Vmd403 Midterm 2

Front 1

What is Cerebrocortical Necrosis?

Back 1

deficient thiamine
mitochondria cannot complete TCA
(2 steps powered by thiamine)
hypoxia/ischemia

Front 2

Advantage of endosymbiosis of eukaryote + mitochondria?

Back 2

Eukaryote: nucleus
Mitochondria: oxidative metabolism

Front 3

Mitochondrial membranes?

Back 3

Inner: bigger, more selective

Front 4

Where does TCA occur?

Back 4

Inside mitochondrial matrix

Front 5

What are electron carriers for TCA?

Back 5

NADH, FADH2

Front 6

Terminal electron acceptor of the Electron Transport Chain

Back 6

Oxygen

Front 7

Mitochondrial diseases

Back 7

-Lactic acidosis
-Thiamine deficiency (cerebrocortical necrosis) (cattle, horses, ruminants, rats)
-Difluoroacetate poisoning (cattle)
-Sorghum-Johnson grass poisoning (cattle, horses)

Front 8

mitochondrial vestiges

Back 8

own membrane, own DNA, own ribosomes, own selectively permeable transporters

Front 9

what gets converted to AcetylCoA to go through TCA?

Back 9

Carbohydrates, proteins, fats

Front 10

Products of TCA (AcetylCoA and Oxygen)?

Back 10

CO2, H2O, & reduced electron carriers (NADH/FADH2)

Front 11

Function of reduced electron carriers in the mitochondria?

Back 11

Create a proton gradient to drive Electron Transport Chain

Front 12

Gas exchange by mitochondria?

Back 12

Reduce O2 to H2O, Produce CO2; major O2 consumer in tissues

Front 13

TCA: C2 + C4 --> C6; Name the players!

Back 13

C2: AcetylCoA
C4: Oxaloacetate
C6: Citrate

Front 14

One AcetylCoA produces (via TCA)?

Back 14

3 NADH
1 FADH2
1 "substrate level" GTP

Front 15

NADH produces (via TCA)?
FADH2?
GTP?

Back 15

NADH: 3 ATP
FADH2: 2 ATP
GTP: ~1 ATP

Front 16

Major TCA cycle regulating enzyme

Back 16

Pyruvate DeHydrogenase (PDH)

Front 17

Substrates & products for PDH?

Back 17

Pyruvate + CoA-SH + NAD+ + Thiamine --> AcetylCoA + NADH + CO2

Front 18

In PDH, electrons for NADH come from?

Back 18

FADH2

Front 19

3 driving reactions of 1st half of TCA?
Common feature of these 3?

Back 19

Citrate synthase
Isocitrate dehydrogenase
a-ketoglutarate dehydrogenase
All have large, negative d-G

Front 20

Function of aconitase & special feature?

Back 20

Isomerization, most sensitive to oxidative stress (dies); targeted by some pesticides

Front 21

2 steps of TCA with oxidative decarboxylation?

Back 21

Isocitrate dehydrogenase (Isocitrate to a-Ketoglutatate)
a-ketoglutarate dehydrogenase (a-ketoglutarate to Succinyl CoA)
BOTH PRODUCE NADH

Front 22

Where does substrate-level phosphorylation happen in TCA?

Back 22

Succinyl-CoA to Succinate via succinyl-CoA synthetase, form CoA-SH and GTP from GDP (and ATP to GTP)

Front 23

Where is succinate dehydrogenase found?

Back 23

IN the mitochondrial membrane

Front 24

Succinate dehydrogenase: substrates?

Back 24

Succinate, receives electrons from succinate and transfers them to FADH to make FADH2-->ETC/ATP, oxidize succinate to make fumarate

Front 25

Fumarase: what kind of rxn?

Back 25

Hydration

Front 26

malate dehydrogenate: how do you keep TCA going? What does MDH have to do with that?

Back 26

Keep LOW oxaloacetate concentrations; equilibrium of MDH lies towards malate, away from OA; keeps TCA going.

Front 27

How many ATP per NADH?

Back 27

6

Front 28

How many ATP per TCA?

Back 28

1 (substrate-level)

Front 29

How many ATP per PDH?

Back 29

6 (one NADH)

Front 30

How many ATP per TCA?

Back 30

~18

Front 31

What 2 steps require Thiamine?

Back 31

PDH (pyruvate to AcetylCoA)
a-ketoglutarate dehydrogenase (a-ketolutarate to succinyl-CoA)

Front 32

2 ways to stop TCA?

Back 32

Thiamine deficiency
Hypoxia

Front 33

Stop TCA: buildup of?

Back 33

pyruvate

Front 34

Excess pyruvate leads to?

Back 34

Pyruvate (Lactate Dehydrogenase) Lactate; Lactic acidosis

Front 35

TCA biosynthesis: citrate

Back 35

Fatty acids, sterols (OUTSIDE mitochondria, in cytosol)

Front 36

Biosynthesis from: a-ketoglutarate

Back 36

Amino acids, nucleotide precursors (purines)

Front 37

Biosynthesis from: succinyl-CoA

Back 37

Porphyrins, heme

Front 38

Biosynthesis from: malate

Back 38

OA to GNG OR OA to aspartate, aspartate to Asn, pyruvte, pyrimidines

Front 39

Other ways to make NADH/FADH2; why TCA?

