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Exam 2 > Biochemistry 2 > Flashcards

Biochemistry 2 Flashcards

1
Q

the 6 enzyme classes (and their functions)

A

1) oxidoreductases: redox reactions
2) transferases: transfer of chemical group
3) hydrolase: lysis by water
4) lyase: cleavage reaction not using water
5) isomerase: change of molecular conformation
6) ligase: joining of 2 compounds

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2
Q

serine protease mechanism

A

Substrate binds.
Ser-195 attacks (Ser is very reactive due to His and Asp).
Transition state is stabilized.
Peptide bond is cleaved via hydrolysis.

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3
Q

active site specificity of chymotrypsin

A

bulky, hydrophobic residues

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4
Q

active site specificity of trypsin

A

positively charged residues (Arg, Lys)

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5
Q

active site specificity of elastase

A

small AAs prevalent in elastin (Gly, Ala, Val)

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6
Q

spontaneous reaction (in terms of Gibb’s free energy)

A

spontaneous if delta G < 0 (negative)

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7
Q

delta G and Keq at equilibrium

A

delta G = 0

Keq = Q

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8
Q

biochemical reactions vs chemical reactions

A

Reactions in the body are never at equilibrium.

Some processes are solid phase reactions (not in solution).

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9
Q

removal of product drives the reaction _________

A

forward

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10
Q

enzymes/catalysts

A

Stabilize the transition state (lower transition state energy).
Do NOT change delta G or Keq.

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11
Q

catabolism

A

Breakdown.

Burn fuel for storage or ATP use.

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12
Q

anabolism

A

Build-up.

Burn ATP for biosynthetic purposes, active transport, mechanical work.

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13
Q

velocity

A

The amount of product formed per unit time.

Initial velocity is equal to the linear part of the curve.

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14
Q

1/2 Vmax

A

where Km = [S]

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15
Q

Km

A

Affinity for a substrate.
Larger Km = weaker affinity.
Never changes.
Always positive.

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16
Q

how to measure enzymatic activity in a sample

A

Michaelis-Menten.

Use saturating amounts of substrate (»>Km).

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17
Q

how to measure substrate levels

A

Michaelis-Menten.

Use low substrate levels with respect to Km.

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18
Q

Kcat

A

Measures the catalytic power of an enzyme.

Kcat = Vmax/[enzyme]

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19
Q

Vmax

A

Maximal activity for a sample.

More enzyme causes a higher Vmax (up to a point).

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20
Q

Lineweaver-Burke Plot

A

1/v = (Km/Vmax) (1/S) + (1/Vmax)

slope: Km/Vmax
x-intercept: -1/Km
y-intercept: 1/Vmax

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21
Q

deficiency of enzyme activity: causes

A

Lack of enzyme.
Defective enzyme.
Lack of substrate/cofactor.

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22
Q

enzyme regulation by location

A

Enzymes are only expressed in certain tissues.

Ex: ALT (alanine transaminase): internal liver enzyme; high levels = lots of damage
Ex: alpha-1 antitrypsin: indicator of liver damage; secreted by liver and taken up by lungs

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23
Q

zymogen

A

Inactive form of the enzyme.
Proteolytic cleavage rapidly opens up the active site.

Ex: prothrombin/thrombin and fibrinogen/fibrin in blood clotting cascade.

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24
Q

blood clotting cascade

A

Damage/trauma activates an enzyme.
Cascade of proteins (1 or 2 trigger, millions activated).
Prothrombin is soluble.
Gamma-carboxylation is added to glutamates on prothrombin (vit K dependent).
Gamma-carboxylation binds Ca2+, so prothrombin can bind to the membrane.
Prothrombin is cleaved to thrombin, an active serine protease, on the membrane.
Fibrinogen is cleaved to fibrin.
Fibrin forms cross-linnked clot.

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25
Q

warfarin/coumadin

A

Vitamin K analogue.
Interferes with gamma-carboxylation of prothrombin.
Reduces over-clotting in patients that clot too readily.

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26
Q

heparin

A

Short-acting anticoagulant.
Promotes antithrombin-thrombin complex formation.
Antithrombin is an inhibitor that binds tightly to thrombin,
Once bound together, the complex is degraded, so it reduces the thrombin available for clotting.
Reduces clotting.

