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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
How are Allosteric enzymes modulated?
Actively by non covalent binding of metabolite to another site than the catalytic site Causes conformational changes
26
These allosteric enzymes facilitate binding
Positive Effetors (activators)
27
These allosteric enzymes prevent binding of substrate
Negative Effectors (inhibitors)
28
Isozymes
Same catalytic function, different primary sequence Different biophysical properties Different binding sites
29
Pro enzymes (Zymogen)
Inactive precursor of enzyme Usually require proteolytic breakdown to become active Form of enzymatic regulation
30
Troponin in MI
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
31
% of calories from protein
10-15%
32
% of calories from fat
25-25%
33
Monosaccharides
Single sugar carbohydrate | Ex: glucose, fructose
34
Disaccharides
Two sugar carbohydrate | Ex: lactose
35
Polysacccharide
Multi sugar carbohydrate | Ex: glycogen
36
Lipid Examples
Fatty acids, triglycerides, membrane lipids, cholesterol and cholesterol esters, lipid soluble vitamins
37
Protein examples
Oligopeptides, polypeptides, amino acids
38
The Essential Amino Acids obtained from the diet
Leucine, isoleucine, valine, histidine, lysine, methionine, phenylalanine, threonine, tryptophan, arginine (in children)
39
Acidic Amino Acids
Aspartic Acid | Glutamic Acid
40
Basic Amino Acids
Arginine Histidine Lysine
41
Duodenum (proximal small intestine) Digests and Absorbs...
Fat Sugars Peptides and AA ``` Iron Folate Calcium Water Electrolytes ```
42
Ileum (distal small intestine) digests and absorbs...
Bile acids Vitamin B12 Water Electrolytes
43
Digested products are absorbed into...
Hepatic Portal System
44
Steatorrhea
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
45
Crohn Disease
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 ```
46
Lipid Soluble vitamins
A, D, K, E
47
Structure and Composition of the Plasma Membrane
Composed of lipids, proteins and carbohydrates Asymmetric bilayer Semi permeable Primary component is phospholipids Amphipathic - hydrophobic tails - hydrophilic heads
48
3 Membrane Lipids
Phospholipids Glycolipids Cholesterol
49
2 Types of Phospholipids
Glycerolphospholipids | Sphingolipids
50
Glycerolphospholipids
Phospholipids with a glycerol backbone | Plus a Phoshphate and two FA
51
Sphingolipids
Phospholipids with sphingosine backbone | Plus long FA and phosphorylcholine
52
Glycolipids
Membrane lipid with sphingosine backbone with a carbohydrate (oligosaccharide) residues OUTER LEAFLET
53
Cholesterol
Membrane lipids with steroid nucleus with hydroxyl group and hydrocarbon side chain EMBEDDED in lipid bilayer
54
Outer Sheet Membrane Lipids
Phosphatidylcholine Sphingomyelin Glycolipids
55
Membrane Lipids of Inner Sheet
Phosphatidylinositol Phosphatidylserine Phosphatidylethanolamine
56
Describe Phosphatidylserine (PS) as a marker for Apoptoosis
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
57
3 Types of Membrane Proteins
Integral Membrane proteins Peripheral proteins Lipid- anchored proteins
58
Integral membrane proteins
Firmly embedded in the membrane Stabilized by hydrophobic interactions with lipids
59
Polytopic Transmembrane proteins
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
60
Peripheral PRoteins
Membrane protein loosely bound to membrane | Electrostatic interactions with lipids or proteins
61
Lipid-anchored proteins
Tethered to membrane | Covalent attachment to a lipid
62
Glycocalyx
Carbohydrate shell on outer sheet of many membranes
63
3 Key Functions of Glycocalyx
Protection Cell Adhesion Cell Identification
64
Blood Type O
Antibodies for A and B H antigen Universal Donor
65
Blood Type A
