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Fall 2013 > BioChem Final > Flashcards

BioChem Final Flashcards

1
Q

How is Gluconeogenesis regulated?

A
  1. Turned on when needed

2. Reciprocally regulated with glycolysis

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2
Q

When does Gluconeogenesis need to be turned on?

A
  • High levels of LACATE = Exercise;
  • High levels of GLYCEROL = High fat diet;
  • High levels of AMINO ACIDS = Starvation (not enough cards) or Diabetes (inhibits glucose to cells) ; Liver will produce glucose for Brain with starvation and DM
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3
Q

What is Reciprocal Regulation?

A

Regulation of enzymes in opposing pathways by the same of similar compounds;

  • One reaction turned ON, while opposing reaction is turned OFF;
  • Prevents futile cycling (going in circles)
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4
Q

How is Gluconeogenesis reciprocally regulated with Glycolysis?

A
  1. PFK (glyco) inhibited by ATP/citrate and activated by AMP/Fructose2-6-bisPO4….while Fructose-1-6-bisphosphatase (gluconeo) is oppositely affected;
  2. Pyruvate Kinase (glyco) is inhibited by Acetyl-CoA…while Pyruvate Carboxylase (glucoeneo) is activated by Acetyl-CoA;
  3. Pyruvate Dehydrogenase Complex (glyco) is also inhibited by Acetyl-CoA
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5
Q

Why does increased Acetyl-CoA INHIBIT Pyruvate Kinase and the Pyruvate Dehydrogenase Complex of GLYCOLYSIS?

A
  • Because there is enough Acetyl-CoA, so pyruvate does not need to be converted to make more, which would be the commitment AWAY from carb synthesis;
  • So Acetyl-CoA is used to direct away from forming more and allow pyruvate to be used in another way
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6
Q

Why does increase Acetyl-CoA ACTIVATE Pyruvate Carboxylase of Gluconeogenesis?

A

-Lots of Acetyl-CoA needs a lot of OAA, so wants to make more OAA to bind and be able to continue into the TCA cycle;

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7
Q

What is the Energy Concern with Gluconeogenesis?

A
  • Very energy expensive process!;
  • Requires 6 ATP (4 ATP + 2 GTP) and 2 NADH to synthesize ONE glucose from TWO pyruvate;
  • Spend MORE to make Glucose with gluconeogenesis than to Breakdown with glycolysis
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8
Q

What must the Sum of the Delta G values be?

A

-Delta G must be NEGATIVE for Glycolysis and Gluconeogenesis for each pathway to be able to occur

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9
Q

What is the Alternative to Hexokinase of glycolysis?

A

Glucose-6-Phosphatase of gluconeogenesis =

-Converts Glucose-6-PO4 back to Glucose

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10
Q

What is the alternative to PFK (phosphofructokinase) of Glycolysis?

A

Fructose-1,6-bisphosphatase of gluconeogenesis =

-Converts Fructose-1,6-bisPO4 back to Fructose-6-PO4

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11
Q

What is the alternative to Pyruvate Kinase of glycolysis?

A

-Pyruvate Decarboxylase (pyruvate to OAA) and then PEP Carboxykinase (OAA to PEP) of gluconeogenesis

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12
Q

What is Glycogen?

A
  • Animal storage form of Glucose;
  • Highly branched polyglucose;
  • Found in the Liver and Muscle
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13
Q

What are the 2 paths of Glycogen Metabolism?

A
  1. Glycogenesis = Synthesis of glycogen from Glucose-6-PO4 (of glycolysis) in times of storage;
  2. Glycogenolysis = Breakdown of Glycogen back into Glucose-6-PO4 to provide glucose in times of need
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14
Q

What is the enzyme for Glycogen SYNTHESIS with Glycogenesis?

A

Glycogen Synthetase = STORES

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15
Q

How is Glucose-6-PO4 from glycolysis converted to GLYCOGEN for storage?

A

GLYCOGEN SYNTHETASE=

  1. Reversible conversion/isomerization to Glucose-1-PO4;
  2. Glucose-1-PO4 undergoes activation to be UDP~glucose;
  3. Converted to Glycogen
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16
Q

2nd step in Glycogen synthesis: Glucose-1-PO4 to UDP~glucose

A
  • UTP REMOVES 2Pi (pyrophosphate) from Glucose-1-PO4 to leave activated UDP~glucose;
  • Removing 2Pi expends ALOT of energy
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17
Q

What is UTP?

