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MCM > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

2 Subdivisions of Coenzymes

A

Co-Substrate (temporary association)

Prosthetic (permanent association)

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2
Q

Co- Substrate Coenzymes

A

Coenzyme that binds and detaches in altered state

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3
Q

Prosthetic Coenzyme

A

Coenzyme part of the enzyme, tightly bound

Example: Heme

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4
Q

Cytochrome C Oxidase Cofactors

A

Copper (Cu)

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5
Q

Heme Protein Cofactors

A

Iron (Fe)

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6
Q

ATPases Cofactors

A

Magnesium (Mg)

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7
Q

Glutathione Peroxidase Cofactor

A

Selenium (Se)

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8
Q

Superoxide Dismutase Cofactor

A

Zinc (Zn)

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9
Q

What is metabolism, and its purpose?

A

Metabolism is a series of biochemical reactions that capture and harness energy from nutrients. Breakdown nutrients to release energy to sustain life, have offspring, continue human existence

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10
Q

2 Goals of Metablolism

A
  1. Produce energy via catabolic pathways

2. Synthesize Biomolecules via anabolic pathways

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11
Q

2 Types of Biochemical reactions

A
  1. Exergonic: release energy, more favorable thermodynamically
  2. Endergonic: require input of energy, not favorable
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12
Q

Free Energy Change (DeltaG)

A

Tells the dynamics of a biochemical reaction, represents the spontaneity and whether the reaction will occur

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13
Q

When Free Energy Change = 0

A

Reaction at equilibrium

Keq = 1

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14
Q

When Keq >1

A

DeltaG <0
Reaction is spontaneous
Proceeds to the right
Exergonic

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15
Q

When Keq<1

A

DeltaG >0
Non spontaneous
Proceed to the left (favors reactants)
Endergonic

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16
Q

Thioester Bond

A

Between thick of Coenzyme A and Carboxylic Acids

Energy released when broken down is equivalent to energy released from hydrolysis of ATP to ADP and Pi

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17
Q

Triphosphate nucleotides

A

Store energy within their phosphoric acid anhydride bonds like ATP

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18
Q

Mass Action (Le Chatelier’s Principle)

A

Keq dependent on the concentrations of the reactants and products
Can alter the concentrations of reactions and products to drive a reaction in a certain direction —> this alters Keq which can tell you whether the product is endergonic or exergonic and the DeltaG

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19
Q

Input of Energy (coupled reactions)

A

Couple an endergonic (non spontaneous) reaction with an exergonic (spontaneous) rxn to use the energy released to power the endergonic rxn
Add the reactions Delta Gs together to determine if the reactions coupled will allow the endergonic reaction to proceed
Must share an intermediate in order to couple
Ex: ATP powers biochemical reactions

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20
Q

Addition/Elimination Reaction

A

Transfer of an atom to a multiple bond or elimination of an atom to form multiple bond

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21
Q

Metalloenzymes

A

Enzymes that require metal ions as a cofactor

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22
Q

LEAD POISONING

  • What is happening
  • Symptoms
A

Inhibits enzymes in heme biosynthesis
Heme is coenzyme of hemoglobin, need for carry oxygen by RBC

Symptoms:
Abdominal pain
Sideroblastic anemia
Irritability
Headaches
Signs of impaired nervous system and encephalopathy
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23
Q

Treatment of Lead Poisoning and Chelating Agents

A

Ca-EDTA with dimercoprol : PB replaces calcium because higher affinity for EDTA than calcium has, Pb-EDTA is then excreted from body

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24
Q

Examples of Irreversible INhibitors

A

Leda, Cyanide, Sulfide, Organophosphates, Aspirin

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25
Q

How are Allosteric enzymes modulated?

A

Actively by non covalent binding of metabolite to another site than the catalytic site

Causes conformational changes

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26
Q

These allosteric enzymes facilitate binding

A

Positive Effetors (activators)

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27
Q

These allosteric enzymes prevent binding of substrate

A

Negative Effectors (inhibitors)

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28
Q

Isozymes

A

Same catalytic function, different primary sequence
Different biophysical properties
Different binding sites

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29
Q

Pro enzymes (Zymogen)

A

Inactive precursor of enzyme
Usually require proteolytic breakdown to become active

Form of enzymatic regulation

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30
Q

Troponin in MI

A

Calcium binds to troponin leading to muscle contraction

Troponin is trimeric, and Tn-I has 3 subunits, with one being in cardiac muscle = cTn-I

Troponin cTn-I used as a bio marker for MI, elevated after MI
Max sensitivity 10-24 hours after MI

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31
Q

% of calories from protein

A

10-15%

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32
Q

% of calories from fat

A

25-25%

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33
Q

Monosaccharides

A

Single sugar carbohydrate

Ex: glucose, fructose

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34
Q

Disaccharides

A

Two sugar carbohydrate

Ex: lactose

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35
Q

Polysacccharide

A

Multi sugar carbohydrate

Ex: glycogen

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36
Q

Lipid Examples

A

Fatty acids, triglycerides, membrane lipids, cholesterol and cholesterol esters, lipid soluble vitamins

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37
Q

Protein examples

A

Oligopeptides, polypeptides, amino acids

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38
Q

The Essential Amino Acids obtained from the diet

A

Leucine, isoleucine, valine, histidine, lysine, methionine, phenylalanine, threonine, tryptophan, arginine (in children)