Antibodies for B | Antigen A
66
Blood Type B
Antibody for A | B antigen
67
Blood Type AB
No antibodies Antigens A and B Universal acceptor
68
Rh Factor
D antigen inherited autosomal dominant fashion
69
Rh+
Express D antigen
70
Rh-
do NOT express D antigen
71
Erythroblastosis Fetalis
Disease in which incompatibility between blood of mother and fetus
72
Mom Rh- and Fetus RHh+
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
73
3 Factors Influencing Membrane Fluidity
Temperature Lipid Composition Cholesterol
74
Temp and Membrane Fluidity
Below Tm = membrane rigid, ordered packing Above Tm = membrane more fluid Too Above Tm can result in membrane being too fluid
75
Melting Temp of membrane
Temp at which membranes switch from fluid to rigid state
76
Lipid Effects on Membrane Fluidity
Saturated Lipids = decreased fluidity Unsaturated Lipids = increased Fluidity
77
Cholesterol effects on membrane fluidity
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
78
Spur Cell Anemia
Elevated Levels of Cholesterol in RBC membrane Decreases fluidity and flexibility RBC membrane breaks when passing through capillaries
79
Ion Concentrations outside Membrane Relatively
Na+ high K+ low Cl- high Ca2+ low
80
Ion Concentrations Inside the Membrane/Cell Relatively
Ca2+ higher Cl- lower K+ higher Na+ lower
81
Voltage Gated Na+ Channel
Brings Na+ into the cell via Facilitated Diffusion
82
Glucose Transporter (ex: GLUT1)
Brings glucose into the cell via facilitated diffusion
83
Ion Channels
Pores or gates, allow charged and polar molecules to pass through membrane down concentration gradient Open and close in response to a stimulus
84
Ligand Gated Ion Channels
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)
85
Voltage Gated Ion Channels
Open and close in response to change in membrane potential | Depolarization triggers the opening to allow specific ions to cross down concentration gradient
86
Tetrodotoxin
Poison in puffer fish that will inactivate Na+ channel
87
Process of transporting monosaccharides from intestinal lumen into enterocyte into the blood is facilitated by both...
Facilitated diffusion and | Active transport
88
What enters intestinal epithelial cells from lumen by SGLT1
Glucose, galactose, and Na+ via secondary active transport
89
What passes via GLUT2 from enterocyte to blood stream
Glucose, galactose, fructose via facilitated diffusion
90
How is fructose transported from lumen of intestine to epithelial cell
Facilitated diffusion by GLUT5 on apical side
91
How is Na+ transported into the blood stream from the epithelial intestinal cell
SGLT1 via primary active transport NA+/K+ ATPase Basolateral membrane
92
Describe Cardiotonic Drugs and Ouabain
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
93
Starch
Polysaccharide of GLUCOSE Carb storage in pants
94
Sucrose
Disaccharide of GLUCOSE and FRUCTOSE Fruits and vegetables
95
Lactose
Disaccharide of GLUCOSE and GALACTOSE Carbs of animal origin
96
Describe Lactose Intolerane
Body cannot digest lactose due to genetic deficiency in lactase Age dependent decrease in production of lactase (enzyme) Gas, belly pain, bloating
97
Blood Glucose regulated by...
Insulin and glucagon
98
Normal Blood Glucose
70-100mg/dL (fasting) Greater than or equal to 140 mg/dL (fed)
99
Hypoglycemia blood glucose levels
Equal to or less than 60 mg/dL
100
Diabetes Mellitus/Hyperglycemia blood glucose levels
Greater than or equal to 126 mg/dL
101
Less than 40 mg/dL blood glucose results in
Convulsions, coma, brain damage, death
102
Glycolysis
Metabolism of glucose | 2 molecules ATP formed
103
2 cell types that require Glucose the most
RBCs - only source of energy because they do not have mitochondria Brain cells favor glucose
104
Gluconeogenesis in the liver is called...