Back 39

Pre-existed aerobic metabolism

Front 40

Define: anaplerotic reaction

Back 40

replenish intermediates as they're used for biosynthetic precursors

Front 41

3 most important intermediates of TCA to be replenished?

Back 41

Pyruvate carboxylase
PEP carboxykinase
Malic enzyme

Front 42

Why is Pyruvate carboxylase important?

Back 42

Keeps OA levels low enough to keep malate going, ensure that it doesn't get too low; it is inactive without AcetylCoA

Front 43

Limiting intermediate of TCA?

Back 43

[Oxaloacetate]

Front 44

In fed state, how is PDH regulated?

Back 44

Phosphorylated to lower activity; phosphorylated by kinases regulated by NADH, AcetylCoA, ATP

Front 45

In fasted state, how is PDH regulated?

Back 45

Kinase activity inhibited by high [pyruvate], unphosphorylated PDH has high activity; Ca++ release activates phosphatase, Ca++ can go through mitochondrial membrane

Front 46

Citrate synthase as a regulator?

Back 46

Substrates: oxaloacetate and acetyl-CoA; [oxaloacetate] very low, citrate synthase is NEVER fully saturated, OA is the limiting factor; pyruvate carboxylase can stimulate TCA

Front 47

Major overall big picture regulator of TCA?

Back 47

Electron transport chain; COMPLETELY coupled!

Front 48

How are reducing agents of TCA oxidized?

Back 48

Oxidized in electron transport chain

Front 49

Where in TCA is FAD required?

Back 49

Succinate dehydrogenase

Front 50

What are NAD+ and FAD for the TCA cycle supplied by?

Back 50

ETC

Front 51

First physiological clinical finding of hypoxia?

Back 51

Encephalopathy

Front 52

What foods contain thiaminase?

Back 52

Decomposed raw fish, bracken fern

Front 53

Clinical symptoms of thiamine deficiency?

Back 53

Neurological

Front 54

What two steps of the TCA require thiamine?

Back 54

Pyruvate dehydrogenase
a-ketoglutarate dehydrogenase

Front 55

Signs of thiamine deficiency?

Back 55

Extensor rigidity, vestibular ataxia

Front 56

Name of thiamine deficiency in sheep?

Back 56

Cerebrocortical necrosis

Front 57

Thiamine deficiency degenerates what neurological type of tissue?

Back 57

Gray matter

Front 58

What can thiamine cause in ruminants?

Back 58

Cortical blindness
Dementia

Front 59

Diagnostic marker of thiamine deficiency?

Back 59

Dysfunctional TCA
High [lactate]
High [pyruvate]
Low red blood cell transketolase activity (G3P<-->Ribose5P)

Front 60

Ischemia

Back 60

Low blood flow

Front 61

Anoxia

Back 61

No oxygen at all
Loss of mitochondrial function
Tissue damage

Front 62

Where does ETC occur?

Back 62

Inner mitorchondrial membrane

Front 63

Where does TCA occur?

Back 63

Mitochondrial matrix

Front 64

ETC is energetically...

Back 64

Exergonic (spontaneous)

Front 65

ETC complexes I and II both feed...

Back 65

CoQ

Front 66

ETC complex III feeds?

Back 66

CytC, some energy will be lost as heat

Front 67

Why is electron flow spontaneous in ETC?

Back 67

Each step has higher affinity for electrons than the last

Front 68

Order of ETC?

Back 68

NADH to complex I/II to CoQ to complex III to CytC to complex IV to 1/2 O2 + 2H + 2e- ==> H2O

Front 69

CoQ is also known as...
And accepts...

Back 69

Ubiquinone
Electrons-- "universal electron acceptor"

Front 70

How was the order of ETC worked out/how do you tell what step is faulty?

Back 70

Lots of heme-like cytochromes (CytC), have unique spectrums if oxidized or reduced

Front 71

Mitochondrial "charged" state?

Back 71

100mV

Front 72

Increased intracellular [ADP] activates what enzyme?

Back 72

ATP synthase

Front 73

Problem with ATP synthase and mitochondrial charge?

Back 73

ATP synthase consumes membrane potential to make ATP from ADP and Pi

Front 74

How does mitochondria restore charge after ATP synthase is activated?

Back 74

ETC: consumes O2, NADH, FADH2

Front 75

Mitochondrial myopathy?

Back 75

Horse-exercise intolerance
Low O2 consumption, high plasma [lactate]
missing complex I --> CoQ, generates NAD+ (complex II insufficient)

Front 76

Why is brown fat brown?

Back 76

Mitochondria

Front 77

How does cyanide induce seizures?

Back 77

Inhibits mitochondrial function

Front 78

Why is brown fat brown?

Back 78

Mitochondria

Front 79

How does cyanide induce seizures?

Back 79

Inhibits mitochondrial function

Front 80

Reactive oxygen species?

Back 80

O2- or `OH

Front 81

What can reactive oxygen species damage?

Back 81

Nucleic acids
Lipid
Protein

Front 82

O2- can react with ______ to form ______

Back 82

NO`
forms Peroxynitrite OR:
React with Fe and H2O2 to form
`OH

Front 83

How does mitochondrial function contribute to reactive oxygen species?