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39
Q

Acidic Amino Acids

A

Aspartic Acid

Glutamic Acid

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40
Q

Basic Amino Acids

A

Arginine
Histidine
Lysine

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41
Q

Duodenum (proximal small intestine) Digests and Absorbs…

A

Fat
Sugars
Peptides and AA

Iron
Folate
Calcium
Water
Electrolytes
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42
Q

Ileum (distal small intestine) digests and absorbs…

A

Bile acids
Vitamin B12
Water
Electrolytes

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43
Q

Digested products are absorbed into…

A

Hepatic Portal System

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44
Q

Steatorrhea

A

Presence of excess fat in stool, potentially fecal incontinence

May occur due to malabsorption of fat (IBS, Celiac disease, etc.)

or maldigestion of fat (decreased lipase activity due to lack of pancreatic function, problems with bile secretion and or production, or obstructed bile duct)

Lipase blocker drugs can also cause steatorrhea

Malabsorption of lipid soluble vitamins A, D, E and K is a concern

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45
Q

Crohn Disease

A

Autoimmune disease
Chronic inflammation and damage of bowel mucosa

Diseased bowel in segments between healthy bowel

Symptoms:
Nutritional deficiencies
Abdominal pain
Diarrhea
Flatulence
Bloating
Itching
Skin lesions
Treatment:
Surgical resection
Pharmacological therapy
Immunosuppressive agents
Nutritional supplements
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46
Q

Lipid Soluble vitamins

A

A, D, K, E

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47
Q

Structure and Composition of the Plasma Membrane

A

Composed of lipids, proteins and carbohydrates

Asymmetric bilayer

Semi permeable

Primary component is phospholipids

Amphipathic

  • hydrophobic tails
  • hydrophilic heads
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48
Q

3 Membrane Lipids

A

Phospholipids
Glycolipids
Cholesterol

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49
Q

2 Types of Phospholipids

A

Glycerolphospholipids

Sphingolipids

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50
Q

Glycerolphospholipids

A

Phospholipids with a glycerol backbone

Plus a Phoshphate and two FA

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51
Q

Sphingolipids

A

Phospholipids with sphingosine backbone

Plus long FA and phosphorylcholine

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52
Q

Glycolipids

A

Membrane lipid with sphingosine backbone with a carbohydrate (oligosaccharide) residues

OUTER LEAFLET

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53
Q

Cholesterol

A

Membrane lipids with steroid nucleus with hydroxyl group and hydrocarbon side chain
EMBEDDED in lipid bilayer

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54
Q

Outer Sheet Membrane Lipids

A

Phosphatidylcholine

Sphingomyelin

Glycolipids

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55
Q

Membrane Lipids of Inner Sheet

A

Phosphatidylinositol

Phosphatidylserine

Phosphatidylethanolamine

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56
Q

Describe Phosphatidylserine (PS) as a marker for Apoptoosis

A

In healthy cells - PS in inner leaflet of bilayer

During apoptosis - PS moves to outer leaflet an serves as a tag/label for recognition by phagocytes to remove the dying cell

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57
Q

3 Types of Membrane Proteins

A

Integral Membrane proteins

Peripheral proteins

Lipid- anchored proteins

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58
Q

Integral membrane proteins

A

Firmly embedded in the membrane

Stabilized by hydrophobic interactions with lipids

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59
Q

Polytopic Transmembrane proteins

A

Integral membrane protein that spans entire lipid bilayer
Weaves in and out several times
Interacts with both internal and external environment

Includes transporters, ion channels, receptors

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60
Q

Peripheral PRoteins

A

Membrane protein loosely bound to membrane

Electrostatic interactions with lipids or proteins

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61
Q

Lipid-anchored proteins

A

Tethered to membrane

Covalent attachment to a lipid

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62
Q

Glycocalyx

A

Carbohydrate shell on outer sheet of many membranes

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63
Q

3 Key Functions of Glycocalyx

A

Protection

Cell Adhesion

Cell Identification

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64
Q

Blood Type O

A

Antibodies for A and B
H antigen
Universal Donor

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65
Q

Blood Type A

A

Antibodies for B

Antigen A

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66
Q

Blood Type B

A

Antibody for A

B antigen

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67
Q

Blood Type AB

A

No antibodies
Antigens A and B
Universal acceptor

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68
Q

Rh Factor

A

D antigen inherited autosomal dominant fashion

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69
Q

Rh+

A

Express D antigen

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70
Q

Rh-

A

do NOT express D antigen

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71
Q

Erythroblastosis Fetalis

A

Disease in which incompatibility between blood of mother and fetus

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72
Q

Mom Rh- and Fetus RHh+

A

Mom produces antibodies during pregnancy for the D antigen that the fetus has
Antibodies cross placenta in second and later pregnancies and can attack the fetus

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73
Q

3 Factors Influencing Membrane Fluidity

A

Temperature

Lipid Composition

Cholesterol

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74
Q

Temp and Membrane Fluidity

A

Below Tm = membrane rigid, ordered packing
Above Tm = membrane more fluid

Too Above Tm can result in membrane being too fluid

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75
Q

Melting Temp of membrane

A

Temp at which membranes switch from fluid to rigid state

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76
Q

Lipid Effects on Membrane Fluidity

A

Saturated Lipids = decreased fluidity

Unsaturated Lipids = increased Fluidity

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77
Q

Cholesterol effects on membrane fluidity

A

Can both increase and decrease fluidity

Membrane already rigid, add cholesterol to make more fluid

Membrane too fluid, add cholesterol to make more rigid/less fluid

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78
Q

Spur Cell Anemia

A

Elevated Levels of Cholesterol in RBC membrane
Decreases fluidity and flexibility
RBC membrane breaks when passing through capillaries