A
  • High energy compound that is dedicated for use ONLY in polysaccharide synthesis;
  • Contain Uridine (found in RNA)
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18
Q

Why does a diphosphate (UDP) still remain after removing 2Pi with UTP?

A

For UDP~glucose, the glucose is attached at C1m making a di-PO4 remain, just moved around;
-Still two TOTAL glucose remaining in the molecule

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19
Q

3rd step in Glycogen synthesis: UDP~glucose to Glycogen

A
  • UDP molecule is REMOVED from the glucose, breaking the high energy bond;
  • Remaining glucose molecule is ADDED to the at the C4 on the NONREDUCING ending of the Glycogen chain to added another branch (C1 already activate);
  • C1 and C4 come from the Alpha-1,4 links of glycogen
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20
Q

What is the enzyme for Glycogen BREAKDOWN with Glycogenolysis?

A

-Glycogen Phosphorylase = BREAKS off a glucose at C1 and adds a PO4

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21
Q

How is Glycogen from storage converted back into Glucose-6-PO4?

A

GLYCOGEN PHOSPHORYLASE=

  1. Breaks glycogen chain off at C1 to take a glucose molecule and adds a Pi from the cytoplasm to created GLUCOSE-1-PO4;
  2. Reversible conversion/isomerization to Glucose-6-PO4
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22
Q

What happens one the Glucose-6-PO4 has been created from the breakdown of Glycogen?

A
  • Liver = Glucose-6-Phosohatase converts to GLUCOSE and sends to blood to raise levels and supply for the Brain;
  • Muscle = Undergoes GLYCOLYSIS to provide its own energy (CANNOT send back to the Blood)
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23
Q

Why can’t the Muscle supply the blood with glucose?

A

-Doesn’t have the enzyme Glucose-6-Phosphatase to converted the Glucose-6-PO4 back into the just glucose

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24
Q

How is Glycogen Synthetase of Glycogen STORAGE controlled ALLOSTERICALLY?

A
  • Glycogen Synthetase 1 (active) INHIBITED by AMP;

- Glycogen Synthetase D (inactive) ACTIVATED by Glucose-6-PO4

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25
Q

How is Glycogen Phosphorylase of Glycogen BREAKDOWN controlled ALLOSTERICALLY?

A
  • Phosphorylase A (active) INHIBITED by glucose (liver);

- Phosphorylase B (inactive) INHIBITED by Glucose-6-PO4 and ATP; ACTIVATED by AMP (muscle)

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26
Q

How do LOW ENERGY LEVELS affect the Glycogen Metabolism and its substrates?

A

HIGH concentration of Pi (during high ATP breakdown) when energy levels are LOW = ACTIVATE Glycogen Phosphorylase to breakdown Glycogen

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27
Q

How do HIGH ENERGY LEVELS affect the Glycogen Metabolism and its substrates?

A

HIGH concentration of UTP when energy levels are HIGH = ACTIVATE Glycogen Synthetase to store as Glycogen

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28
Q

What Hormones affect Glycogen Metabolism?

A
  • Glucagon;
  • Epinephrine;
  • Insulin
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29
Q

How do Glucagon and Epinephrine control Glycogen Metabolism?

A

-GLUCAGON (Liver)= Lowers blood glucose;
=EPINEPHRINE (Muscle) = Provides energy with glucose;
*Both INCREASE breakdown and INHIBIT synthesis of Glycogen

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30
Q

How does Insulin control Glycogen Metabolism?

A
  • Allows glucose to enter cells;
  • Released when HIGH BLOOD glucose concentration;
  • INCREASES synthesis and INHIBITS breakdown of Glycogen
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31
Q

How does Glucagon and Epinephrine act on the cell?

A
  • Peptide Hormones that DO NOT enter the cells, just act on the SURFACE;
  • Bind to receptor which sends signal across the cell membrane = SIGNAL TRANSDUCTION
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32
Q

How does Signal Transduction work?

