saturated and when can ADH not oxidize ethanol?

A

Cytoplasm of Liver cells

NAD

1mM or 5 mg/dl

3 to 4 times Km
conc. beyond 4 times Km

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7
Q

What is the toxic level for ethanol?

What allows ethanol to enter cells easily?

What happens when ADH is saturated?

A

50-100 mg/dl

High lipid solubility

Spill over and metabolism by MEOS

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8
Q

Describe what happens to ethanol

A

Ethanol –> Acetylaldehyde –> Acetate

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9
Q

Does MEOS directly produce NADH?

A

No but it creates acetaldehyde which when oxidized produces NADH

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10
Q

Which oxidizing system is able to oxidize a variety of compounds such as ethanol, FA, aromatic hydrocarbons, steroids, barbiturate drugs?

It also is associated with Endoplasmic Reticulum

A

Microsomal Ethanol Oxidizing System

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11
Q

Certain enzymes of MEOS are “inducible” what does this mean and significance?

A

Ethanol in high conc. can induce synthesis of these enzymes which results in hepatocytes being able to metabolize ethanol much better

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12
Q

What are two problems associated with acetaldehyde toxicity?

A

Impedes the formation of microtubules in liver cells

Cause the development of perivenular fibrosis

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13
Q

Does Alcohol Dehydrogenase (used to convert Ethanol to acetaldehyde) deplete or create NADH?

A

CREATES NADH

Depletes NAD+

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14
Q

What does elevated NADH signal?

A

Metabolic shift toward reduction so…

Inhibits krebs
Decreased fat burning
Increased FA synthesis (fatty liver)
Lactic Acidemia (Increased lactic acid)

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15
Q

What are the four basic steps of Fatty Acid Oxidation? (NADH is a product)

A

Oxidation
Hydration
Oxidation
Thiolysis

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16
Q

What are the three basic steps to Fatty Acid Synthesis? (NADPH is a reactant)

A

Reduction
Dehydration
Reduction

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17
Q

Where do lipids tend to accumulate?

A

In most tissue where ethanol is metabolized

Fatty liver, myocardium, Renal tubules

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18
Q

What is the reactant, enzyme, and product of TAG synthesis?

A

DHAP, Glycerol 3-phosphate dehydrogenase, and Glycerol 3 Phosphate

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19
Q

What is the Reactant, Enzyme, and Product for Lactate Production?

A

Pyruvate, Lactate Dehydrogenase, and Lactate

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20
Q

What is an Acyl?

A

Fatty acid attached to something

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21
Q

What is a fatty acid?

A

A carboxyl group and a carbon chain

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22
Q

Study the Chart from Biochem one

A

DAMMIT

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23
Q

Are the fatty acids on a TriAcylGlycerol usually saturated or unsaturated?

A

First is Saturated
Second is Unsaturated
Third is Either

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24
Q

Are Triglycerides Oxidized or reduced?

Anhydrous or Hydrous?

How many kcal per gram?

A

Reduced

Anhydrous

9

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25
Q

A 150 pound male has how many kcal of triglycerides?

A

100,000 kcal triglycerides

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26
Q

Which muscle type stores more fat? How much more?

A

Type 1 (aerobic) store two to three times more fat than type 2

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27
Q

Does exercise reduce or increase IMTG in type one muscle fibers?

Is the IMTG replenished faster after aerobic or resistance exercise?

A

Reduce

Resistance

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28
Q

Compare IMTG concentrations and insulin sensitivity in Normal population

Athletes

Obese people

A

Lower IMTG and Moderate insulin sensitive

Higher IMTG and greater insulin sensitive

Higher IMTG and low insulin sensitivity

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29
Q

What enzymes get a TAG to DAG to MAG?

MAG to FFA?

MAG to LCFA+Glycerol?

A

Adipose Triglyceride Lipase (ATGL)
Hormone Sensitive Libase (HSL)

Monoacylglycerol Lipase (MGL)

MonoacylGlycerol Lipase (MGL)

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30
Q

What gets LCFA+Glycerol to MAG?

MAG to DAG?

DAG to TAG?

A

Glycerol-3-phosphate acytltransferase (GPAT)

Acylglycerol-3-phosphate acyltransferase (AGPAT)

Diacylglycerol acyltransferase (DGAT)

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31
Q

What is the protein that breaks down lipoproteins at the surface of capillaries? (mostly skeletal muscle, heart and adipose tissue) It releases FFAs into tissue.

Where is it produced?

A

Lipoprotein Lipase

Produced by muscle and fat cells

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32
Q

Does excersise increase or decrease lipoprotein lipase in skeletal muscle?

A

Increase!