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79
Q

Ion Concentrations outside Membrane Relatively

A

Na+ high
K+ low
Cl- high
Ca2+ low

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80
Q

Ion Concentrations Inside the Membrane/Cell Relatively

A

Ca2+ higher
Cl- lower
K+ higher
Na+ lower

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81
Q

Voltage Gated Na+ Channel

A

Brings Na+ into the cell via Facilitated Diffusion

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82
Q

Glucose Transporter (ex: GLUT1)

A

Brings glucose into the cell via facilitated diffusion

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83
Q

Ion Channels

A

Pores or gates, allow charged and polar molecules to pass through membrane down concentration gradient

Open and close in response to a stimulus

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84
Q

Ligand Gated Ion Channels

A

Respond to ligands, ligand facilitates opening of channel to allow transport of ions down concentration gradient

Ex: Gutamate Receptor (an antagonist used to treat Alzheimer’s = Mimantine/Namenda)

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85
Q

Voltage Gated Ion Channels

A

Open and close in response to change in membrane potential

Depolarization triggers the opening to allow specific ions to cross down concentration gradient

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86
Q

Tetrodotoxin

A

Poison in puffer fish that will inactivate Na+ channel

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87
Q

Process of transporting monosaccharides from intestinal lumen into enterocyte into the blood is facilitated by both…

A

Facilitated diffusion and

Active transport

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88
Q

What enters intestinal epithelial cells from lumen by SGLT1

A

Glucose, galactose, and Na+ via secondary active transport

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89
Q

What passes via GLUT2 from enterocyte to blood stream

A

Glucose, galactose, fructose via facilitated diffusion

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90
Q

How is fructose transported from lumen of intestine to epithelial cell

A

Facilitated diffusion by GLUT5 on apical side

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91
Q

How is Na+ transported into the blood stream from the epithelial intestinal cell

A

SGLT1 via primary active transport
NA+/K+ ATPase
Basolateral membrane

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92
Q

Describe Cardiotonic Drugs and Ouabain

A

Inhibit Na+/K+ ATPase on cardiac myocytes

Causes increase in Na+ inside the cell, which then leads to increase in Ca2+ due to slowing of NCX

Increased Ca2+ leads to stronger excitation and contraction of cardiac muscle

Used with CHF and arrhythmia

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93
Q

Starch

A

Polysaccharide of GLUCOSE

Carb storage in pants

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94
Q

Sucrose

A

Disaccharide of GLUCOSE and FRUCTOSE

Fruits and vegetables

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95
Q

Lactose

A

Disaccharide of GLUCOSE and GALACTOSE

Carbs of animal origin

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96
Q

Describe Lactose Intolerane

A

Body cannot digest lactose due to genetic deficiency in lactase

Age dependent decrease in production of lactase (enzyme)

Gas, belly pain, bloating

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97
Q

Blood Glucose regulated by…

A

Insulin and glucagon

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98
Q

Normal Blood Glucose

A

70-100mg/dL (fasting)

Greater than or equal to 140 mg/dL (fed)

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99
Q

Hypoglycemia blood glucose levels

A

Equal to or less than 60 mg/dL

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100
Q

Diabetes Mellitus/Hyperglycemia blood glucose levels

A

Greater than or equal to 126 mg/dL

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101
Q

Less than 40 mg/dL blood glucose results in

A

Convulsions, coma, brain damage, death

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102
Q

Glycolysis

A

Metabolism of glucose

2 molecules ATP formed

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103
Q

2 cell types that require Glucose the most

A

RBCs - only source of energy because they do not have mitochondria

Brain cells favor glucose

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104
Q

Gluconeogenesis in the liver is called…

A

De Novo Synthesis

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105
Q

How does glucose get across the cell membrane into the cell

A

Via glucose transporters (GLUTs) in the cell membrane

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106
Q

GLUT 1

A

Ubiquitous but high in RBCs and BRAIN

High affinity for Glucose

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107
Q

GLUT 2

A

Main glucose transporter in the liver

Low affinity for glucose

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108
Q

GLUT 3

A

Main glucose transporter in neurons

High affinity for glucose

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109
Q

GLUT 4

A

Present in skeletal muscle, heart, adipose tissue

Regulated and dependent of insulin in order to transport glucose

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110
Q

Describe GLUT4 and how it comes to transport glucose in the PM

A
  1. Stored in vesicles within the cells
  2. Insulin signaling causes the vesicles to fuse to the PM to allow GLUT4 to be present in the PM
  3. GLUT4 then is able to induce glucose uptake
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111
Q

Under aerobic conditions, what can happen to pyruvate

A

Pyruvate can be completely oxidized generating much more ATP

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112
Q

Where does glycolysis occur within the cell?

A

Cytoplasm

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113
Q

3 Phases of Glycolysis

A
  1. Investment: requires 2 ATP
  2. Splitting: one 6 carbon molecule into 2, 3 carbon molecules
  3. Recoup/Payoff: 4 ATP molecules generated
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114
Q

He Okinawa and glucokinase are…

A

Isozymes that both phosphorylation glucose to G6P

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115
Q

In what cell types does Hexokinase work to phosphorylate glucose to G6P?

A

All cells

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116
Q

What cell types does Glucokinase work to phosphorylate glucose to G6P?

A

Liver
Pancreatic B cells

More specific than Hexokinase

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117
Q

What is the purpose of phosphorylation game glucose to G6P in glycolysis?