A
  • Peptide hormones DON’T enter cells;
  • Bind to specific receptor proteins in cell membrane of the outer surface of target cells;
  • Cause a conformational change in receptor protein ;
  • Then, causes a conformational change in ADENYL CYCLASE on the inner surface of the membrane making it ACTIVE
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33
Q

What occurs when Adenyl Cyclase is ACTIVATED?

A

-Catalyzes the conversion of ATP to CYCLIC AMP by the removal of 2Pi (pyrophosphate)

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34
Q

What is the “Cascade Mechanism” of Signal Transduction?

A
  • The amplification of small amounts of message to bring about a large amount of results in a short amount of time;
  • Adenyl cycles enzyme works over and over again increasing the amplifying the number of responses each time
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35
Q

What is the mechanism for Covalent Modification?

A
  1. Add PO4 to enzyme;
  2. Conformational change occurs;
  3. Increase or decreases enzyme activity (totally on or off)
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36
Q

What happens to the Cyclic AMP to continue glycogen breakdown?

A

-Protein Kinase covalently modifies it by adding the Regulatory molecule to CAMP and leaving the catalytic molecule free

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37
Q

What is the free Catalytic Subunit then used for in glycogen breakdown?

A
  1. Activates Phosphorylase Kinase by adding PO4 ;
    AND
  2. Inactivates Glycogen Synthetase (the glycogen storage enzyme) by adding a PO4;
    =RECIPROCAL REGULATION
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38
Q

What is the next step with Activated Phosphorylase Kinase in Glycogen breakdown?

A

-Phosphorylase Kinase then ACTIVATES Glycogen Phosphorylase by adding a PO4 (major breakdown enzyme)

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39
Q

What is the final step with Activated Glycogen Phosphorylase (has a PO4)?

A
  • Catalyzes the Addition of a Pi from the cytoplasm to the NON-Reducing end of glycogen to create Glucose-1-PO4 which will then isomerize into Glucose-6-PO4;
  • Now can be used by the Liver or the Muscle
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40
Q

Why does Glycogen Breakdown use Reciprocal Regulation to INACTIVE Glycogen Synthetase?

A
  • Active Glycogen Synthetase STORES glycogen;
  • During times of Glucose need, glycogen does NOT NEED to be stored, so using the sam enzyme to activate breakdown and inactivate storage is highly efficient
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41
Q

What are Phosphatases?

A
  • Allosteric controls that RETURN Covalently Modified enzymes back to their ORIGINAL form by removing the PO4;
  • Can either be returning it to active or inactive, whatever is the normal state
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42
Q

Why can Glycogen be broken down so quickly to provide glucose in sudden need?

A

-The molecule is highly branched allowing it to be broken down at all the branches and quickly catabolized back to glucose as the cascade mechanism amplifies the enzymatic reaction at each point

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43
Q

What happens when the breakdown of CAMP is inhibited by Caffeine?

A

-More energy will released in at once because the CAMP will hang around longer activating more enzymes than normal

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44
Q

Where does GALACTOSE enter carb metabolism?

A

-Through UDP-Glucose and into the Glycogen pathway to become Glucose-1-PO4 and onto Glucose-6-Phosphate to be used in Glycolysis

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45
Q

Where does MANNOSE enter carb metabolism?

A

-Through Fructose-6-Phosphate into the Glycolysis pathway

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46
Q

Where does FRUCTOSE enter carb metabolism?

A

-Through DHAP and Glyceraldehyde to Glyceraldehyde-3-PO4 and into the Glycolysis pathway

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47
Q

What is the Pentose Phosphate Pathway?

A
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48
Q

Where does the Pentose Phosphate pathway occur?

A
  • In the liver, mammary glands, testes, and adrenal cortex in animals;
  • Tissues that carry out ALOT of biosynthesis, so need a lot of NADPH and the accompanying electrons
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49
Q

What are the FUNCTIONS of the Pentose Phosphate Pathway?

A
  1. Alternative route for glucose oxidation to CO2 and H2O (another form of complete breakdown);
  2. Energy released in oxidation is used to make NADPH (12 NADPH/glucose);
  3. Allows interconversion of 3,4,5,6,7 C sugars to inter into glycolysis (transaldolases and transketolases);
  4. Biosynthesis of ribose-5-PO4 from glucose-6-PO4;
  5. In plants, many some type of enzymes used for photosynthesis
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50
Q

Why is the Pentose Phosphate pathway important for the generation of NADPH?