Back 83

Electrons from ETC (CoQ) react directly with O2 to form O2-

Front 84

Phagocyte: what can happen to make reactive oxygen species?

Back 84

NADPH oxidase provides electrons to make O2 to O2-

Front 85

O2- can create what toxic substance?

Back 85

H2O2

Front 86

H2O2 reacts with what to make an OH- radical?

Back 86

Fe and O2-

Front 87

H2O2 reacts with what to make hypochlorite radical?

Back 87

Myeloperoxidase

Front 88

How do reactive species damage the cell?

Back 88

Membrane lysis (phopholipid gets reduced) due to kinks in the tails, formed by "lipid hydroperoxide"

Front 89

Lipid hydroperoxide: how does it work? (step-by-step)

Back 89

OH- reacts with C in tail, takes an electron
Now, C` will react with molecular O2
Peroxyl radical CO2` reacts with neighboring carbon
New C`, known as lipid hyrdoperoxide
SELF-PROPAGATING

Front 90

Substrates to quench reactive oxygen species?

Back 90

Tocopherol and ascorbic acid to ascorbate
Glutathione peroxidase

Front 91

Why is complex II working on CoA insufficient (why is complex I so important)?

Back 91

Complex I regenerates NAD+ for Glycolysis/TCA

Front 92

When oxidized, PUFA can form?

Back 92

Lipid Hydroperoxide

Front 93

What happens to a lipid hydroperoxide?

Back 93

PLA2 clips off FA tail
Glutathione Peroxidase reduces peroxide to an alcohol, requiring selenium as a cofactor

Front 94

Ultimate source of electrons in reducing reactive oxygen species?

Back 94

Glutathione

Front 95

How is tocopherol regenerated?

Back 95

Dehydrosascorbate reductase reduces ascorbic acid to ascorbate, regenerating tocopherol

Front 96

Reaction mediated by superoxide dismutase?

Back 96

Takes 2 O2- and makes H2O2 + O2 (not good either, but enzymes get rid of H2O2)

Front 97

Enzyme that removes H2O2?

Back 97

Catalase

Front 98

GSH?
GSSG?

Back 98

GSH: reduced glutathione; ultimate reducing power/e- source
GSSG: oxidized glutathione

Front 99

Enzyme that replenishes GSH? Reducing source?

Back 99

Glutathione reductase
Reducing source: NADPH

Front 100

Disease associated with antioxidant deficiency?

Back 100

White Muscle Disease

Front 101

Coenzyme for Glutathione Peroxidase?

Back 101

Selenium

Front 102

Treatment for White Muscle Disease?

Back 102

Selenium, Tocopherol

Front 103

Heinz Body Anemia: Cause, trigger, Dx, consequences?

Back 103

Cause: reactive thiols in cat Hb
Trigger: Onions, tylenol (high thiosulfates) increase oxidative stress
Dx: Deformed and lysing RBC, hemolytic anemia
Tx: antioxidants, N-acetyl cysteine to promote intracellular glutathione

Front 104

Heinz Body Anemia: when is it good?

Back 104

Easier to lyse cells that have malaria to get rid of it

Front 105

Which 2 amino acids and other biosynthetic substrate can NEVER be used for GNG?

Back 105

Leucine, Lysine, fatty acids

Front 106

What is the only biosynthetic substrate that can be formed from fatty acids? What term can therefore be applied to fatty acids?

Back 106

Acetyl CoA
Ketogenic

Front 107

Precursors for GNG

Back 107

Lactate
Pyruvate
Glycerol
Proprionate
Glucogenic amino acids

Front 108

What state is GNG used in?

Back 108

Fasting

Front 109

Using lactate as the substrate, where is NADH for GNG produced? Using pyruvate?

Back 109

Lactate Dehydrogenase (lactate)
Malate dehydrogenase (pyruvate)

Front 110

How is lactic acid cleared in the skeletal muscle?

Back 110

Taken through TCA to form H2O + CO2

Front 111

How is lactate cleared in the liver?

Back 111

Taken through GNG

Front 112

Treatment for White Muscle Disease?

Back 112

Selenium, Tocopherol

Front 113

Heinz Body Anemia: Cause, trigger, Dx, consequences?

Back 113

Cause: reactive thiols in cat Hb
Trigger: Onions, tylenol (high thiosulfates) increase oxidative stress
Dx: Deformed and lysing RBC, hemolytic anemia
Tx: antioxidants, N-acetyl cysteine to promote intracellular glutathione

Front 114

Heinz Body Anemia: when is it good?

Back 114

Easier to lyse cells that have malaria to get rid of it

Front 115

Which 2 amino acids and other biosynthetic substrate can NEVER be used for GNG?

Back 115

Leucine, Lysine, fatty acids

Front 116

What is the only biosynthetic substrate that can be formed from fatty acids? What term can therefore be applied to fatty acids?

Back 116

Acetyl CoA
Ketogenic

Front 117

Precursors for GNG

Back 117

Lactate
Pyruvate
Glycerol
Proprionate
Glucogenic amino acids

Front 118

What state is GNG used in?