A

Traps glucose in the cell

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118
Q

What is Hexokinase’s affinity to glucose

A

HIGH, functional even at low concentrations of glucose

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119
Q

What is Glucokinase’s affinity for glucose

A

Low affinity for glucose

Most active when high glucose, like after a meal

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120
Q

Where does Glucokinase go in the presence of Fructose 6–P?

A

Translocation to the nucleus

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121
Q

What is PFK1 activated by?

A

AMP

F2,6BP

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122
Q

What is PFK1 inhibited by?

A

ATP, citrate

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123
Q

What inhibits Hexokinase?

A

Glucose 6 Phosphate

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124
Q

What activated glucokinase?

A

Glucose
Fructose 1 Phosphate
Insulin

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125
Q

What inhibits glucokinase?

A

Fructose 5 Phosphate

Glucagon

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126
Q

Hormonal Regulation of PFK1

What stimulates?
What inhibits?

A

Insulin stimulates

Glucagon inhibits

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127
Q

With hormonal regulation, what activates PFK1 activity?

A

High insulin

Low glucagon

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128
Q

With hormonal regulation, what inhibits PFK1 activity?

A

High glucagon

Low insulin

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129
Q

What activates Pyruvate Kinase (PK)?

A

F1,6BP

Insulin

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130
Q

What inhibits Pyruvate Kinase (PK)?

A

ATP
Alanine
Glucagon

131
Q

When is Pyruvate Kinase (PK) active?

A

High insulin

Which dephosphorylates PK

132
Q

When is Pyruvate Kinase (PK) inhibited?

A

High glucagon

Which phosphorylate PK

133
Q

Why is glycolysis inhibited at rest?

A

Negative feedback of G6P on Hexokinase inhibiting Hexokinase

Lots of ATP around inhibits PFK1 and Pyruvate Kinase

134
Q

4 Fates of Pyruvate

A
  1. Reduced to lactate
  2. Oxidized in TCA Cycle to acetyl CoA and then CO2
  3. Converted to Alanine
  4. Converted to ethanol
135
Q

What do most defects in glycolysis enzymes cause and what cell type is impacted the most?

A

Most defects lead to ineffective glycolysis and cause hemolytic anemias

Because RBCs are the cells impacted the most because they lack mitochondria

136
Q

What happen to RBCs when there is a deficiency in glycolysis?

A

ATP deficiency
Disruption of ion gradients
Reduced cell viability
Destruction of RBCs causes hemolytic anemia

137
Q

Why are brain cells particularly dependent on glucose?

A

Glucose is one of the only fuel molecules that can cross the blood brain barrier (BBB)

138
Q

How does the brain obtain glucose during starvation?

A

From the liver via gluconeogenesis

139
Q

What, besides glucose, can the brain use as fuel as the last resort?

A

Ketone bodies

140
Q

What happens to carbohydrate metabolism in the FED STATE

A

Abundant glucose

Increase uptake and trapping of glucose in the cell

Production of glycogen

Decreased gluconeogenesis

Increase in insulin

141
Q

What happens to carbohydrate metabolism in the FASTING STATE

A

Low glucose

Low insulin

Decrease uptake of glucose

More catabolism

Less storage

Increase in gluconeogenesis and glycogenolysis

142
Q

Type 1 Diabetes

A

Severe insulin deficiency due to loss of pancreatic beta cells

143
Q

Type 2 Diabetes

A

Insulin resistance that progresses to loss of beta cell function

144
Q

Hemolytic Anemia

A

Premature destruction of RBCs

145
Q

What are some of the many causes of Hemolytic Anemia?

A

Inherited defects in RBC membranes causing the cell to break

Hemoglobinopathies leading to cell conformation and collapse

Nutritional deficiencies

Infections

Defects in glycolysis enzymes

146
Q

Grams of glucose the body needs per day

A

160 grams

147
Q

Daily glucose requirement of brain in grams

A

About 120 grams

148
Q

Amount of glucose present in body fluids in grams

A

About 20 grams

149
Q

Amount of glucose readily available from glycogen in grams

A

About 190 grams

Only enough for one day

150
Q

What is Gluconeogenesis? Where does it occur? What are the major precursors?

A

Concerts Pyruvate —> glucose

Occurs in liver, kidney, small intestine

Major precursors are lactate, amino acids, glycerol

151
Q

Where is the gluconeogenesis enzyme Pyruvate Carboxylase (PC) found?

A

Mitochondria

152
Q

Which enzyme is the rate limiting step in gluconeogenesis?

A

Fructose 1,6 - biphosphatase

153
Q

Where is glucose 6 phosphatase located?

A

Lumen of the endoplasmic reticulum

154
Q

Cori Cycle

A

Takes lactate produced from anaerobic glycolysis in RBC and exercising muscle to…

Gluconeogenesis in the liver

Leaves muscle cell or RBC —> into the blood —> liver —> gluconeogenesis occurs to produce pyruvate from lactate —> pyruvate goes through gluconeogenesis to produce glucose

155
Q

Precursors of GLuconeogenesis

A

Glycerol (lipid degradation)

Propionate (degradation of odd numbered FA)

Alanine (protein degradation, pyruvate)

Amino Acids (protein degradation)

156
Q

F1,6BP deficiency

A

Disorder of Gluconeogenesis

Deficiency in ATP production because cannot make glucose from pyruvate

Presents in infancy or early childhood

157
Q

Von Gierke Disease (GSD1a)

A

Deficiency in Glucose 6- Phosphatase (in gluconeogenesis)

Free glucose is not formed and released into bloodstream by the liver

158
Q

Dietary source of Fructose

A

Sucrose —> FRUCTOSE + glucose

159
Q

Dietary source of Galactose

A

Lactose —> GALACTOSE + glucose

160
Q

Which GLUT uptakes fructose?