A
  • Traps the energy as needed electrons in the needed Redox coenzyme for SYNTHETIC pathways (NADPH);
  • Can be used to generate NADH;
  • NADPH is used by antioxidant enzymes
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51
Q

How can NADH be used to create NADH with the Pentose Phosphate Pathway?

A

-Remove electrons from NADPH and give them to NAD+;
-Generates NADH and NADP+;
(NEVER move Phosphate, just electrons)

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52
Q

How many ATP could come from the Pentose Phosphate Pathway?

A

-12 NADPH produced per glucose;
= ~36 ATP if converted to NADH and sent to ETC;
(3 ATP generated per NADH)

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53
Q

What are Lipids?

A

Variety of biological molecules that are soluble in NON-POLAR solvents, but NOT in water;
-Either Saponifiable or Non-sapinofiable

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54
Q

What are Saponifiable Lipids?

A

Can be broken down to at least one fatty acid + an alcohol

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55
Q

What lipids are Saponifiable?

A
  1. Fatty acids and derivatives (building blocks)
  2. Triaclglycerols (storage)
  3. Phosphoacylglycerolds (membranes)
  4. Sphingolipids (nerve tissue)
  5. Glycolipids (carb conjugates)
  6. Wax esters (lubricants, coatings)
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56
Q

What lipids are Non-Saponifiable?

A
  1. Isoprenoids (Terpenes, Steroids) = 5-C

2. Derivatives of Arachidonic acid (Prostaglandins, Leuokotrienes, Thromboxanes)

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57
Q

What are Fatty Acids?

A 
Long, chain monocarboxylic acids;
-Long carbon chain is HYDROPHOBIC;
-Carboxylic acid group is HYDROPHILIC due to separation of charge
=AMPHIPHILIC overall ;
-Saturated or Unsaturated
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58
Q

What are Saturated Fatty Acids?

A
  • Contain NO double bonds;
  • Saturated with Hydrogens;
  • Lack of double bonds allows them to stack together very closely making them SOLID at room temp
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59
Q

Myristic

A

SATURATED Fatty Acid;

14:0

60
Q

Palmitic

A

SATURATED Fatty Acid;

16:0

61
Q

Stearic

A

SATURATED Fatty Acid

18:0

62
Q

How are fatty acid chains denoted?

A
  • First number is the total number of carbons;
  • Second numer is the number of double bonds
  • Triangle and following numbers give placement of the double bond
63
Q

What are Unsaturated Fatty Acids?

A
  • Contain at least one or more DOUBLE bonds;
  • Double bonds in nature are highly “Cis” (H’s on the same side) creating kinds in the chain;
  • Don’t stack tightly making them liquids at room temp
  • “Oleic” means unsaturated
64
Q

How are double bonds counted in Fatty Acids?

A

-First C from the Carboxylic Acid end is the number placement given to the double bond

65
Q

Palmitoleic

A

UNSATURATED Fatty Acid;

16:1:^9

66
Q

Oleic

A

UNSATURATED Fatty Acid;

18:1:^9

67
Q

Linoleic

A

UNSATURATED Fatty Acid;

18:2:^9,12

68
Q

What are Triacylglycerols?

A
  • Triglycerides, NEUTRAL fats;

- Consist of 3 Fatty Acids linked to a Glycerol backbone

69
Q

How are the fatty acids and glycerol backbone of triglycerides linked?

A
  • Ester linkage formed through a condensation rxn and removal of water (3 H2O);
  • Links the OH (carboxyl end) of each fatty acid to the H of each alcohol group on the glycerol
70
Q

What are the roles of triglycerides in animals?

A
  1. Major storage and transport form of fatty acids - highly efficient;
  2. Insulation (Blubber)
71
Q

What makes triglycerides such efficient storage?

A
  1. Hydrophobic = don’t attract water, so store more energy in a lot let space and with less weight (unlike carbs that have water and heavy O attached);
  2. Less oxidized = carbs have -OH groups which make them heavy and take up space and attract water
    * Fatty acids are ~2X more efficient use of space than carbs
72
Q

What are Phosphoacylglycerols?