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27
Q

elastase inhibition

A

Elastase is released by lung neutrophils to neutralize foreign particles.
Alpha1-antitrypsin/alpha1-antiprotease inhibit elastase normally.
If alpha1-antitrypsin is defective, then unregulated elastase activity destroys elastin, causing scarring and emphysema.

Defective alpha1-antitrypsin caused by smoking (oxidation of sulfur to sulfoxide).
Treatment: intravenous alpha1-antitrypsin.

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28
Q

phosphorylation of protein

A

Phosphorylation/dephosphorylation modifies the charge of an AA residue.
Changes structure/function/activity of enzyme.

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29
Q

competitive inhibitors

A

Interact with binding site.
Same Vmax.
Increased Km (decreased affinity).

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30
Q

noncompetitive inhibitors

A

Do not interfere with substrate binding.
Decreased Vmax.
Same Km.

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31
Q

irreversible inhibitors

A

Type of non-competitive inhibitor.
Modifies the enzymatic AAs.
Decreases Vmax.
Same Km.

Ex: DIFP inhibits serine proteases

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32
Q

allosteric affectors

A

Inhibit or activate.
Usually multiple subunits (cooperativity).
Have R and T forms.
Do not follow Michaelis-Menten kinetics.
Often regulate a reaction pathway.
Highly regulatable by substrate concentration.

Ex: PFK-1: AMP activates, ATP inhibits

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33
Q

product inhibition

A

The immediate product of an enzyme binds to the enzyme and inhibits its activity.

Ex: hexokinase: G6P inhibits

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34
Q

feedback inhibition

A

The product inhibits an earlier step of the reaction.

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35
Q

Retinoblastoma

A

Rb+, Rb+ is normal
Loss of one Rb+ –> predisposed to develop tumor.
Loss of two Rb+ –> induces tumor formation.

E2F needed for transcription of genes needed for cell growth.
E2F is regulated by pRB.
Phosphorylated pRb is inactive which allows E2F to transcribe genes for S phase growth.
Phosphorylation state of pRb is regulated by cdks (cyclin D or E).
Cell growth is accelerated if pRb is lost.

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36
Q

p53

A

p53 is stabilized by phosphorylation that occurs during stress.
When DNA is damaged, p53 induces transcription of p21 gene.
p21 binds to cdk/cyclin complex and halts the cycle.
p21 binds to PCNA and inhibits replication fork.

p53 halts the cell cycle and prevents apoptosis.
Without p53, p21 is not induced, the cell cycle is not halted, and cells will replicate damaged DNA.

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37
Q

Rb gene suppresses

A

retinoblastoma

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38
Q

p53 gene suppresses

A

sarcomas, carcinomas

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39
Q

NFC-1 gene suppresses

A

neuroblastoma

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40
Q

APC gene suppresses

A

colon, stomach

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41
Q

BRCA gene suppresses

A

breast cancer

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42
Q

oncogenes

A

Activate cell division in response to growth factor stimulation.
Dominant effect: only 1 gene needs to be altered.

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43
Q

Signal Transduction

A

Signals from outside the cell affects gene expression.
Receptors penetrate cell membrane and have enzymatic activity.
Phosphorylation of Tyr residues allow interactions with other members of cascade.
Tumor cells can generate their own growth signals.

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44
Q

altered growth factors

A

Simian Sarcoma (sis) oncogene encodes PDGF molecule and can induce signal transduction.

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45
Q

altered growth factor receptors

A

Mutant forms stimulate growth even in absence of growth factor.
Ex: epidermal growth factor receptor
Family members: ErbB, HER2

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46
Q

Ras signalling

A

Ras is active when bound to GTP, and inactive when bound to GDP (switches between states by GAP).
Causes signal transduction to nucleus.
Mutant Ras is locked “on” –> excessive signal transduction.

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47
Q

NF1 gene

A

Encodes neurofibromin protein.
Neurofibromin contains a GAP domain, possibly acts through Ras.
Neurofibromatosis: benign neurofibromas on skin due to defective signal transduction.

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48
Q

c-Fos and c-Jun

A

Transcription factors.
Bind to AP1 sites.
Too much of these cause continuous growth due to too much signal transduction.

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49
Q

Myc gene

A

Myc is a transcription factor that regulates 15% of all genes (~3,000 genes).
Myc binds to enhancer sequence and recruits HATs.
Mutant Myc upregulates genes involved in cell proliferation.