A

GLUT5

161
Q

Which transporter takes up Galactose and Glucose?

A

SGLT1

162
Q

Pentose Phosphate Pathway (PPP)

A

Another oxidative pathway for glucose metabolism

Produces no energy
Produces the sugar for DNA and RNA formation
Produces NADPH

163
Q

Where does Pentose Phosphate pathway occur?

A

Cytosol

164
Q

G6P dehydrogenase

A

Rate limiting step of pentose phosphate pathway

Oxidizes G6P

Reduces NADP+ to NADPH

165
Q

What is Glutathione and what is it regenerated by?

A

Antioxidant that detoxifies H2O2

Regenerated by NADPH

166
Q

How does high demand of Ribose 5P affect PPP?

A

OXIDATIVE PHASE favored to produce Ribulose 5P

167
Q

How does a high demand for NADPH affect PPP?

A

Non Oxidative products shunted into gluconeogenesis for re entry into PPP which produces NADPH

168
Q

What type of cells have very high PPP activity?

A

Phagocytic cells

169
Q

What types of bonds link together glucose molecules in a chain of glycogen?

A

Alpha 1,4 glycosidic bonds

170
Q

What type of bonds are at branch points of glycogen?

A

Alpha 1,6 glycosidic bonds

171
Q

Non reducing end of glycogen

A

Contain a terminal glucose with a free hydroxyl group at Carbon 4

172
Q

Reducing end of glycogen

A

Consists of glucose monomer connected to a protein called glycogenin

173
Q

Glycogenin of glycogen is connected to what part of the glycogen?

A

Reducing end

174
Q

Which end of glycogen is degraded and extended from?

A

Non reducing end

175
Q

Where is glycogen stored?

A

Mainly liver and muscle

But also other tissue

176
Q

How is glycogen stored?

A

As granules

177
Q

What all does a granule contain ?

A

Glycogen but also the enzymes needed for glycogen metabolism

178
Q

Liver glycogen function

A

Regulates blood glucose levels

179
Q

Muscle glycogen function

A

Provides reservoir of fuel (glucose) for physical activity

180
Q

Three Key steps of Glycogenesis

A
  1. Trapping and Activation of Glucose
  2. Elongation of a glycogen primer
  3. Branching of glycogen chains
181
Q

2 Key steps of Glycogenolysis

A
  1. Chain Shortening

2. Branch transfer and release glucose

182
Q

What does the enzyme Phosphoglucomutase do?

A

Reversible isomerizes G6P to G1P in glycogenesis (production of glycogen)

183
Q

What does the enzyme UDP-glucose pyrophosphorylase do?

A

Activates glucose in glycogenesis and generates UDP-glucose

184
Q

What does the enzyme glycogen synthase (GS) do?

A

Catalyzes transfer of glucose from UDP-glucose to non reducing end of the glycogen chain

185
Q

What does the enzyme glucose (4:4) transferase do?

A

Branching enzyme

Breaks a fragment of glycogen chain off once it reaches 11 residues to create a branch

186
Q

What does Glycogen phosphorylase (GP) use as a cofactor?

A

Pyridoxal phosphate (vitamin B6)

187
Q

What does Glycogen Phosphorylase (GP) do?

A

Catalyzes cleavage of glucose residues from non reducing end of glycogen

188
Q

What happens to Glu-1-P in the liver

A

Glu-1-P converted to Glu-6-P then to Glucose by glucose 6 phosphatase

Released into blood stream

189
Q

What happens to Glu-1-P in the muscle?

A

Skeletal and cardiac muscle lack glucose 6 phosphatase so cannot hydrolysis Glu-6-P

Instead generate energy via glycolysis and TCA cycle

190
Q

Rate limiting step of glycogenesis

A

Glycogen Synthase

191
Q

Rate limiting step for Glycogenolysis

A

Glycogen phosphorylase

192
Q

Glycogen synthase is active when…

A

It is dephosphorylated

193
Q

Glycogen synthase is inactive when…

A

It is phosphorylate

194
Q

Glycogen phosphorylase is active when…

A

It is phosphorylated

195
Q

Glycogen phosphorylase is inactive when…

A

It is dephosphorylated

196
Q

Why is Glycogenesis favored in FED STATE

A

Blood glucose is high

Insulin high

Cellular ATP high

197
Q

Why is Glycogenolysis favored in FASTING STATE?

A

Blood glucose is low

Glucagon High

198
Q

Why is Glycogenolysis favored during EXERCISE?

A

Cellular calcium high in exercising muscles

AMP high from breakdown of ATP

199
Q

Does Glucagon act on muscle?

A

No

200
Q

Prediabetic/ at risk Glucose level

A

100-125 mg/dL fasting

> 140 mg/dL fed

201
Q

Diabetes Mellitus Glucose levels

A

> 126 mg/dL fasting

> 199 mg/dL Fed

202
Q

Type 2 diabetes

A

INsulin resistance - not binding to insulin receptor

203
Q

4 Key enzymes for Insulin Regulation of Glucose and Glycogen

A

GLUT4

Protein Kinase B (PKB)

Protein Phosphatase 1 (PP1)

Glycogen synthase kinase 3 (GSK3)

204
Q

Key enzymes and second messengers of regulation by Glucagon of glucose and glycogen

A

G protein

Adenylate Cyclase (AC) and cAMP

Protein Kinase A (PKA)

Protein phosphatase 1 (PP1)

Phosphorylase kinase (PK)

205
Q

Other names for the Krebs Cycle?