A

(POLAR)

  • 2 fatty acids chain linked to a glycerol through an ester;
  • glycerol is then linked to a phosphate;
  • phosphate is then linked to al alcohol;
  • Fatty acids are HYDROPHOBIC;
  • Phosphate group is HYDROPHILIC
73
Q

What makes a Lecithin?

A

The group that is attached to a Phoshoacylglycerol at the Phosphate end is Choline;
= PHOSPHATIDYLCHOLINE

74
Q

What are the roles of Phosphoacylglycerols?

A
  • Structural components of membranes (hydrophilic head and hydrophobic tails);
  • Surfactants (alveoli of the lungs);
  • Emulsification for the digestion of lipids in aqueous blood stream (micelle formation)
75
Q

What are Sphingolipids?

A

(POLAR)

-Glycolipids containing a backbone of sphingoid bases, amino alcohols that includes SPHINGOSINE

76
Q

What are the roles of Sphingolipids?

A
  • Components of animal and plant membranes;
  • Especially important in NERVE CELLS;
  • Constant turnover is critical! - if can’t be turned over, nerve cells will degenerate and cause death
77
Q

What is a Ceramide?

A

-Sphingosine backbone with ONLY a fatty acid

78
Q

What is a Sphinomyelin?

A

-Sphingosine backbone with a fatty acid, and a PO4 attached to choline

79
Q

What are Cerebrosides?

A

-Sphingosine backbone with a fatty acid and a SIMPLE carb attached

80
Q

What are Gangliosides?

A

-Sphingosine backbone with a fatty acid and a COMPLEX carb attached

81
Q

What are Glycolipids?

A

-Carb and lipid together

82
Q

What are Wax Esters?

A

-Fatty acid attached to an alcohol with varying hydrocarbon chains on either end

83
Q

What are the roles of Wax Esters?

A

-Protective coatings on leaves, stems, fruit (plants), skin, and fur (animals)

84
Q

What are Non-Saponifiable?

A
  1. Isoprenoids = Terpenes and Steroids

2. Derivatives of Arachidonic Acid (20C Chain fatty acids)

85
Q

What are Isoprenoids?

A
  • 5 carbon unit that contains a double bond and some asymmetry;
  • Allows them to link in various ways (head to head, head to tail, etc)
86
Q

What are Terpenes?

A

Long chains;

  • Plants = oils, frangrances, pigments;
  • Animals = precursor to cholesterol, involved in covalent modification to change enzyme function;
  • Vitamins = A, E, K (fat soluble)
87
Q

What are Steroids?

A
  • Type of lipids that contain a characteristic arrangement of four cycloalkane rings that are joined to each other;
  • Core contains 17 carbons with 3 cyclohexane rings and 1 cyclopentane;
  • Differ in substituents on rings, double bonds, and stereochemistry
88
Q

What are the various Steroids?

A
  1. Cholesterol
  2. Steroid hormones
  3. Bile salts
  4. Vitamin D
89
Q

Cholesterol

A
  • Very critical to membrane structure
  • Precursor to other steroids
  • Body can produce whether or not consumed in the diet
90
Q

Steroid Hormones

A
  • Progesterone;
  • Testosterone;
  • Estradiol;
  • Cortisol
  • Very similar derivatives of cholesterol
91
Q

Bile Salts

A
  • Synthesized in the LIVER;

- Aid the digestion/emulsification of dietary lipids through the formation of micelles = AMPHIPHILIC

92
Q

Vitamin D

A

-We make precursors but rely heavily on sunlight for production

93
Q

What are the Derivatives of 20C Chain Fatty acids (Arachidonic)?

A
  1. Prostaglandins
  2. Thromboxanes
  3. Leukotrienes
94
Q

What are Prostaglandins?

A
  • Derivative of arachidonic acid with “hairpin” structure;
  • Wide variety of structure, so wide variety of function;
  • Increase body temp (fever);
  • Pain and inflammation;
  • Platelet aggregation;
  • Gastric mucus production to protect stomach lining
95
Q

What are Thromboxanes?

A
  • Platelets (Thrombocytes);

- Form blood clots

96
Q

How do NSAIDS work?

A
  • INHIBIT Cyclooxygenase (Cox);
  • This blocks Prostaglandin and Thromboxanes and therefore ALL of their functions;
  • Beneficial to block pain, but blocking gastric secretions can cause ulcers
97
Q

What are the Isozymes of Cox?