Back 118

Fasting

Front 119

Using lactate as the substrate, where is NADH for GNG produced? Using pyruvate?

Back 119

Lactate Dehydrogenase (lactate)
Malate dehydrogenase (pyruvate)

Front 120

How is lactic acid cleared in the skeletal muscle?

Back 120

Taken through TCA to form H2O + CO2

Front 121

How is lactate cleared in the liver?

Back 121

Taken through GNG, known as the "Cori Cycle"

Front 122

Why do carnivores use GNG?

Back 122

High protein diet, need glucose

Front 123

Why do herbivores use GNG?

Back 123

All the glucose in the high-carb diet is taken up by the microbes

Front 124

% of BG from GNG after:
22 hours fasting?
46 hours fasting?

Back 124

22: 65%
46: 100%

Front 125

In lactic acidosis, which regulatory enzyme senses low pH? What pathway does it shut down?

Back 125

PFK, shuts down glycolysis

Front 126

Alternate enzyme for PK in GNG?

Back 126

Pyruvate carboxylase and PEPCK

Front 127

What step of GNG will consume NADH that will be produced either by LDH or malate dehydrogenase?

Back 127

Glyceraldehyde 3 Phosphate Dehydrogenase

Front 128

What enzyme replaces PFK in GNG?

Back 128

Fructose biphosphate

Front 129

What enzyme replaces hexokinase in GNG?

Back 129

Glucose 6 Phosphatase, in liver/kidney cortex only!

Front 130

What 2 substrates does pyruvate carboxylase require to convert pyruvate to OA? What coenzyme does this?

Back 130

HCO3- and ATP
Coenzyme: biotin

Front 131

What are the allosteric activators for pyruvate carboxylase?

Back 131

Acetyl CoA
ATP

Front 132

3 TCA inhibitors?

Back 132

Acetyl CoA
NADH
ATP

Front 133

What high-energy bond(s) is/are used in forming PEP from pyruvate?

Back 133

GTP to GDP (PEPCK)
ATP to ADP (PC)

Front 134

F16BPase: activators?
inhibitors?

Back 134

Activator: citrate
Inhibitor: F2,6BP, AMP

Front 135

Pathway from G6P to glycogen?

Back 135

G6P via PGM to G1P via UDP-Glucose phosphorylase to UDP-glucose via glycogen synthase to glycogen

Front 136

Dysfunctional glucose transport system at the level of G6Pase-name that disease?

Back 136

VonGierke Disease

Front 137

2 main TCA inhibitors

Back 137

ATP, NADH

Front 138

How many bonds (inc. NADH) for GNG from pyruvate? from lactate?

Back 138

12-pyruvate
6-lactate

Front 139

How is proprionyl CoA produced?

Back 139

Produced from oxidation of odd-number fatty acids

Front 140

Proprionyl CoA is used significantly for GNG in what kind of animal?

Back 140

Ruminants

Front 141

Proprionyl CoA requires what form of energy to form OA? What cofactor is necessary?

Back 141

ATP
Cofactor: B12

Front 142

Where does the glycerol used in GNG come from?

Back 142

Lipolysis of adipose tissue

Front 143

Name of the pathway by which glycerol is used in GNG?

Back 143

Glycerol-phosphate pathway

Front 144

Where is glycerol GNG restricted to? Why?

Back 144

Liver; Adipose does not contain glycerol kinase to form G3P from glycerol

Front 145

Glucose lactate cycle is also known as...

Back 145

Cori Cycle

Front 146

Where is the Cori cycle predominant?

Back 146

RBC, skeletal muscle

Front 147

Where is the lactate from the Cori cycle taken?

Back 147

Liver

Front 148

What happens in the liver during Cori Cycle?

Back 148

Lactate goes through GNG to glucose to maintain blood glycemia

Front 149

Transamination of pyruvate is involved in which GNG pathway?

Back 149

Glucose alanine cycle

Front 150

Where and how is pyruvate shuttled in the glucose alanine cycle? What is the major advantage of the glucose alanine cycle?

Back 150

From skeletal muscle to liver as alanine, gets rid of NH3 in urea

Front 151

Why is the glucose alanine cycle bad?

Back 151

You're degrading protein from skeletal muscle to maintaing glycemia

Front 152

How does skeletal muscle remove lactate to form glucose?

Back 152

Glucose lactate cycle/Cori cycle

Front 153

How expensive is the Cori cycle? Why bother?

Back 153

6ATP per glucose formed, but it reduces O2 debt after exercise, restores pH, allows you to have glucose store for prey/predator

Front 154

Most important step of glycolysis/GNG for regulation?

Back 154

PFK/F16BPase

Front 155

Most important effector of Glycolysis/GNG?

Back 155

F26BP (activator for glycolysis, inhibitory for GNG)

Front 156

Pyruvate carboxylase only has high activity when what substrate is high?

Back 156

Acetyl CoA

Front 157

Long term activating hormone of GNG?

Back 157

Cortisol

Front 158

Actions of cortisol?

Back 158

Increase enzyme production of:
PEPCK
F16BPase
G6Pase

Front 159

Fast hormonal activator of GNG?