De Novo Synthesis
105
How does glucose get across the cell membrane into the cell
Via glucose transporters (GLUTs) in the cell membrane
106
GLUT 1
Ubiquitous but high in RBCs and BRAIN High affinity for Glucose
107
GLUT 2
Main glucose transporter in the liver Low affinity for glucose
108
GLUT 3
Main glucose transporter in neurons High affinity for glucose
109
GLUT 4
Present in skeletal muscle, heart, adipose tissue Regulated and dependent of insulin in order to transport glucose
110
Describe GLUT4 and how it comes to transport glucose in the PM
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
111
Under aerobic conditions, what can happen to pyruvate
Pyruvate can be completely oxidized generating much more ATP
112
Where does glycolysis occur within the cell?
Cytoplasm
113
3 Phases of Glycolysis
1. Investment: requires 2 ATP 2. Splitting: one 6 carbon molecule into 2, 3 carbon molecules 3. Recoup/Payoff: 4 ATP molecules generated
114
He Okinawa and glucokinase are...
Isozymes that both phosphorylation glucose to G6P
115
In what cell types does Hexokinase work to phosphorylate glucose to G6P?
All cells
116
What cell types does Glucokinase work to phosphorylate glucose to G6P?
Liver Pancreatic B cells More specific than Hexokinase
117
What is the purpose of phosphorylation game glucose to G6P in glycolysis?
Traps glucose in the cell
118
What is Hexokinase’s affinity to glucose
HIGH, functional even at low concentrations of glucose
119
What is Glucokinase’s affinity for glucose
Low affinity for glucose | Most active when high glucose, like after a meal
120
Where does Glucokinase go in the presence of Fructose 6–P?
Translocation to the nucleus
121
What is PFK1 activated by?
AMP | F2,6BP
122
What is PFK1 inhibited by?
ATP, citrate
123
What inhibits Hexokinase?
Glucose 6 Phosphate
124
What activated glucokinase?
Glucose Fructose 1 Phosphate Insulin
125
What inhibits glucokinase?
Fructose 5 Phosphate Glucagon
126
Hormonal Regulation of PFK1 What stimulates? What inhibits?
Insulin stimulates Glucagon inhibits
127
With hormonal regulation, what activates PFK1 activity?
High insulin | Low glucagon
128
With hormonal regulation, what inhibits PFK1 activity?
High glucagon | Low insulin
129
What activates Pyruvate Kinase (PK)?
F1,6BP | Insulin
130
What inhibits Pyruvate Kinase (PK)?
ATP Alanine Glucagon
131
When is Pyruvate Kinase (PK) active?
High insulin | Which dephosphorylates PK
132
When is Pyruvate Kinase (PK) inhibited?
High glucagon | Which phosphorylate PK
133
Why is glycolysis inhibited at rest?
Negative feedback of G6P on Hexokinase inhibiting Hexokinase Lots of ATP around inhibits PFK1 and Pyruvate Kinase
134
4 Fates of Pyruvate
1. Reduced to lactate 2. Oxidized in TCA Cycle to acetyl CoA and then CO2 3. Converted to Alanine 4. Converted to ethanol
135
What do most defects in glycolysis enzymes cause and what cell type is impacted the most?
Most defects lead to ineffective glycolysis and cause hemolytic anemias Because RBCs are the cells impacted the most because they lack mitochondria
136
What happen to RBCs when there is a deficiency in glycolysis?
ATP deficiency Disruption of ion gradients Reduced cell viability Destruction of RBCs causes hemolytic anemia
137
Why are brain cells particularly dependent on glucose?
Glucose is one of the only fuel molecules that can cross the blood brain barrier (BBB)
138
How does the brain obtain glucose during starvation?
From the liver via gluconeogenesis
139
What, besides glucose, can the brain use as fuel as the last resort?
Ketone bodies
140
What happens to carbohydrate metabolism in the FED STATE
Abundant glucose Increase uptake and trapping of glucose in the cell Production of glycogen Decreased gluconeogenesis Increase in insulin
141
What happens to carbohydrate metabolism in the FASTING STATE
Low glucose Low insulin Decrease uptake of glucose More catabolism Less storage Increase in gluconeogenesis and glycogenolysis
142
Type 1 Diabetes
Severe insulin deficiency due to loss of pancreatic beta cells
143
Type 2 Diabetes
Insulin resistance that progresses to loss of beta cell function
144
Hemolytic Anemia
Premature destruction of RBCs
145
What are some of the many causes of Hemolytic Anemia?