A

Tricarboxylic acid cycle (TCA)

The Citric Acid Cycle

206
Q

Where does the TCA cycle take place?

A

Mitochondria

207
Q

TCA cycle is amphibolic, what does that mean?

A

Catabolism and Anabolism

208
Q

What is the overall function of TCA

A

Oxidizing carbon fuels for harvesting high energy electrons

209
Q

What molecules can contribute to the Acetyl CoA pool feeding the TCA cycle?

A

Fats
Polysaccharides
Proteins

210
Q

What is the activated form of acetate?

A

Acetyl CoA

211
Q

How does pyruvate enter the mitochondria to become Acetyl CoA and partake in TCA?

A

Via mitochondrial pyruvate carrier (MPC)

212
Q

What enzyme decarboxylates pyruvate into Acetyl CoA for TCA?

A

Pyruvate Dehydrogenase Complex (PDC)

213
Q

In a phosphatase deficiency how is PDC affected and what are the consequences?

A

PDC is phosphorylate and there for INACTIVE

Results in Lactic Acidosis (build up of lactic acid)

CNS effected the most

214
Q

In a High Energy State PDC/PDH is inhibited, by what?

A

ATP
Acetyl CoA
NADH

215
Q

In Low Energy State PDH/PDC is being activated, by what?

A

ADP
Pyruvate
High calcium levels

216
Q

Which step in TCA is rate limiting and what enzyme catalyzes this step?

A

Step 3: isocitrate to a-ketoglutarate

Isocitrate dehydrogenase

217
Q

The enzyme a-ketoglutarate dehydrogenase does what in TCA? Is it regulated?

A

A-ketoglutarate to Succinylcholine-CoA

Yes, regulated

218
Q

Products of TCA

A

2 CO2
1 FADHs
1 GTP
3 NADH

219
Q

What high energy substance is produced by TCA via substrate level phosphorylation?

A

GDP

220
Q

When cellular ATP levels are low, the activity of TCA cycle is…

A

Increased

221
Q

When cellular ATP levels are high, the TCA cycle is…

A

Inhibited

222
Q

What is the inhibition of TCA called when there are high levels of cellular ATP?

A

Mitochondrial ETC Inhiition

223
Q

Why is TCA cycle considered ANAPLEROTIC?

A

Reactions provide intermediate for replenishing the TCA cycle

224
Q

What are the two major anaplerotic reactions replenishing the TCA cycle?

A
  1. Degradation of AA

2. Carboxylation of Pyruvate

225
Q

Citrate from the TCA cycle can leave the mitochondria and be converted to?

A

Back into Acetyl CoA and then into FA and isprenoids

226
Q

Malate from the TCA cycle can leave the mitochondria and be converted into what?

A

First converted into OAA then phophoenopyruvate (PEP) and then finally to glucose

227
Q

Succinyl CoA can leave the TCA cycle and the mitochondria to be converted into?

A

Porphyrins then Heme

228
Q

Oxaloacetate (OAA) can be taken from TCA cycle to produce?

A

AAs:

Aspartate (Asp)
Asparagine (Asn)

229
Q

A-ketoglutarate can leave the TCA cycle and mitochondria to be converted to?

A

AAs:

Glutamate (Glu)
Glutamine (Gln), Proline (Pro), Arginine (Arg)

230
Q

Where does oxidative phosphorylation occur?

A

Mitchondrial Inner Membrane

231
Q

Two types of Redox Reactions

A
  1. The electron only transfer

2. Reducing equivalent transfer (Redox couples)

232
Q

Oil Rig

A

Oxidation Is Loss of electron

Reduction Is Gain of electrons

233
Q

The electron only transfer

A

Redox reaction where electrons are transferred between two METAL IONS

234
Q

Reducing - equivalent Transfer (Redox couple)

A

Transfer of a proton and an electron

235
Q

Standard Redox Potential (Eo’)

A

A measure of the affinity of a Redox pair of electrons

Unit: Volt (V)

236
Q

Lower Eo’ has low or higher affinity for electrons? Gives up or accepts electrons?

A

Lower affinity

Gives up electrons

237
Q

Higher Eo’ has a higher or lower affinity for electrons? Gives up or accepts electrons?

A

Higher affinity

Accepts electrons

238
Q

Eo’ of Reducing Agent

A

Smaller Eo’

Donates electrons

239
Q

Eo’ of Oxidizing Agent

A

Larger Eo’

Accepts electrons

240
Q

Relation of Delta Eo’ to Delta Go’

A

Inversely related

241
Q

3 Key Goals of OxPhos

A
  1. To transfer electrons
  2. Establish proton gradient
  3. Synthesize ATP
242
Q

Two factors of the Proton Motive Force that drives ATP synthesis?

A
  1. pH gradient: proton concentration high in intermembrane space of mitochondria, low in matrix
  2. Membrane potential: positive within intermembrane space and negative within matrix
243
Q

Membrane protein that catalyzes ATP synthesis

A

ATP synthase (Complex V)

244
Q

Cty-c in ETC

A

Receives electrons from complex III and gives electrons to complex IV

Attached to surface of inner membrane on intermembrane space

245
Q

CoQ (ubiquinone)

A

Electrons from complex II to complex III

Embedded in inner membrane

246
Q

Which complex does NADH provide electrons to in ETC?