Back 159

Glucagon

Front 160

Upstream actions of glucagon to speed up GNG?

Back 160

GPCR: high cAMP, PKA

Front 161

Inhibitory hormone of GNG?

Back 161

Insulin

Front 162

What does insulin activate?

Back 162

Glycolysis
Lipogenesis

Front 163

What major substrate determines the fate of Pyruvate?

Back 163

Acetyl CoA (excess will increase pyruvate carboxylase action and GNG)

Front 164

What are the major and minor inhibitors of F16BPase?

Back 164

Major: F26BP
Minor: AMP

Front 165

What is the major activator of F16BPase?

Back 165

Citrate

Front 166

What are the activators/inhibitors of F26BP?

Back 166

Activator: PFK2
Inhibitor: F26BPase
Can be the same enzyme, depends

Front 167

How does glucagon inhibit glycolysys?

Back 167

Glucagon to cell to GPCR cAMP to PKA to phophorylate F26BPase (now active) to INACTIVATE F26BP by lowering concentration of F26BP

Front 168

What 2 things inhibit PK in the liver?

Back 168

Alanine, ATP

Front 169

Glucokinase is NOT regulated by what regulator of the other hexokinases?

Back 169

G6P

Front 170

Km of Glucokinase compared to the other hexokinases?

Back 170

High

Front 171

When lactate is the substrate for GNG, how is is transported out of the mitochondria?

Back 171

Aspartate

Front 172

What is required in the mitochondria in order for lactate to be transported out as aspartate?

Back 172

Glu INTO mitochondria
a-ketoglutarate OUT of mitochondria
Limited by the presence of these substrates

Front 173

Whether transported out as aspartate or malate, GNG will still occur because either of these substrates will be converted to WHAT outside of the mitochondria?

Back 173

Oxaloacetate

Front 174

If using pyruvate as the substrate for GNG, how does it exit the mitochondria?

Back 174

Malate

Front 175

What enzyme catalyzes malate formation from pyruvate inside the mitochondria? What does it produce?

Back 175

Malate dehydrogenase, produces NAD+

Front 176

Once out of the mitochondria, how does malate get converted to oxaloacetate for GNG? What does it produce?

Back 176

Malate dehydrogenase, produces NADH

Front 177

What does liver use to pay the bill for GNG?

Back 177

Lipids and fats--FA oxidation, create a lot of AcetylCoA, lots of ketone bodies, also make a lot of FADH/NADH to be put through ETC to make ATP for this process

Front 178

Ruminant characteristics?

Back 178

Cloven hoof
No upper incisors
4-compartment stomach, fermentation in 3 of them
Chew cud

Front 179

name of the small cranial part of the ruminant stomach

Back 179

reticulum

Front 180

Pseudoruminant: class?

Back 180

Camelids

Front 181

Large herbivore, non-fermenting?

Back 181

Equids

Front 182

Most important type of microbes?

Back 182

Bacteria

Front 183

Less important microbes?

Back 183

Fungi, protozoa

Front 184

Rumen characteristics that make it ideal for microbes (good fermentation bath)?

Back 184

Dark, wet, warm, constant pH, nutrients supplied, waste removed

Front 185

What type of metabolism must microbes of the rumen use?

Back 185

Reductive catabolism (no O2)
CHO + ADP to VFA + CH4 + ATP

Front 186

What is TCA used for in ruminants?

Back 186

Metabolite interchange

Front 187

What type of energy source are plants?

Back 187

Carbohydrates

Front 188

Ruminant characteristics?

Back 188

Cloven hoof
No upper incisors
4-compartment stomach, fermentation in 3 of them
Chew cud

Front 189

name of the small cranial part of the ruminant stomach

Back 189

reticulum

Front 190

Pseudoruminant: class?

Back 190

Camelids

Front 191

Large herbivore, non-fermenting?

Back 191

Equids

Front 192

Most important type of microbes?

Back 192

Bacteria

Front 193

Less important microbes?

Back 193

Fungi, protozoa

Front 194

Rumen characteristics that make it ideal for microbes (good fermentation bath)?

Back 194

Dark, wet, warm, constant pH, nutrients supplied, waste removed

Front 195

What type of metabolism must microbes of the rumen use?

Back 195

Reductive catabolism (no O2)
CHO + ADP to VFA + CH4 + ATP

Front 196

What is TCA used for in ruminants?

Back 196

Metabolite interchange

Front 197

What type of energy source are plants?

Back 197

Carbohydrates in the form of polysaccharides

Front 198

4 main polysaccharides of plants?

Back 198

Starch
Pectin
Hemicellulose
Cellulose

Front 199

Starch-linkage, where it's found, how it is hydrolyzed, where it's digested

Back 199

Glu a-1,4
Found in seeds, tubers
Hydrolyzed by amylase
Can be digested in small intestine

Front 200

Pectin: what it's made of, where it's found, how & by what it is hydrolyzed

Back 200

Galacturonic acid + arabinose
Fruit and leaves
Microbial hydrolysis only, via pectinesterases

Front 201

Hemicellulose: what it's made of, where it's found, how & by what it is hydrolyzed

Back 201

xylose + arabinose
Fiber of leaves and stems
Microbial hydrolysis only, via hemicellulases

Front 202

Cellulose: linkage, where it's found, how it's hydrolyzed, what can hydrolyze it?