A
  • Cox-1 = controls normal physiological functions of Postaglandins and Thromboxanes;
  • Cox-2 = controls inflammation
98
Q

What occurs when NSAIDS block Cox 1?

A

-Inhibit Blood Clotting and Cytoprotection = NOT always good

99
Q

Why is it beneficial to ONLY block Cox-2?

A
  • Cox-2 controls pain/inflammation, so creating drugs that only fit into its active site allows other physiological functions to continue as normal;
  • Celebrex for arthritis can get around the CH3 that blocks other NSAIDS
100
Q

What are Leukotrienes?

A
  • Control the contraction of smooth muscles in the lungs;
  • Involved in Asthma and anaphylactic shock;
  • Typically blocked by inhalers
101
Q

What is the Emulsification of Lipids?

A
  • Lipids are NOT broken down completely before absorbed (unlike carbs and proteins);
  • Bile salts and phospholipids (AMPHIPHILIC) create micelles around the lipids allowing them to be suspended and transported in the aqueous blood stream
102
Q

How are the AMPHIPHILIC structure of the micelles arranged?

A
  • Hydrophilic headed is OUT toward the solution;

- Hydrophobic tails are IN toward the lipid

103
Q

What are Lipoproteins?

A

-Micelle structures that are composed of amphiphilic lipids and proteins that transport digested lipids

104
Q

What determines the function of each type of Lipoprotein>

A
  • Point of synthesis;
  • Lipids composition;
  • Protein content (at least 9 different apoproteins can be used)
105
Q

What are the classes of Lipoproteins?

A
  1. Chylomicrons;
  2. VLDL (Very Low Density)
  3. LDL (Low Density)
  4. HDL (High Density)
106
Q

What are the Chylomicrons?

A
  • Largest Lipoproteins that go from the blood to the lymphatic system;
  • Mostly made of triglycerides
107
Q

How are Chylomicrons used?

A

Transported from the Intestinal Mucosa to either…

  • peripheral tissues where triglycerides are used for energy OR
  • Liver where triglyceridesa are used for energy/ketones or repackaged to be sent to other parts of the body
108
Q

What are VLDLs?

A
  • About 50% triglycerides;

- Transport from the LIVER (packaged) and sent to the adipose tissues for storage

109
Q

What are LDLs?

A
  • BAD cholesterol;
  • Transports cholesterol throughout the body (needed by tissues and hormones);
  • Problems occur when LDL’s try and carry too much cholesterol and drop in in the vessels and other wrong places causing damage
110
Q

What are HDLs?

A
  • GOOD cholesterol;
  • Mostly PROTEINS;
  • Favors delivery of EXCESS cholesterol to liver for elimination;
  • Initiates Bile Salt synthesis (made from cholesterol) = removing cholesterol, forces body to used stores to make more bile;
  • Cleans up what the LDLs loose
111
Q

How is Fatty Acid Oxidation MOBILIZED?

A
  • Signal Transduction that is initiated by Epinephrine;

- Followed by Covalent Modification

112
Q

Signal Transduction of Mobilizing FA Oxidation

A
  1. Epinephrine binds Adipose Tissue receptor;
  2. Receptor activates Adenyl cyclase (inner membrane);
  3. Catalyzes the formation of CAMP and 2Pi (from ATP);
  4. cAMP activated protein kinase through binding of the regulatory subunit
    …Then covalent modification
113
Q

Covalent Modification of Mobilizing FA Oxidation

A
  1. Activated protein kinase activates Hormone sensitive Lipase with the ADDITION of a PO4;
  2. Activated Lipase-PO4 catalyzes triglyceride breakdown into glycerol + free fatty acids
114
Q

What happens to the free fatty acids after mobilization?

A

The free fatty acids are carried by SERUM ALBUMIN (protein) through the blood stream to the peripheral tissues (skeletal and heart muscles);
-DOES NOT go to the brain

115
Q

What is the Activation for fatty acid Oxidation?