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50
Q

Burkitt’s Lymphoma

A

Translocation involving chromosome 8 (encodes Myc gene) .
When translocated, Myc is constituitively expressed.
Leads to leukemia and lymphomas.

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51
Q

HPV (and other DNA viruses)

A

T-antigen sequesters Rb and p53.
Takes “brakes” off the cell cycle.
E7 targets Rb.
E6 targets p53

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52
Q

characteristics of cancer

A 
Evade apoptosis.
Self-sufficiency in growth signals.
Insensitive to anti-growth signals.
Limitless replication potential (increased telomerase activity).
Angiogenesis.
Tissue invasion.
Metastasis.
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53
Q

Familial Adenomatous Polyposis Coli (APC)

A

Loss of APC causes colon cancer.

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54
Q

maltose

A

glucose + glucose

alpha 1,4 linkage

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55
Q

lactose

A

glucose + galactose

beta 1,4 linkage

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56
Q

sucrose

A

glucose + fructose

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57
Q

amylose

A

Linear.
Polyglucose.
alpha 1,4 linkages.

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58
Q

amylopectin

A

Branched.
Polyglucose.
Mostly alpha 1,4 linkages.
Some alpha 1,6 linkages to create branches.

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59
Q

cellulose

A

Polyglucose.
Linear.
Beta 1,4 linkages.
Humans cannot digest.

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60
Q

glycosaminoglycans (GAGs)

A 
Long: 500+ sugars.
Linear.
Repeating disaccharides.
Highly negative (carboxylates, sulfates).
Highly hydrated.
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61
Q

major GAGs

A

Chondroitin sulfate: bone, cartilage, cornea formation.
Keratan sulfate: cornea, CT.
Dermatan sulfate: binds LDL to plasma walls.
Heparan sulfate: aortic wall, basement membrane.
Heparin: anticoagulant.
Hyaluronic acid: cell migration, lubricant

62
Q

conjugated sugars

A

Gangliosides: lipids added to sugars.
Glucouronic acid + sugar: more soluble, easier to excrete.

Require activation of sugar by UTP.

63
Q

glycation of proteins

A

Occurs without enzyme or cofactor.

Formation of A1C in the blood gives “history” of glucose levels in blood.

64
Q

glycoproteins

A

Produced enzymatically.

Secreted or have exterior-facing domains (exception is O-Glc-Nac.

65
Q

O-linked glycoproteins

A

On Ser/Thr.

Adds 1 residue at a time.

66
Q

N-linked glycoproteins

A

On Asn.
Added in a 14 sugar block.
Constructed on a dolichol phosphate lipid.
Processing occurs during trafficking from ER to Golgi.

67
Q

Hunter Disease

A

Congenital disease of glycosylation.

Lack of iduronate sulfatase.

68
Q

Pompe Disease

A

Lack of acid a glucosidase.
Target for gene therapy.
Congenital disease of glycosylation.

69
Q

I-cell Disease

A

Failure of mannose-6-phosphate trafficking system.
Multi-enzyme disease.
Congenital disease of glycosylation.

70
Q

mucins

A

Main component of mucus.
Line/protect epithelial surfaces.
Glycoprotein.

71
Q

proteoglycans

A

Core protein O-linked to glycosaminoglycan.
Aggregate on hyaluronic acid.
Hydrated –> provides cushioning.
Charged –> can bind GFs, cytokines, chemokines.
Found in cartilage, dentin, predentin.

72
Q

glycosylation in biological recognition

A

Protein recognition of carbohydrate structures occurs via lectin domains.
Differentiate ABO blood groups.
Allows viruses/bacteria to infect.
Mediate cell-cell contact.

73
Q

importance of glycosylation

A 
Assist in protein folding in ER.
Regulate activity.
Intracellular transport (mannose-6-P).
Regulate half-life of serum proteins.
First defense in innate immunity.
74
Q

Selectin-Carbohydrate interactions

A

Make contact to slow leukocytes to a roll.

Controls leukocyte trafficking.

75
Q

calories from lipids

A

9 kcal/g

76
Q

calories from proteins

A

4 kcal/g

77
Q

calories from carbohydrates

A

4 kcal/g

78
Q

digestion of polysaccharides

A

Mouth: alpha amylase.
Small intestine: pancreatic amylase, brush border disaccharideases (lactase, sucrose-isomaltase).
Colon: bacteria digest unabsorbed carbs.