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
Grams of glucose the body needs per day
160 grams
147
Daily glucose requirement of brain in grams
About 120 grams
148
Amount of glucose present in body fluids in grams
About 20 grams
149
Amount of glucose readily available from glycogen in grams
About 190 grams Only enough for one day
150
What is Gluconeogenesis? Where does it occur? What are the major precursors?
Concerts Pyruvate —> glucose Occurs in liver, kidney, small intestine Major precursors are lactate, amino acids, glycerol
151
Where is the gluconeogenesis enzyme Pyruvate Carboxylase (PC) found?
Mitochondria
152
Which enzyme is the rate limiting step in gluconeogenesis?
Fructose 1,6 - biphosphatase
153
Where is glucose 6 phosphatase located?
Lumen of the endoplasmic reticulum
154
Cori Cycle
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
Precursors of GLuconeogenesis
Glycerol (lipid degradation) Propionate (degradation of odd numbered FA) Alanine (protein degradation, pyruvate) Amino Acids (protein degradation)
156
F1,6BP deficiency
Disorder of Gluconeogenesis Deficiency in ATP production because cannot make glucose from pyruvate Presents in infancy or early childhood
157
Von Gierke Disease (GSD1a)
Deficiency in Glucose 6- Phosphatase (in gluconeogenesis) Free glucose is not formed and released into bloodstream by the liver
158
Dietary source of Fructose
Sucrose —> FRUCTOSE + glucose
159
Dietary source of Galactose
Lactose —> GALACTOSE + glucose
160
Which GLUT uptakes fructose?
GLUT5
161
Which transporter takes up Galactose and Glucose?
SGLT1
162
Pentose Phosphate Pathway (PPP)
Another oxidative pathway for glucose metabolism Produces no energy Produces the sugar for DNA and RNA formation Produces NADPH
163
Where does Pentose Phosphate pathway occur?
Cytosol
164
G6P dehydrogenase
Rate limiting step of pentose phosphate pathway Oxidizes G6P Reduces NADP+ to NADPH
165
What is Glutathione and what is it regenerated by?
Antioxidant that detoxifies H2O2 Regenerated by NADPH
166
How does high demand of Ribose 5P affect PPP?
OXIDATIVE PHASE favored to produce Ribulose 5P
167
How does a high demand for NADPH affect PPP?
Non Oxidative products shunted into gluconeogenesis for re entry into PPP which produces NADPH
168
What type of cells have very high PPP activity?
Phagocytic cells
169
What types of bonds link together glucose molecules in a chain of glycogen?
Alpha 1,4 glycosidic bonds
170
What type of bonds are at branch points of glycogen?
Alpha 1,6 glycosidic bonds
171
Non reducing end of glycogen
Contain a terminal glucose with a free hydroxyl group at Carbon 4
172
Reducing end of glycogen
Consists of glucose monomer connected to a protein called glycogenin
173
Glycogenin of glycogen is connected to what part of the glycogen?
Reducing end
174
Which end of glycogen is degraded and extended from?
Non reducing end
175
Where is glycogen stored?
Mainly liver and muscle But also other tissue
176
How is glycogen stored?
As granules
177
What all does a granule contain ?
Glycogen but also the enzymes needed for glycogen metabolism
178
Liver glycogen function
Regulates blood glucose levels
179
Muscle glycogen function
Provides reservoir of fuel (glucose) for physical activity
180
Three Key steps of Glycogenesis
1. Trapping and Activation of Glucose 2. Elongation of a glycogen primer 3. Branching of glycogen chains
181
2 Key steps of Glycogenolysis
1. Chain Shortening | 2. Branch transfer and release glucose
182
What does the enzyme Phosphoglucomutase do?