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33
Q

Give an overview of Fat Burning

A
  1. Mobilize (get FA off of glycerol
    TAG->DAG->MAG->FFA
  2. Activate (attach the FA to Coenzyme A)
    FFAs -> Acyl CoA
  3. Beta Oxidation (prepare molecule for Krebs)
    OHOT
  4. Enter Aerobic system (Krebs and ETS)
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34
Q

Fat Breakdown Overview and Enzymes used

A 
Mobilize fat from TG form
   Lipases
Bring Fat to Mito
Activate FA
   Acyl CoA Synthetase and Pyrophosphatase
Transport FA into mito matrix
    CPT and Carnitine
Beta Oxidation
     OHOT (Acyl CoA Dehydrogenase)
Enter Aerobic system
     Multiple Dehydroenases
Make ATP
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35
Q

Epinephrine, Norepinephrine, Glucagon, ACTH, Cortisol are all associated with what?

Insulin?

A

Stimulating Lipolysis

Inhibiting it

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36
Q

Regulation of Lipases are controlled by what?

A

Hormones

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37
Q

Explane Hormone Sensitive Lipase (HSL) and its correlation with Adult Onset Diabetes

Adipose Tryglyceride Lipase (ATGL) and type 2 diabetics?

HSL skeletal muscle protein content reduced or elevated in type two diabetics?

A

HSL much higher specific activity for DAG than TAG with diabetes
HSL is strongly inhibited by insulin

Muscle ATGL elevated a lot with type two ppl

Reduced

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38
Q

What does OHOT stand for?

A

Oxidation
Hydration
Oxidation
Thiolysis

39
Q

What is interesting about any FA that enters the muscle to be oxidized?

A

It must be chaperoned by a protein, FABPc (cytoplasmic fatty acid binding protein) escorting it to the surface of the mitochondria

40
Q

What is the name for when Coenzyme A is attached to FA and creates Acyl CoA using Acyl CoA Synthetase enzyme?

Where does this occur?

Is ATP consumed or produced in this process?

What happens next?

A

Activation

Outer Mitochondrial Membrane

Consumed

Enter the Mitochondria

41
Q

What does Carnitine Palmitoyltransferase Complex consist of?

Responsible for?

Is it considered the RATE LIMITING STEP? (CPT I)

A

CPT I, Acylcarnitine Translocase, CPT II

Transport of LCFA

YES

42
Q

What refers to the four steps that occur prior to having fat enter the Aerobic system?

What enzymes go with the steps?

A

Beta Oxidation (OHOT)

O: Acyl CoA Dehydrogenase
H: Enoyl CoA Hydratase
O: L-3-Hydroxyacyl CoA Dehydrogenase
T: Beta-Ketothiolase

43
Q

What are the results of Beta Oxidation?

A

Both FADH2 and NADH products (go to ETC)

Acetyl CoA Product (enters krebs)

The FA (Acyl CoA) is two carbons shorter each time you run Beta Oxidation (OHOT)

44
Q

Which two additional enzymes are required for Unsaturated FA Degradation?

Which bonds do they go with?

A

Reductase and Isomerase

Odd numbered double bonds = Isomerase
Even numbered ones = Reductase and Isomerase

45
Q

Instead of OHOT what is it for Unsaturated FA?

List steps and enzymes that go with them

A 
Oxidation - Acyl CoA Dehydrogenase
Reductase - 2,4-Dienoyl CoA Reductase
Isomerase - Isomerase
Hydration - Enoyl CoA Hydratase
Oxidation - L-3-Hydroxyacyl CoA Dehydrogenase
Thiolysis - Beta Ketothiolase
46
Q

Difference between Odd-Chain FA and Even?

A

Both are degraded 2 by 2 but Odd are left with Propionyl CoA

47
Q

Fat Oxidation Overview

A 
Hormones are released during exercise or fasting
Lipases release FA from tracylglycerols
Bring FA to Mito
Activation 
     (Acyl CoA Synthetase and Pyrophosphatase)
Transport into matrix
     CPT and Carnitine
Beta Oxidation
Each round of Beta Oxidation releases Acetyl CoA
Acetyl CoA enters aerobic system
     Dehydrogenases
Make ATP
48
Q

Key enzymes for Fat Burning

A

Lipases (HSL) free FA from triglycerides

Acyl CoA Synthetase activates FA for transport

Acyl CoA Dehydrogenase
First enzyme of OHOT
Oxidizes AcylCoA

49
Q

What three things are Inhibitors for Fat burning?

Stimulators?

A

Insulin, High energy charge (ATP), NADH or FADH2

Glucagon, Low energy charge (ADP/AMP), NAD+ or FAD

50
Q

What is the other name for the Pentose Phosphate Pathway?

A

Hexose Monophosphate Pathway

51
Q

What does the PPP make?

What are they needed for?

Main enzyme?