A
  1. Free fatty acids (carried by serum albumin) uses ATP and combines with CoA-SH;
  2. Generates Fatty acyl~CoA + AMP + 2Pi (pyro);
    Enzyme = Acyl-CoA synthetase;
    *Removing 2Pi requires ALOT of energy to create the high energy thioester bond of Fatty acyl~CoA
116
Q

Where does Activation fatty acid oxidation take place?

A

Cytoplasm of the cell!;

Must be transported to Mitochondria for full oxidation

117
Q

How is Fatty acyl~CoA transported into the Mitochondria>

A
  1. Fatty acyl~Co-A is combined with CARNITINE to make Fatty acyl-Carnitine + CoA (removed);
    (Enzyme = Carnitine Acyl Transferase);
  2. Fatty acyl-carnitine is transported across the mitochondrial membrane;
  3. Fatty acid is recombined with a Co-A back in to FA~CoA;
  4. Carnitine is sent back out to cytoplasm
118
Q

Handing the fatty acid to Carnittine is….

A
  • the COMMITMENT to the breakdown (oxidation) of fatty acids;
  • Allosterically controlled by Malonyl-CoA
119
Q

What is the goal of Beta-Oxidation of Fatty Acids?

A
  • Breaks them down into 2C units at a time so they they may be used for energy and allowed to enter into the TCA cycle;
  • Need to convert the -CH3 (methyl) on the end when broken into a C=O;
  • Oxidation-Hydration-Oxidation
120
Q

Mechanism for Beta-Oxidation of Fatty Acids

A
  • Oxidation-Hydration-Oxidation:
    1. Used FAD-requiring dehydrogenase for oxidation and create a double bond;
    2. Directional addition of H20 to add water across the double done, hydration;
    3. NAD-linked oxidation of alcohol to a ketone;
    4. Can then be split by Thiolysis with CoA-SH into 2C units
121
Q

What results from Beta-Oxidation of Fatty Acids?

A
  • The free 2C units are combines with CoASH to generate Acetyl-CoA which will then enter into the TCA cycle and be used to energy;
  • The remaining portion that already had ~SCoA goes back to the oxidation cycle
122
Q

How much energy is generated PER SPIRAL of beta-oxidation of fatty acids?

A

1 FADH2 = 2 ATP;
1 NADH + H+ = 3 ATP:
Total = 5 ATP/spiral;
and, each AcCoa entering TCA yields 12 ATP each

123
Q

Can fatty acids be used to generate glucose?

A

NO;
Fatty acids enter the TCA cycle as Acetyl-CoA;
Acetyl-CoA can NEVER be used to make glucose because of the 2 carbons that are lost in the TCA cycle as CO2

124
Q

Why does fatty acid breakdown yield more energy (net ATPs) than glucose?

A

Because of the long chain of lots of carbon in fatty acids vs. just the 6 carbons of glucose;
Each time 2 carbons is broken off of a fatty acid chain 12 ATP are created along with 5 ATP from the cofactors

125
Q

Why does glucose weigh so much more than fatty acids?

A
  • Carbs contain hydroxyl groups that contain heavy molecules of oxygen, while fatty acids only have hydrogens attached;
  • Carbs are also hydrophilic, making them attract water to add water weight;
  • Hydrophobic fatty acids remain on their own
126
Q

How much more energy efficient are fatty acids than glucose?

A

-Per weight unit, fatty acids are ~ 2x more energy efficient

127
Q

What are the 2 concerns of the LIVER if the supply of Carbs is severely limited?

A

[Starvation and diabetes]

  1. maintaining blood glucose, especially for the brain;
  2. energy to support its own cellular activities
128
Q

How does the Liver try to maintain blood glucose without carbs?

A
  1. First - Initiates GLYCOGEN breakdown first (short term, about a days worth);
  2. Second - starts breaking down proteins to use the Amino Acids for Gluconeogenesis to create glucose = uses ATP and depletes the intermediates of the TCA
129
Q

What can’t fatty acids be used by the liver to respond to blood glucose levels?

A

Fatty acids are converted to Acetyl-CoA which CANNOT generated glucose!!

130
Q

What becomes limited as the Liver uses up Amino Acids stores to maintain blood glucose?

A
  • The TCA intermediates (that can come from amino acids) become limited;
  • Limited availability therefore limits the cycle creating OAA which slows the cycle and limits glucose and energy production
131
Q

How does the Liver try to meet its own energy needs without carbs?