Reversible isomerizes G6P to G1P in glycogenesis (production of glycogen)
183
What does the enzyme UDP-glucose pyrophosphorylase do?
Activates glucose in glycogenesis and generates UDP-glucose
184
What does the enzyme glycogen synthase (GS) do?
Catalyzes transfer of glucose from UDP-glucose to non reducing end of the glycogen chain
185
What does the enzyme glucose (4:4) transferase do?
Branching enzyme Breaks a fragment of glycogen chain off once it reaches 11 residues to create a branch
186
What does Glycogen phosphorylase (GP) use as a cofactor?
Pyridoxal phosphate (vitamin B6)
187
What does Glycogen Phosphorylase (GP) do?
Catalyzes cleavage of glucose residues from non reducing end of glycogen
188
What happens to Glu-1-P in the liver
Glu-1-P converted to Glu-6-P then to Glucose by glucose 6 phosphatase Released into blood stream
189
What happens to Glu-1-P in the muscle?
Skeletal and cardiac muscle lack glucose 6 phosphatase so cannot hydrolysis Glu-6-P Instead generate energy via glycolysis and TCA cycle
190
Rate limiting step of glycogenesis
Glycogen Synthase
191
Rate limiting step for Glycogenolysis
Glycogen phosphorylase
192
Glycogen synthase is active when...
It is dephosphorylated
193
Glycogen synthase is inactive when...
It is phosphorylate
194
Glycogen phosphorylase is active when...
It is phosphorylated
195
Glycogen phosphorylase is inactive when...
It is dephosphorylated
196
Why is Glycogenesis favored in FED STATE
Blood glucose is high Insulin high Cellular ATP high
197
Why is Glycogenolysis favored in FASTING STATE?
Blood glucose is low Glucagon High
198
Why is Glycogenolysis favored during EXERCISE?
Cellular calcium high in exercising muscles AMP high from breakdown of ATP
199
Does Glucagon act on muscle?
No
200
Prediabetic/ at risk Glucose level
100-125 mg/dL fasting >140 mg/dL fed
201
Diabetes Mellitus Glucose levels
>126 mg/dL fasting >199 mg/dL Fed
202
Type 2 diabetes
INsulin resistance - not binding to insulin receptor
203
4 Key enzymes for Insulin Regulation of Glucose and Glycogen
GLUT4 Protein Kinase B (PKB) Protein Phosphatase 1 (PP1) Glycogen synthase kinase 3 (GSK3)
204
Key enzymes and second messengers of regulation by Glucagon of glucose and glycogen
G protein Adenylate Cyclase (AC) and cAMP Protein Kinase A (PKA) Protein phosphatase 1 (PP1) Phosphorylase kinase (PK)
205
Other names for the Krebs Cycle?
Tricarboxylic acid cycle (TCA) The Citric Acid Cycle
206
Where does the TCA cycle take place?
Mitochondria
207
TCA cycle is amphibolic, what does that mean?
Catabolism and Anabolism
208
What is the overall function of TCA
Oxidizing carbon fuels for harvesting high energy electrons
209
What molecules can contribute to the Acetyl CoA pool feeding the TCA cycle?
Fats Polysaccharides Proteins
210
What is the activated form of acetate?
Acetyl CoA
211
How does pyruvate enter the mitochondria to become Acetyl CoA and partake in TCA?
Via mitochondrial pyruvate carrier (MPC)
212
What enzyme decarboxylates pyruvate into Acetyl CoA for TCA?
Pyruvate Dehydrogenase Complex (PDC)
213
In a phosphatase deficiency how is PDC affected and what are the consequences?
PDC is phosphorylate and there for INACTIVE Results in Lactic Acidosis (build up of lactic acid) CNS effected the most
214
In a High Energy State PDC/PDH is inhibited, by what?
ATP Acetyl CoA NADH
215
In Low Energy State PDH/PDC is being activated, by what?
ADP Pyruvate High calcium levels
216
Which step in TCA is rate limiting and what enzyme catalyzes this step?