79
Q

lactose intolerance

A

Failure to digest lactose.
Common in African/Asian descent.
Increases with age.
Can be caused by illness that injures the mucosa.

80
Q

brush border - simple diffusion

A

Simple diffusion down gradient.

Only “rare” sugars.

81
Q

brush border - facilitated diffusion

A

Increases rate of transport down a gradient.
Most common.
Responsive to insulin – increases the number of GLUT4 receptors on the membrane of skeletal muscle, fat, WBC.
Not responsive to insulin – all other transporters, in RBC, brain, pancreas, intestine, brain, kidney.

82
Q

brush border – active transport

A

Increases transport rates even against a gradient.
Needed in order to get Na+ out of the cell.

SGLT (sodium linked) indirectly uses active transport.
Glucose and Na+ enters the cell through SGLT-1.
Glucose exits the cell into blood bia facilitated diffusion through GLUT-2.
ATP is needed to pump Na+ out of cell.

83
Q

active transport of glucose in kidney

A

Prevents loss of glucose to urine.

84
Q

factors affecting glycemic index

A

Sugar content (glucose high, fructose low).
Type of starch (amylose low, amylopectin high).
Physical barriers (bran low).
Viscosity of soluble fiber (apple).
Fat and protein content (affects gastric transport).
Acid content (affects gastric transport).
Food processing (rolled oats low, quick oats high).
Cooking (al dente high).

85
Q

complete glycolysis reaction

A

glucose + 2 Pi + 2ADP –> 2 pyruvate + 2ATP + 2NADPH + 2H+ + 2 H2O

86
Q

glycolysis net reaction

A

glucose + 2ADP + 2Pi –> 2 lactate + 2ATP + 2 H2O

87
Q

red blood cells

A

Lack mitochondria.
Depend on glycolysis for ATP production.
Produce lactate to regenerate NAD+.

88
Q

Most common glycolytic disorder in RBCs

A

Pyruvate kinase deficiency.

Causes persistent anemia.

89
Q

Tarui’s Disease

A

Mutations in PFK-1.

Causes exercise intolerance.

90
Q

abnormal pyruvate kinase

A

Four isozymes: M1 (muscle), M2 (muscle), L (liver), R (RBC).

Defect in a PK causes a disorder in that tissue.

91
Q

hexokinase

A

Can phosphorylate other hexoses.
Ubiquitous (in many tissues).
Lower Km (higher affinity) for glucose.
Inhibited by G6P.

92
Q

Glucokinase

A

Can only phosphorylate glucose.
Only in liver and pancreatic B cells.
Higher Km (lower affinity) for glucose.
NOT inhibited by G6P.

Takes glucose out of circulation.

93
Q

MODY

A

Mature Onset Diabetes in the Young.
NOT associated with obesity or high blood lipid levels.
Pancreatic B cells do produce insulin.
Associated with mutations in glucokinase gene, or genes for TFs that regulate transcription of liver/pancreatic B cell genes.
Without glucokinase, the amount of ATP produced in response to elevated blood sugar is reduced, causing less insulin secretion.

94
Q

glyceraldehyde-3-phosphate DH

A

Uses phosphate and NAD+.
Negative cooperativity.
Less sensitive to changes in substrate concentration.
Much lower Km.

95
Q

NAD+

A 
Required to make GA3P (and DHAP).
Must be recycled to continue glycolysis.
NAD+>>>NADH.
Precursor to niacin.
Intermediate to tryptophan synthesis.
Deficiencies cause D3 (dematitis, diarrhea, dementia).
96
Q

pellagra

A 
Niacin/NAD+ deficiency.
Places with corn.
Causes D3 (dermatitis, diarrhea, dementia) and death.
97
Q

glucose-6-phosphate can also be used for

A

glycogen, polysaccharides, glycoproteins, ribose, NADPH

98
Q

fructose-6-phosphate can also be used for

A

ribose, pentoses

99
Q

glyceraldehyde-3-phosphate can also be used for

A

ribose, pentoses

100
Q

dehydroxyacetone phosphate can also be used for

A

fat/phospholipid metabolism

101
Q

3-phosphoglyceride can also be used for

A

serine

102
Q

ACoA can also be used for

A

FAs, cholesterol, steroid hormones, oxidative metabolism

103
Q

2-deoxyglucose

A

Used for PET imaging.