Back 202

Glu b-1,4
Fiber of leaves and stems
Microbial hydrolysis only, via cellulases

Front 203

Less important microbes?

Back 203

Fungi, protozoa

Front 204

Rumen characteristics that make it ideal for microbes (good fermentation bath)?

Back 204

Dark, wet, warm, constant pH, nutrients supplied, waste removed

Front 205

What type of metabolism must microbes of the rumen use?

Back 205

Reductive catabolism (no O2)
CHO + ADP to VFA + CH4 + ATP

Front 206

What is TCA used for in ruminants?

Back 206

Metabolite interchange

Front 207

What type of energy source are plants?

Back 207

Carbohydrates in the form of polysaccharides

Front 208

4 main polysaccharides of plants?

Back 208

Starch
Pectin
Hemicellulose
Cellulose

Front 209

Starch-linkage, where it's found, how it is hydrolyzed, where it's digested

Back 209

Glu a-1,4
Found in seeds, tubers
Hydrolyzed by amylase
Can be digested in small intestine

Front 210

Pectin: what it's made of, where it's found, how & by what it is hydrolyzed

Back 210

Galacturonic acid + arabinose
Fruit and leaves
Microbial hydrolysis only, via pectinesterases

Front 211

Hemicellulose: what it's made of, where it's found, how & by what it is hydrolyzed

Back 211

xylose + arabinose
Fiber of leaves and stems
Microbial hydrolysis only, via hemicellulases

Front 212

Cellulose: linkage, where it's found, how it's hydrolyzed, what can hydrolyze it?

Back 212

Glu b-1,4
Fiber of leaves and stems
Microbial hydrolysis only, via cellulases

Front 213

What compound cannot by metabolized by either mammalian or microbial cells?

Back 213

Lignin

Front 214

Digestibility of Starch/Pectin?
Of Hemicellulose/Cellulose?

Back 214

Starch/Pectin: 90%
Hemicellulose/Cellulose: 40-70%

Front 215

How do bacteria digest cellulose/hemicellulose?

Back 215

Attach to the plant particles and erode away with flagellae; holes known as frassbetten

Front 216

All plant compounds go through what pathway?

Back 216

Polysaccharide to monosaccharide to pyruvate to volatile fatty acids

Front 217

What is made from pyruvate in the ruminant?

Back 217

Volatile fatty acids (VFAs) + CH4 + CO2

Front 218

Volatile Fatty Acids?

Back 218

2C: Acetic (Ac), CH3COOH
3C: Proprionic (Pr)
4C: Butyric (Bu)
AKA short-chain fatty acids

Front 219

pKa of VFAs relative to the rumen?

Back 219

VFA: 4.8
rumen: 6-7
highly ionized

Front 220

Molar ratio: Ac:Pr:Bu

Back 220

69:20:11

Front 221

Chief energy source for ruminants?

Back 221

VFAs absorbed from rumen

Front 222

3 modes of acetate production in ruminants?

Back 222

via PDH
via PFO (bad, produces CH4 from H2)
Formate: minor pathway, HAS to produce CH4

Front 223

Balanced reaction of acetate formation in the ruminant?

Back 223

Hexose + 4ADP --> 2 acetate + 2CO2 + 4ATP + 8 reducing equivalents

Front 224

What happens to Acetyl CoA in the ruminant?

Back 224

Phosphorylate it, use acetate kinase to produce acetate and 2ATP

Front 225

Glucose to butyrate-how much ATP?

Back 225

Hexose + 3ADP --> butyrate + 2CO2 + 3ATP + 4 reducing equivalents

Front 226

What pathway produced proprionate in ruminants? What energy forms are consumed/produced? What are the 2 variants of this pathway, and when are they used?

Back 226

Succinate pathway (backwards TCA)
Consumes NADH (from acetate production), produces ATP indirectly, leading to low yield
High grain (starch): pathway will be all in one cell
High forage (cellulose): Pathway split between 2 cells

Front 227

Succinate pathway & production of proprionate requires what vitamin?

Back 227

B12 and trace cobalt

Front 228

How could you produce proprionate without B12/cobalt in the diet?

Back 228

By using lactate instead of pyruvate

Front 229

What are the 2 possible fates of H2 in the rumen produced from pyruvate to acetate?

Back 229

CH4 OR some form of reducing power

Front 230

Proprionate synthesis, balanced equation?

Back 230

Succinate pathway:
Hexose + 4ADP + 4 reducing power --> 2 proprionate + 4ATP
Lactate pathway:
Hexose + 2ADP + 4 reducing power --> 2 proprionate + 2 ATP

Front 231

Most common gas in the rumen?

Back 231

CO2

Front 232

2nd most abundantly PRODUCED gas in the rumen?

Back 232

H2 but concentration <1%, used for methane, mostly from PFO rather than PDH or formic acid

Front 233

2nd most COMMON gas in the rumen?

Back 233

CH4, a metabolic dead-end

Front 234

Advantage to lactate over succinate pathway for proprionate production?

Back 234

Keeps pH of the rumen from getting too low

Front 235

What gas increases when methanogens are inhibited?