A

Complex I

247
Q

Where does reduced FADH2 join to ETC?

A

CoQ

248
Q

What molecules inhibit complex I of ETC?

A

Amytal

Rotenone

Myxothiazol

Piercidin A

249
Q

What inhibits complex II in the ETC?

A

Mason ate

250
Q

What inhibits Complex III of ETC?

A

Antimycin

251
Q

What inhibits complex IV of ETC?

A

CO

Cyanide

H2S

252
Q

What inhibits ATP synthase (complex V) of ETC?

A

Oligomycin

253
Q

How does a High [ATP]/[ADP] affect OxPhos and ATP production?

A

Inhibits OxPhos because have plenty of ATP

254
Q

What happens to OxPhos/ATP production with a Low [ATP]/[ADP]?

A

OxPhos is activated

Need more ATP

255
Q

Describe what occurs when the ETC proton gradient is disrupted?

A

Phosphate does not bind with ADP to form ATP, it uncoupled form the electron transfer

Protons Renee tear the mitochondrial matrix from the inner membrane space

  • causes acceleration of TCA cycle and electron transfer to O2
  • ATP synthase is inhibited

Heat is generated by the cell

256
Q

Two Shuttle systems for reduced NADH which cannot cross the mitochondrial membrane

A
  1. Malate aspartate shuttle

2. Glycerophosphate shuttle

257
Q

Where does Malate Aspartate Shuttle operate and where does it generate reduced NADH?

A

Operated in heart, liver, kidney

Generates reduced NADH in mitochondrial matrix

258
Q

Where does the GLycerophosphate shuttle operate and where does it generate reduced FADH2?

A

Operates in skeletal muscle and brain

Generates reduced FADH2 in the inner mitochondrial membrane

259
Q

Functions of Lipids

A

Fuel stores
Structural components
Signaling molecules

260
Q

What is the major source of carbon for FA synthesis?

A

Dietary carbohydrates

261
Q

Where does FA synthesis occur?

A

Mainly in the liver

Adipose tissue

Brain, kidneys, lactating mammary glands

262
Q

FA Synthesis occurs in two different locations, where?

A

Cytosol and mitochondria

263
Q

Precursor of FA synthesis

A

Acetyl CoA

264
Q

Phase I of FA Synthesis

A

Cytosolic entry of Acetyl CoA

265
Q

Phase II of FA Synthesis

A

Generation of Malonyl CoA

Rate limiting step

266
Q

Phase III of FA synthesis

A

Fatty acid chain formation

267
Q

Which enzyme catalyzes the chain formation of FA?

A

Fatty Acid Synthase

268
Q

What promotes and inhibits ATP citrate lyase enzyme in FA synthesis?

A

Glucose and Insulin promote

PUFA and leptin inhibit

269
Q

Which enzyme converts OAA and Acetyl CoA to citrate in FA synthesis?
Why does it do this?

A

Citrate Synthase

Because Acetyl CoA needs to leave mitochondria and enter the cytosol for FA synthesis and it cannot freely pass the membrane and there is not a shuttle for it

270
Q

What enzyme converts citrate back to OAA and Acetyl CoA in FA synthesis?

A

ATP citrate lyase

271
Q

In FA synthesis, which enzyme catalyzes carboxylation of Acetyl CoA to Malonyl CoA (the rate limiting step)?

A

Acetyl CoA carboxylase

272
Q

What promotes and inhibits Acetyl CoA carboxylase enzyme in FA synthesis?

A

Promoted by Citrate and insulin

Inhibited by glucagon, epinephrine, high [AMP], palmitate, PUFA

273
Q

What does Acetyl CoA Carboxylase (ACC) use as a coenzyme?

A

Biotin

274
Q

What enzyme in FA degradation does Malonyl CoA inhibit?

A

Carnitine Acyltransferase

275
Q

What enzyme converts Malonyl CoA to Palmitate (FA) in FA synthesis?

A

Fatty Acid Synthase

276
Q

What promotes and inhibits Fatty Acid Synthase enzyme in the synthesis of FA?

A

Promoted by insulin, glucocorticoid hormones

Inhibited by PUFA

277
Q

How many carbon units are added and degraded at a time during FA synthesis and degradation?

A

2 carbons

278
Q

How many proteins make up Fatty Acid Synthase?

A

8

7 enzyme activities
1 acyl carrier protein

279
Q

Flexible arm of Acyl Carrier Protein (ACP) of FAS

A

Has a phoshphopantetheine group that picks up substrate and take to the next enzyme

280
Q

General reactions of FA synthesis?

A

Condensation, Reduction, Dehydration, Reduction

281
Q

PUFAs

A

Polyunsaturated Fatty Acids

282
Q

What stimulates ATP citrate lyase?

A

Phosphorylation

283
Q

Would long chain FA upregulate or down regulate Acetyl CoA Carboxylase

A

Down regulate

284
Q

Acetyl CoA Carboxylase (ACC) and its activity as a diner versus polymer

A

INACTIVE as a dimer

ACTIVE as a polymer

The longer it is, the more active it is

285
Q

Gene expression of Acetyl CoA Carboxylase up regulated by…

A

High carb/low fat diet

286
Q

Describe the allosteric effect of FAS regulation

A

Presence of phosphorylate day sugar increases FAS activity

287
Q

What represses FAS at gene level?

A

High fat diets
Starvation
High PUFA

All lower synthesis of FAS

288
Q

What induces FAS synthesis at the gene level?