A

Ribose and NADPH

Ribose needed for DNA, RNA, other molecules
NADPH needed for reductive biosynthesis, detox, respiratory bursts, antioxidant regeneration

GLucose 6 phosphate dehydrgenase

52
Q

When new cells are being created, the PPP is stimulated or inhibited?

How bout when process consumes NADPH what happens to PPP?

A

Stimulated

Stimulated

53
Q

What is the location of the Hexose Monophosphate Pathway? (PPP)

How many NADPH per glucose 6-P?

ATP produced or consumed?

A

Cytosol

2

NO ATP produced or consumed

54
Q

What is a Nucleoside?

Nucleotide?

A

Base + Sugar

Base + Sugar + Phosphate

55
Q

Anything that consumes ribose does what to PPP?

A

STIMULATES PPP

56
Q

What are the main products and their purposes of PPP

A

Ribose 5-P : Nuceic Acids, ATP, CoA, NAD FAD

NADPH +H: Reductive Bosynthesis, Free rad elim.
NADPH +H Detox, Respiratory Burst

Glyceraldehyde 3-P
Fructose 6-P Glycolysis

57
Q

Which is oxidized in the electron transport chain to make ATP? NADPH or NADH

Which is an electron donor during reductive biosynthesis, respiratory burst, detox, and regeneration of antioxidants?

A

NADH

NADPH

58
Q

What do the oxidative reactions of PPP do?

The Non-Oxidative ones?

A

Make NADPH

Ribose 5-P can be converted into products to be used in Glycolysis

It can also be used to make nucleotides and nucleic acids

59
Q

What are the 4 individual steps of PPP?

A

Dehydration of glucose 6-P

Hydrolysis of 6-P gluconate gamma lactone

Oxidative Decarboxylation
6-P gluconate to yield Ribulose 5-P

Isomerization
Ribulose 5-P to Ribose 5-P

60
Q

What is the main enzyme for PPP?

Two reactants?

Product?

A

Glucose 6-P Dehydrogenase

Glucose 6-P and NADP+ are reactants

Makes NADPH as a product

61
Q

What are the enzymes that go along with the four steps of PPP?

A

Glucose 6-P Dehydrogenase (Dehydrogenation)

Lactonase (Hydrolysis)

6-phosphogluconate dehydrogenase (oxidative decarboxylation)

Nothing for Isomerization?

62
Q

Molecules move back and forth from PPP and what other pathway?

Which enzymes act as “The Link” between these pathways?

A

Glycolysis

Transketolases and Transaldolases build a reversible link between PPP and glycolysis

63
Q

What are the “Fantastic Four” ways NADPH is utilized?

A

Reductive Biosynthesis

Detoxification

Respiratory Bursts

Antioxidant Regeneration

64
Q

What does Reductive Biosynthesis mean?

A

Building things by adding electrons (From NADPH)

Build fat, cholesterol, steroid hormones, bile salts

65
Q

What does detoxification mean?

A

Maxing toxins more water soluble for execration by adding electrons (from NADPH)

Toxins then excreted in urine

66
Q

Which process makes detoxification occur? Where does this process come from?

How are molecules made more water soluble?

A

Livers P450 monoxegenase system
Endoplasmic reticulum in liver contain system

Addition of hydroxyl groups (OH)

67
Q

What does Respiratory Burst mean?

What happens?

A

This means creating “harsh chemistry” to kill bad guys (non-self like bacteria) by using electrons from NADPH

White blood cells take in more oxygen. O2 and electrons (from NADPH) make very reactive molecules

Reactive molecules and nonself bacteria are sequestered in a vesicle where bacteria dies

68
Q

What are the roles of Hydrogen Peroxide and Myeloperoxidase in Harsh Chemistry?

A

Hydrogen Peroxide used to create reactive species to destroy. (bacteria, viruses, other non self )

Myeloperoxidase is an enzyme that makes hypochlorus acid from hydrogen peroxide

69
Q

What does Antioxidant Regeneration mean?

A

Adding electrons (from NADPH) to antioxidants so they can keep protecting the body from free radicals

70
Q

What are three common Reactive Species?

A

O2-

H2O2 Hydrogen Peroxide

.OH Hydroxyl

71
Q

What three things do Free radicals and Reactive Species attack?

A

Polyunsaturated fat in phospholipids

Protein in cells

Nucleic acids in DNA

72
Q

What is the name of the process by which electronically excited molecules are inactivated?

A

Quenching (this is usually an antioxidant giving an electron to the free radical)

73
Q

When free radicals are quenched, antioxidants get what?

When antioxidants get regenerated they get what?

A

Oxidized

Reduced

74
Q

What are three enzymes that may also quench free radicals?