Back 235

H2

Front 236

As H2 increases, which pathway of decarboxylation of pyruvate is inhibited most? Which VFA will be favored, and which decreased?

Back 236

PFO
Favor: Proprionate
Reduce: Acetate

Front 237

How do you inhibit methanogens?

Back 237

Feed high-grain (starch) diet so that lactic acid acidifies the rumen, inhibits methanogens
Administer methanogen-specific antibiotics (resistance not a concern)

Front 238

VFA ratio of a high-forage diet?
Moles of CH4 per mole of hexose?

Back 238

73:17:10
0.7mol CH4 per mol Hexose

Front 239

VFA ratio of a high-grain diet?
Moles of CH4 per mole of hexose?

Back 239

45:47:8
0.3mol CH4 per mol Hexose

Front 240

H2 vs. H+?

Back 240

H+ acidifies rumen, high with high-grain diet, produced from lactic acid
H2: produced from PFO pathway, constitutively goes to CH4, inhibits PFO in high concentration

Front 241

Free energy change from hexose in aerobic vs. anaerobic metabolism?

Back 241

both 50% efficient, but aerobic produces 10x as much ATP.

Front 242

High forage vs. high grain diet for %VFA to %CH4?

Back 242

High forage: 20% methane, 75%VFA
High grain: 10%methane, 85%VFA

Front 243

Sources of NH3 for microbes to synthesize AAs/proteins?

Back 243

Plant/animal proteins or nucleic acids
NH4 salts (taste bad)
Urea (if palatable)

Front 244

Too much urea will create what in the ruminant?

Back 244

NH3 toxicity

Front 245

How do you feed lipids/fats to cattle?

Back 245

Protected (seed husks) or globules (powder) to bypass the rumen

Front 246

Vitamin synthesis in rumen? Which ones, and where?

Back 246

Rumen: All B vitamins, Vitamin K (need cobalt to make B12)
Liver: Vitamin C
High grain diet can destroy niacin, thiamin
CANNOT make: A, D, E

Front 247

What do ruminants use to "activate" VFA for metabolism?

Back 247

a CoA synthetase, produce VFA-CoA

Front 248

Acetate metabolism-where? What tissues does it wind up in?

Back 248

Not rumen--portal vein to liver, not liver so circulation; produces AcetylCoA, most common in heart, skeletal muscle, adipose, mammary

Front 249

Main fat precursor in ruminants?

Back 249

Acetate/AcetylCoA

Front 250

Proprionate metabolism-when does it supply the most energy?

Back 250

high-grain diet

Front 251

Proprionate metabolism--where?

Back 251

Not in the rumen, well in the liver!

Front 252

Proprionate metabolism requires what? What pathway does it use?

Back 252

Requires B12, goes down succinyl pathway to GLUCOSE

Front 253

Butyrate metabolism-where? What does it become?

Back 253

Rumen wall, some escapes to mammary glands, stinky cheese
Becomes ketone body
Ketone bodies high in fed ruminants

Front 254

GNG: 2 main precursors in ruminants?

Back 254

AAs
Proprionate

Front 255

When is GNG highest in ruminants?

Back 255

FED state

Front 256

Ruminant fat synthesis comes from what VFA?

Back 256

Acetate to AcetylCoA...to TAG

Front 257

Very little fat synthesis in liver from glucose in ruminants; why?

Back 257

Can't activate acetate to AcetylCoA, lacks glucokinase

Front 258

Very little fat synthesis from glucose in mammary in ruminants; why?

Back 258

Lacks a citrate shuttle, no way to get AcetylCoA out of the mitochondria

Front 259

Mammary and adipose tissue of ruminants use what precursor for fat synthesis?

Back 259

Acetate

Front 260

Most ketone synthesis in ruminants comes from what VFA?

Back 260

Butyrate

Front 261

Which is more common: ovine pregnancy toxemia or bovine ketosis?

Back 261

Pregnancy toxemia; cannot shuttle glucose away from the fetus like the cow can shuttle away from milk production

Front 262

Which animals' brains CAN use ketones?
Which can't?

Back 262

Can: Humans, rats
Can't: Cows, dogs, pigs

Front 263

Types of lipids (5)?

Back 263

Fatty Acids
Triglycerides
Phospholipids
Cholesterol
Lipoprotein

Front 264

Fatty acids can be modified in what way?

Back 264

Saturated or unsaturated

Front 265

What are essential fatty acids from the diet?

Back 265

Linoleic acids

Front 266

What is a fatty acid important to inflammatory precursors?

Back 266

Arachadonic acid

Front 267

Another word for fatty acid synthesis?

Back 267

Lipogenesis

Front 268

What are the 2 precursors that can be used for fatty acid synthesis?

Back 268

Arachadonic aci
Carbohydrates

Front 269

What enzyme controls lipogenesis?

Back 269

AcetylCoA Carboxylase

Front 270

What hormone regulates fatty acid synthesis?

Back 270

Insulin

Front 271

What tissue does most lipogenesis occur in?

Back 271

Liver

Front 272

What is the shuttle that gets AcetylCoA out of the mitochondria and into the cytosol for fatty acid synthesis?