A

Adipose tissue is mobilized;

  • Fatty acids converted to Acetyl-CoA and enter TCA:
  • TCA NOT functioning properly due to loss of intermediates (AcCoA can’t make glucose);
  • Low OAA = build up of OAA leading to a 4C compound Acetoacetyl-CoA
132
Q

What is Acetoacetyl-CoA?

A
  • The result of the build up of high concentration of Acetyl-CoA due to low OAA levels (TCA not working);
  • It is the precursor to Ketone bodies
133
Q

What are the Ketone bodies?

A 
[Metabolic acidosis]
-Acetoacetate (acidic);
-Acetone ("sweet breath");
-Beta-OH butyrate (acidic);
=Build up due to a lack of adequate glucose and the ability to use up Acetyl-CoA by combining with OAA (limited)
134
Q

What is caused by the build up of EXCESS ketone bodies?

A
  • High sugar and acid in blood:
  • Blood = DECREASES pH;
  • Ketosis - mild, ok (dieting);
  • Ketoacidosis - difficulty transporting O2, leads to coma
135
Q

What occurs in the LUNGS with excess ketones?

A

[Respiratory alkalosis]

  • Tries to help relieve acidosis;
  • Releases acetone;
  • Removes CO2 to increase blood pH (deep breathing)
136
Q

What occurs in the URINE with excess ketones?

A
  • Ketone cause an overload of the renal balance;
  • Raise in osmotic pressure;
  • Dehydration (due to removal of H2O to balance);
  • Thirst due to water loss;
  • Plasma volume drops;
  • Shock = renal failure
137
Q

WHERE does fatty acid SYNTHESIS occur?

A

Liver and adipose tissue where it is stored

138
Q

WHEN does fatty acid synthesis occur?

A

When excess Acetyl-CoA is present from…

  • Carbs;
  • Proteins (Ketogenic that form AcCoa, not glycogenic)
139
Q

How does fatty acid synthesis DIFFER from Beta-Oxidation (breakdown)?

A
  1. Occurs in the Cyto (breakdown in mito);
  2. Multi-enzyme complex b/c in cyto vs. separate enzymes in mito;
  3. Uses Acyl-Carrier Protein vs. CoA;
  4. Uses NADPH (Synthetic cofactor)
140
Q

How is Acetyl-CoA transported back to the Cytoplasm to be used for Fatty Acid Synthesis?

A

-AcCoA from pyruvate or AAn’s combined with OAA to make Citrate;
-Citrate is carried across the mito membrane;
-Once in cytoplasm uses ATP and another CoenzymeA to remake Acetyl-CoA and OAA
[Citrate cleavage enzyme]

141
Q

How is fatty acid synthesis ACTIVATED?

A

Formation of Malonyl-CoA;
-Carboxylation of a 2C free fatty acid to make the end methyl (CH3) reactive;
-Uses ATP, HCO3- (CO2) and Biotin;
[AcCoA carboxylase]

142
Q

How is AcCoa Carboxylase controlled?

A
  • ACTIVATED by Citrate;

- INHIBITED by Fatty acyl~CoA

143
Q

What order does Breakdown of Fatty Acids occur?

A
  1. Activation;

2. Transport (Point of CONTROL, handing to Carnitine)

144
Q

What order does Synthesis of Fatty Acids occur?

A
  1. Transport;

2. Activation (Point of CONTROL, carboxylation to malonyl-CoA)

145
Q

What is the Reciprocal Regulation of Fatty Acid breakdown/synthesis?

A
  • Breakdown is INHIBITED by Malonyl-CoA;

- Synthesis fi INHIBITED by Fatty acyl~CoA

146
Q

What are the overall Steps of Fatty Acid Breakdown and the cofactors?

A

[Mitochondria];

  1. Oxidation (FADH2)
  2. Reduction (add H2O)
  3. Oxidation (NADH)
    * Coenzyme A is attached at all steps
147
Q

What are the overall steps of Fatty Acid Synthesis and the cofactors?

A

[Cytoplasm]

  1. Reduction (NADPH);
  2. Dehydration (remove H2O);
  3. Reduction (NADPH)
    * ACP (Acyl-Carrier Protein) attached at all steps

Fall 2013 (6 decks)

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