A

Superoxide Dismutase (quenches superoxide)

Catalase (quenches hydrogen peroxide)

Glutathione Peroxidase (quenches hydrogen peroxide)

75
Q

What is the location and function of Superoxide Dismutase (SOD)

A

Extracellular
Cytoplasm
MItochondria

Eliminate Superoxide and produce Hydrogen Peroxide

76
Q

Catalase Location and Function

A

Mostly in cell peroxisomes
Smaller amounts in cytoplasm, mitochondria, microsomes

Eliminate Hydrogen Peroxide!
Nutrophils have lots of catalase

77
Q

Remember this!

A

ANYTHING THAT CONSUMES NADPH STIMULATES PPP

78
Q

What are the 6 KEY enzymes of PPP?

A 
Glucose 6-Phosphate Dehydrogenase
    main enzyme makes NADPH
Superoxide Dismutase
     Turns superoxide to hydrogen peroxide
Catalase
     turns hydrogen peroxide to water
Glutathione Peroxidase
     Turns hydrogen peroxide to water
Myeloperoxidase
     Turns hydrogen peroxide to hypochlorus acid         
     (respiratory burst)
Cytochrome P-450 mono-oxygenase system
     Adds OH groups to aromatic and aliphatic 
     compounds (detox)
79
Q

Does eating fat stimulate fat synthesis?

A

NO! Eating SUGAR does!

80
Q

Give Fat synthesis overview

A

Eat sugar (lots of blood glucose)

Rest (energy charge is high muscle glycogen up)

Muscle hexokinase is inhibited by glucose 6 phosphate (more glucose not brought into muscle)

Liver glucokinase stimulated by lots of glucose and NOT inhibited by glucose 6 phosphate

Liver runs glycolysis (lots of ATP and Acetyl CoA)

ATP inhibits icocitrate dehydrogenase stop TCA

Citrate spills out and is acetyl CoA is given back

Acytyl CoA turned to malonyl CoA

Fatty acid synthase keeps adding malyonyl coAs to a growing FA

Palmitate (16:0) is eventually created

81
Q

Eating carbs raises blood glucose so insulin is secreted and glucose enters the cells…. then what three questions are asked?

A

Do you have enough energy

Enough stored carbs?

What should I do know?

82
Q

When will glucose move from blood to muscle?

A

As long as conc. of glucose is lower in muscle and transporters are available

83
Q

You eat carbs, glucose blood up, insulin spike, fat and muscle glucose transport know what happens if the muscle is full of glycogen?

If its not?

A

Glucose goes to the LIVER

Glucose is stored as Glycogen

84
Q

Does exercise increase or decrease glucose uptake in skeletal muscle?

A

INCREASE A TON

85
Q

Glucose goes from blood to muscle when the blood glucose conc. is higher than the muscle glucose conc. What is done to keep the conc. in the muscle low comparatively>?

A

A phosphate is added to glucose in the muscle which makes it into glucose 6 phosphate and not glucose.

86
Q

How does muscle say NO to incoming glucose?

A

If there is high energy charge and glycogen is full then PFK is inhibited

This causes glucose 6 phosphate to accumulate

Which inhibits hexokinase

Which inhibits glucose 6 phosphate and causes glucose accumulation

Glucose accumulation in the muscle brings the muscle and blood conc. of glucose to equal therefore preventing facilitated diffusion into muscle!

87
Q

What Four steps does Fatty Acid Synthase make sure happens?

A

Condenses (adds malonyl CoA)

Reduces

Dehydrates

Reduces

88
Q

Functions of cholesterol?

A

Essential component of cell membranes!

Precursors to bile salts and steroid hormones

89
Q

Where is cholesterol made? (structures)

Where do reactions take place?

A

Liver is primary site but also intestine adrenal cortex and gonads

Cytosol!

90
Q

What does HMG-CoA reductase do?>

A

Turns HMG-CoA to Mevalonate which is on its way to becoming cholesterol

91
Q

What are the ingredients for cholesterol? What are they the same as?

Main enzyme?

First unique compound in cholesterol synthesis?

A

Acetyl CoA, NADPH, and ATP.
Same as ingredients for building FA

HMG CoA Reductase

Mevalonate

92
Q

Describe Proglycogen

Macroglycogen

A

More sensative to dietary carbs
Synthesized more rapidly following post exercise glycogen depletion, plateau after 24 hours

Synthesis is slower and more constant may last for 48 hours post exercise. Responsible for cargo loading

93
Q

Where do we store our glycogen? (structures)

Where in those structures?

A

LIver and skeletal muscle

Cytosol

94
Q

Glycogen synthesis overview

A

Phosphoralate Glucose (hexokinase or gluckinase)

Make UDP-GLucose (pyrophosphatase)

Initiation (connect glucose to glycogenin)

Elongation of the chain (glycogen synthase adds glucose)

Branching (4:6 transfer)

Biochem 2 (2 decks)

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