Step 3: isocitrate to a-ketoglutarate Isocitrate dehydrogenase
217
The enzyme a-ketoglutarate dehydrogenase does what in TCA? Is it regulated?
A-ketoglutarate to Succinylcholine-CoA Yes, regulated
218
Products of TCA
2 CO2 1 FADHs 1 GTP 3 NADH
219
What high energy substance is produced by TCA via substrate level phosphorylation?
GDP
220
When cellular ATP levels are low, the activity of TCA cycle is...
Increased
221
When cellular ATP levels are high, the TCA cycle is...
Inhibited
222
What is the inhibition of TCA called when there are high levels of cellular ATP?
Mitochondrial ETC Inhiition
223
Why is TCA cycle considered ANAPLEROTIC?
Reactions provide intermediate for replenishing the TCA cycle
224
What are the two major anaplerotic reactions replenishing the TCA cycle?
1. Degradation of AA | 2. Carboxylation of Pyruvate
225
Citrate from the TCA cycle can leave the mitochondria and be converted to?
Back into Acetyl CoA and then into FA and isprenoids
226
Malate from the TCA cycle can leave the mitochondria and be converted into what?
First converted into OAA then phophoenopyruvate (PEP) and then finally to glucose
227
Succinyl CoA can leave the TCA cycle and the mitochondria to be converted into?
Porphyrins then Heme
228
Oxaloacetate (OAA) can be taken from TCA cycle to produce?
AAs: Aspartate (Asp) Asparagine (Asn)
229
A-ketoglutarate can leave the TCA cycle and mitochondria to be converted to?
AAs: Glutamate (Glu) Glutamine (Gln), Proline (Pro), Arginine (Arg)
230
Where does oxidative phosphorylation occur?
Mitchondrial Inner Membrane
231
Two types of Redox Reactions
1. The electron only transfer | 2. Reducing equivalent transfer (Redox couples)
232
Oil Rig
Oxidation Is Loss of electron Reduction Is Gain of electrons
233
The electron only transfer
Redox reaction where electrons are transferred between two METAL IONS
234
Reducing - equivalent Transfer (Redox couple)
Transfer of a proton and an electron
235
Standard Redox Potential (Eo’)
A measure of the affinity of a Redox pair of electrons Unit: Volt (V)
236
Lower Eo’ has low or higher affinity for electrons? Gives up or accepts electrons?
Lower affinity | Gives up electrons
237
Higher Eo’ has a higher or lower affinity for electrons? Gives up or accepts electrons?
Higher affinity | Accepts electrons
238
Eo’ of Reducing Agent
Smaller Eo’ | Donates electrons
239
Eo’ of Oxidizing Agent
Larger Eo’ | Accepts electrons
240
Relation of Delta Eo’ to Delta Go’
Inversely related
241
3 Key Goals of OxPhos
1. To transfer electrons 2. Establish proton gradient 3. Synthesize ATP
242
Two factors of the Proton Motive Force that drives ATP synthesis?
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
Membrane protein that catalyzes ATP synthesis
ATP synthase (Complex V)
244
Cty-c in ETC
Receives electrons from complex III and gives electrons to complex IV Attached to surface of inner membrane on intermembrane space
245
CoQ (ubiquinone)
Electrons from complex II to complex III Embedded in inner membrane
246
Which complex does NADH provide electrons to in ETC?
Complex I
247
Where does reduced FADH2 join to ETC?
CoQ
248
What molecules inhibit complex I of ETC?
Amytal Rotenone Myxothiazol Piercidin A
249
What inhibits complex II in the ETC?
Mason ate
250
What inhibits Complex III of ETC?
Antimycin
251
What inhibits complex IV of ETC?
CO Cyanide H2S
252
What inhibits ATP synthase (complex V) of ETC?
Oligomycin
253
How does a High [ATP]/[ADP] affect OxPhos and ATP production?
Inhibits OxPhos because have plenty of ATP
254
What happens to OxPhos/ATP production with a Low [ATP]/[ADP]?
OxPhos is activated | Need more ATP
255
Describe what occurs when the ETC proton gradient is disrupted?