Back 272

Acetyl CoA to citrate inside the mitochondria, leave the mitochondria as citrate, enzyme citrate lyase in the cytosol produces OA and Acetyl CoA

Front 273

What are the substrates and products of the reaction catalyzed by AcetylCoA carboxylase?

Back 273

Substrates: AcCoA + ATP + HCO3-
Products: malonylCoA + ADP + Pi

Front 274

What effectors regulate AcetylCoA carboxylase? What is the active and inactive form?

Back 274

Active: unphosphorylated
Positive: Citrate (indicates the fed state), protein phosphatase (insulin), ATP
Negative: PalmitoylCoA, PKA (high AMP due to Glucagon/Epinephrine, low ATP)

Front 275

What enzyme catalyzes MalonylCoA forming its product? What is the other substrate & the product?

Back 275

Fatty acid synthase
Other substrate: ACP
Product: MalonylACP

Front 276

What is needed to form palmitate?

Back 276

Substrates: 2 Acetyl CoA, one Malonyl ACP

Front 277

What is the reducing power used in lipogenesis? Where does this reducing power come from?

Back 277

NADPH; from PPP

Front 278

What are the 2 key enzymes regulating fatty acid synthesis?

Back 278

AcetylCoA Carboxylase
Fatty acid synthase

Front 279

How can fatty acids be modified? What enzymes help with this?

Back 279

Elongases and desaturases

Front 280

Purpose of synthesizing long chain fatty acids?

Back 280

Energy storage

Front 281

How are fatty acids stored? How are they transported?

Back 281

Stored as triglycerides esterified to glycerol; transported in blood bound to albumen

Front 282

What is the fate of fatty acids synthesized in liver vs. adipose?

Back 282

Adipose: will be stored there
Liver: will be exported as VLDL

Front 283

What advantage is there to storing fat over glycogen? What is the energy content of fat and carbohydrates?

Back 283

Advantage: fat is lighter (not hydrated)
Fat: 9kcal/g
Carbohydrates: 4kcal/g

Front 284

What is the specific molecule that fatty acids bind to and form TAG? What enzyme catalyzes this reaction?

Back 284

a-glycerol phosphate
acetyltransferase

Front 285

Phospholipid function?

Back 285

Lipid bilayer, signaling

Front 286

Cholesterol function?

Back 286

Membrane fluidity
Steroid hormones
Bile acids & salts--fat digestion, absorption

Front 287

How is cholesterol synthesized? What is the rate-limiting step?

Back 287

Acetyl CoA to
HMG CoA, reduced in several steps to
Cholesterol
HMG CoA is rate-limiting!

Front 288

What are lipoproteins composed of?

Back 288

Triglyceride
Cholesterol
Phospholipid
Protein (apo-lipoprotein)

Front 289

Function of lipoprotein?

Back 289

Transport cholesterol and triglyceride between organs and tissues

Front 290

What is the apolipoprotein of VLDL and LDL?

Back 290

ApoB-100

Front 291

Apolipoprotein of chylomicron?

Back 291

Apo-B 48

Front 292

Apolipoprotein of Hdl?

Back 292

Apo-A1

Front 293

Lipoprotein classes, smallest to largest?

Back 293

HDL<LDL<VLDL<Chylomicron

Front 294

What is the mechanism of LPL enzyme?

Back 294

Takes VLDL or chylomicron that is excreted by liver and in the target tissue (adipose, muscle, heart) it cleave the TG to allow fatty acid uptake.

Front 295

What tissue type is LPL found in?

Back 295

Capillary epithelium

Front 296

LPL is active with the release of what hormone? What is the exception to this?

Back 296

Insulin
Exception: heart will use LPL in the fasted state to spare glucose for the brain

Front 297

Where is HSL found?

Back 297

Adipose tissue

Front 298

What is the rate-limiting enzyme in adipocytes for fat metabolism?

Back 298

HSL

Front 299

What does HSL do in adipocytes?

Back 299

Hydrolyzes TG to release glycerol and free fatty acids from the adipose tissue to the rest of the body

Front 300

How is HSL regulated?

Back 300

Activated by phosphorylation cascade from Glucagon/epinephrine/GPCR
Inhibited by high levels of insulin in the fed state or in fight-or-flight

Front 301

What are the 3 steps of fatty acid oxidation?

Back 301

1. Fatty acid activation
2. Transport across membranes
3. b-oxidation

Front 302

What does the first step of fatty acid oxidation involve?

Back 302

Forms a FA Acyl CoA

Front 303

What does the second step of fatty acid oxidation involve?

Back 303

Transporting across the membrane of the mitochondria as 'carnitine' via a carnitine carrier protein and the enzymes carnitine palmitoyl transferase I and II

Front 304

What does the third step of fatty acid oxidation involve?

Back 304

b-oxidation: each round generates GTP and reducing power in the form of NADH & FADH2

Front 305

How much net ATP can be produced from oxidizing a 14C fatty acid?

Back 305

112 ATP/mol

Front 306

When does FA oxidation take place?

Back 306

Either after a high-fat, low-CHO meal or in the fasted state (insulin will be low)

Front 307

What compound blocks fatty acid oxidation while lipogenesis is occurring?

Back 307

Malonyl CoA