A

Insulin
Glucocorticoid hormones
High carb/low fat diets

All increase synthesis of FAS

289
Q

Where does elongation of FA occur?

A

Smooth ER or mitochondria

290
Q

What does the smooth ER pathway of FA elongation use as a carbon donor?

A

Malonyl CoA

291
Q

What does the mitochondria pathway of FA elongation use as carbon donor?

A

Acetyl CoA

292
Q

What is desaturation of FA?

A

Introduction of double bonds

293
Q

What enzyme catalyzes desaturation of FA? Where does it occur? What is used to desaturated?

A

Acyl CoA Desaturases

Occurs in Smooth ER

Use HADPH or NADH and oxygen

294
Q

What are the four desaturasees that humans have ?

A

4, 5, 6, and 9

Cannot go past 9 when creating double bonds in humans

295
Q

What induces and reduces gene expression of desaturases?

A

Induced by insulin
Suppressed by dietary PUFAs

Dietary cholesterol induces delta 9 desaturase BUT suppresses all others

296
Q

Essential Fatty Acids

A

Linoleum Acid: used to make arachidonic acid

Linolenic acid: use to make eicosapentanoid acid

Used as precursors to build off of

297
Q

Phase I of FA oxidation (degradation)

A

Fatty Acid Activation

Occurs in cytosol

298
Q

Phase II of FA oxidation (degradation)

A

Beta Oxidation

Occurs mostly in the mitochondrial matrix

299
Q

What enzyme during FA oxidation activates FA with CoA to produce Fatty acyl CoA in order for FA to enter mitchondria?

A

Fatty Acyl CoA synthetase

300
Q

What enzyme in FA oxidation removes CoA from Fatty acyl CoA and adds carnitine to get the FA from the mitochondrial intermembrane space into the matrix?

A

Carnitine palmitoyltransferase I (CPT I)

RATE LIMITING

301
Q

What inhibits CPT I in the oxidation of FA?

A

Malonyl CoA

302
Q

Carnitine-acyl carnitine translocase

CACT) (Acyl Carnitine Traslocase) (Carnitine Shuttle

A

Shuttles Fatty acyl carnitine in FA oxidation from the inter membrane space across the inner membrane to the matrix

303
Q

What enzyme in FA oxidation converts Fatty acyl carnitine to Fatty acyl CoA in the matrix?

A

Carnitine palmitoyltransferase II (CPT II)

This releases carnitine which is then reused

304
Q

Beta Oxidation of FA Oxidation generates

A

Acetyl CoA (enter TCA)

FADH2 (ETC)

NADH (ETC)

305
Q

Four main steps fo B oxidation

A
  1. Oxidation
  2. Hydration
  3. Oxidation
  4. Thiolysis
306
Q

Which enzyme converts Fatty acyl CoA to Trans Fatty envoys CoA (oxidation)?

A

Acyl CoA dehydrogenase

Generates FADH2

307
Q

Which enzyme converts trans fatty enoyl CoA to B-hydroxyacyl CoA in FA oxidation (hydration step)?

A

Enoyl CoA Hydratase

308
Q

What enzyme converts B-hydroxyacyl CoA to B-ketoacyl via oxidation in FA oxidation?

A

3-hydroxyacyl CoA Dehydrogenase

309
Q

What enzyme cleaves B-ketoacyl CoA into Acetyl CoA and Fatty acyl CoA through thiolysis in FA oxidation?

A

Acetyl CoA acecyltransferase

310
Q

Two novel enzymes required for degradation of unsaturated FA

A

Reductase: reduces double bond

Isomerase: moves the disruptive bond

311
Q

Where does B-oxidation of very long FAs occur? Does it produce ATP? What does it produce? Is there some way to prevent this product from being toxic?

A

B-oxidation occurs in peroxisomes

Does not produce ATP

Produces hydrogen peroxide H2Oo2

Contains a catalase that converts H2O2 into H2O to prevent toxicity

312
Q

Where very large FA go through B oxidation in peroxisomes there is one step different, which step is it and what is the enzyme used?

A

Very first step, instead of ACAD, uses…

Acyl-CoA oxidase - the FADH2 produced here is then used to produce the hydrogen peroxide instead of being sent to the TCA cycle

313
Q

Three main ketone bodies

A
  1. Acetoacetate
  2. B-Hydroxybutyrate
  3. Acetone
314
Q

Where are ketone bodies produced?

A

Liver only

315
Q

Energy source first few hours of fasting

A

Blood glucose, followed by glycogen

316
Q

Energy source after 1 day of fasting

A

Triacylglycerids stored in adipose tissues

317
Q

Energy source after 3 days of fasting

A

Ketone bodies made in liver and proteins in muscles break down

318
Q

Energy source after 1-2 weeks of starvation

A

Brain switches to ketone bodies

319
Q

Energy source after 2-3 months of starvation

A

TAGs depleted, proteins are main source

Leads to coma and death

320
Q

Physiological Keaton’s is

A

Mild to moderate increase in ketone oldies

Can handle this

Fasting, during pregnancy, prolonged exercise, ketogenic diets

321
Q

Pathological ketoacidosis

A

When glucagon/insulin ratio is increased, favoring FA breakdown

Acidic condtions

Fatal

322
Q

Where does synthesis of ketone bodies occur?

A

Mitochondrial matrix of hepatocytes (liver)

323
Q

Can RBCs utilize ketone bodies

A

No

324
Q

What tissues/organs utilize ketone bodies?

A

Brain, muscle, kidneys

MCM (1 decks)

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