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
Two Shuttle systems for reduced NADH which cannot cross the mitochondrial membrane
1. Malate aspartate shuttle | 2. Glycerophosphate shuttle
257
Where does Malate Aspartate Shuttle operate and where does it generate reduced NADH?
Operated in heart, liver, kidney Generates reduced NADH in mitochondrial matrix
258
Where does the GLycerophosphate shuttle operate and where does it generate reduced FADH2?
Operates in skeletal muscle and brain Generates reduced FADH2 in the inner mitochondrial membrane
259
Functions of Lipids
Fuel stores Structural components Signaling molecules
260
What is the major source of carbon for FA synthesis?
Dietary carbohydrates
261
Where does FA synthesis occur?
Mainly in the liver Adipose tissue Brain, kidneys, lactating mammary glands
262
FA Synthesis occurs in two different locations, where?
Cytosol and mitochondria
263
Precursor of FA synthesis
Acetyl CoA
264
Phase I of FA Synthesis
Cytosolic entry of Acetyl CoA
265
Phase II of FA Synthesis
Generation of Malonyl CoA | Rate limiting step
266
Phase III of FA synthesis
Fatty acid chain formation
267
Which enzyme catalyzes the chain formation of FA?
Fatty Acid Synthase
268
What promotes and inhibits ATP citrate lyase enzyme in FA synthesis?
Glucose and Insulin promote PUFA and leptin inhibit
269
Which enzyme converts OAA and Acetyl CoA to citrate in FA synthesis? Why does it do this?
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
What enzyme converts citrate back to OAA and Acetyl CoA in FA synthesis?
ATP citrate lyase
271
In FA synthesis, which enzyme catalyzes carboxylation of Acetyl CoA to Malonyl CoA (the rate limiting step)?
Acetyl CoA carboxylase
272
What promotes and inhibits Acetyl CoA carboxylase enzyme in FA synthesis?
Promoted by Citrate and insulin Inhibited by glucagon, epinephrine, high [AMP], palmitate, PUFA
273
What does Acetyl CoA Carboxylase (ACC) use as a coenzyme?
Biotin
274
What enzyme in FA degradation does Malonyl CoA inhibit?
Carnitine Acyltransferase
275
What enzyme converts Malonyl CoA to Palmitate (FA) in FA synthesis?
Fatty Acid Synthase
276
What promotes and inhibits Fatty Acid Synthase enzyme in the synthesis of FA?
Promoted by insulin, glucocorticoid hormones Inhibited by PUFA
277
How many carbon units are added and degraded at a time during FA synthesis and degradation?
2 carbons
278
How many proteins make up Fatty Acid Synthase?
8 7 enzyme activities 1 acyl carrier protein
279
Flexible arm of Acyl Carrier Protein (ACP) of FAS
Has a phoshphopantetheine group that picks up substrate and take to the next enzyme
280
General reactions of FA synthesis?
Condensation, Reduction, Dehydration, Reduction
281
PUFAs
Polyunsaturated Fatty Acids
282
What stimulates ATP citrate lyase?
Phosphorylation
283
Would long chain FA upregulate or down regulate Acetyl CoA Carboxylase
Down regulate
284
Acetyl CoA Carboxylase (ACC) and its activity as a diner versus polymer
INACTIVE as a dimer ACTIVE as a polymer The longer it is, the more active it is
285
Gene expression of Acetyl CoA Carboxylase up regulated by...
High carb/low fat diet
286
Describe the allosteric effect of FAS regulation
Presence of phosphorylate day sugar increases FAS activity
287
What represses FAS at gene level?
High fat diets Starvation High PUFA All lower synthesis of FAS
288
What induces FAS synthesis at the gene level?
Insulin Glucocorticoid hormones High carb/low fat diets All increase synthesis of FAS
289
Where does elongation of FA occur?
Smooth ER or mitochondria
290
What does the smooth ER pathway of FA elongation use as a carbon donor?
Malonyl CoA
291
What does the mitochondria pathway of FA elongation use as carbon donor?
Acetyl CoA
292
What is desaturation of FA?
Introduction of double bonds
293
What enzyme catalyzes desaturation of FA? Where does it occur? What is used to desaturated?
Acyl CoA Desaturases Occurs in Smooth ER Use HADPH or NADH and oxygen
294
What are the four desaturasees that humans have ?
4, 5, 6, and 9 Cannot go past 9 when creating double bonds in humans
295
What induces and reduces gene expression of desaturases?
Induced by insulin Suppressed by dietary PUFAs Dietary cholesterol induces delta 9 desaturase BUT suppresses all others
296
Essential Fatty Acids
Linoleum Acid: used to make arachidonic acid Linolenic acid: use to make eicosapentanoid acid Used as precursors to build off of
297
Phase I of FA oxidation (degradation)
Fatty Acid Activation Occurs in cytosol
298
Phase II of FA oxidation (degradation)
Beta Oxidation Occurs mostly in the mitochondrial matrix
299
What enzyme during FA oxidation activates FA with CoA to produce Fatty acyl CoA in order for FA to enter mitchondria?
Fatty Acyl CoA synthetase
300
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?
Carnitine palmitoyltransferase I (CPT I) RATE LIMITING
301
What inhibits CPT I in the oxidation of FA?
Malonyl CoA
302
Carnitine-acyl carnitine translocase | CACT) (Acyl Carnitine Traslocase) (Carnitine Shuttle
Shuttles Fatty acyl carnitine in FA oxidation from the inter membrane space across the inner membrane to the matrix
303
What enzyme in FA oxidation converts Fatty acyl carnitine to Fatty acyl CoA in the matrix?
Carnitine palmitoyltransferase II (CPT II) This releases carnitine which is then reused
304
Beta Oxidation of FA Oxidation generates
Acetyl CoA (enter TCA) FADH2 (ETC) NADH (ETC)
305
Four main steps fo B oxidation
1. Oxidation 2. Hydration 3. Oxidation 4. Thiolysis
306
Which enzyme converts Fatty acyl CoA to Trans Fatty envoys CoA (oxidation)?
Acyl CoA dehydrogenase Generates FADH2
307
Which enzyme converts trans fatty enoyl CoA to B-hydroxyacyl CoA in FA oxidation (hydration step)?
Enoyl CoA Hydratase
308
What enzyme converts B-hydroxyacyl CoA to B-ketoacyl via oxidation in FA oxidation?
3-hydroxyacyl CoA Dehydrogenase
309
What enzyme cleaves B-ketoacyl CoA into Acetyl CoA and Fatty acyl CoA through thiolysis in FA oxidation?
Acetyl CoA acecyltransferase
310
Two novel enzymes required for degradation of unsaturated FA
Reductase: reduces double bond Isomerase: moves the disruptive bond
311
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?
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
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?
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
Three main ketone bodies
1. Acetoacetate 2. B-Hydroxybutyrate 3. Acetone
314
Where are ketone bodies produced?
Liver only
315
Energy source first few hours of fasting
Blood glucose, followed by glycogen
316
Energy source after 1 day of fasting
Triacylglycerids stored in adipose tissues
317
Energy source after 3 days of fasting
Ketone bodies made in liver and proteins in muscles break down
318
Energy source after 1-2 weeks of starvation
Brain switches to ketone bodies
319
Energy source after 2-3 months of starvation
TAGs depleted, proteins are main source Leads to coma and death
320
Physiological Keaton’s is
Mild to moderate increase in ketone oldies Can handle this Fasting, during pregnancy, prolonged exercise, ketogenic diets
321
Pathological ketoacidosis
When glucagon/insulin ratio is increased, favoring FA breakdown Acidic condtions Fatal
322
Where does synthesis of ketone bodies occur?
Mitochondrial matrix of hepatocytes (liver)
323
Can RBCs utilize ketone bodies
No
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What tissues/organs utilize ketone bodies?
Brain, muscle, kidneys

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