Targets hexokinase.

104
Q

arsenate

A

Targets GA3P DH.

Substitutes for phosphate.

105
Q

flouride

A

Targets enolase.

106
Q

PET imaging

A

Shows hotspots for glycolysis.
Can see if metabolic activity in tumor is knocked out.
Detects metastasis.

107
Q

% ethanol absorption in stomach? intestine?

A

20% stomach
80% intestine

Eating food slows gastric emptying, thus slows absorption (esp. fatty foods)

108
Q

factors affecting elimination rate of ethanol

A

Sex (male > female).
Body composition (fat > lean).
Tolerance (experience > novice).
Alleles (ADH).

109
Q

NAD/NADH levels in alcohol metabolism

A

Alcohol clearance produces lots of NADH.
High NADH inhibits gluconeogenesis, promotes triglyceride synthesis.
Acetaldehyde increases TFs driving FA synthesis.

110
Q

MEOS

A 
Microsomal Ethanol Oxidizing System.
Activated with chronic alcohol consumption.
Cytochrome p450 based.
Smooth ER.
2/3 of total ethanol oxidation.
Affects drug metabolism.
Inducible.
111
Q

ADH1B*2

A

Polymorphism of ADH1.
Common in asian descent.
Ethanol is metabolized more quickly, less of an effect.

112
Q

ADH2*2

A

Polymorphism of ADH2.
Common in asian descent.
Converts acetaldhyde to acetic acid, but is slow.
Acetaldehyde causes facial flushing, high HR.
Uncomfortable.

113
Q

Disulfiram/Antabuse

A

Inhibits ADH2.
Creates an unpleasant reaction to alcohol.
FDA-approved for treatment of alcohol use disorder.

114
Q

thiamine deficiency

A

Common in alcoholics (poor diet, absorption).
Wernicke’s Encephalopathy.
Korsakoff’s Psychosis.

115
Q

Wernicke’s Encephalopathy

A 
Thiamine deficiency.
C - confusion
O - opthalmoplegia
A - ataxia
T - thiamine treatment
116
Q

Korsakoff’s Psychosis

A 
Thiamin deficiency.
R - retrograde amnesia
A - anterograde amnesia
C - confabulation
K - Korsakoff's psychosis
117
Q

metabolism of ethylene, methanol

A

Metabolized by same enzymes as ethanol.
Produce toxins (cause death, blindness, kidney failure).
Treatment: give ethanol.
Drug: Fomepizole (inhibits ADH, not v effective).

118
Q

thiamine cofactor

A

Used in PDH and Isocitrate DH.
Vitamin B1.
Does carboxylations and 2 carbon transfers.
Deficiency leads to beri-beri and Wernicke’s.

119
Q

lipoate cofactor

A

Used in PDH and isocitrate DH.
Activates acetate.
Target of arsenic.

120
Q

FAD cofactor (specifically in PDH/isocitrate DH)

A

Regenerates lipoate so rxn can continue.

Vitamin B2/riboflavin.

121
Q

riboflavin deficiency

A

cheilosis

glossitis

122
Q

beri-beri

A

Thiamine deficiency.
DRY: peripheral neuropathy, tingling hands/feet, involuntary eye movement.

WET: cardiac issues

123
Q

PDH complex deficiency (results and therapies)

A 
Metabolic acidosis (build up of lactate, pyruvate, alanine).
Neurological disorders ( cerebellar dysfunction).
Therapies:
Cofactor supplementation (maximize enzyme activity).
Ketogenic diet (reduce pyruvate load).
Bicarbonate (control acidosis).
Dichloroacetate (reduce PDH inhibition, to treat acidosis).
124
Q

metabolic disease associated with succinate DH

A

phaeochromocytoma,

paraganglioma

125
Q

metabolic disease associated with fumarase

A

leiomyomas

126
Q

metabolic disease associated with isocitrate DH

A

tumors (gliomas, AML)

127
Q

transketolase

A

transfers 2 carbons using thiamine

128
Q

transaldolase

A

transfers 3 carbons

129
Q

rate-limiting step of PPP

A

1st step (G6P –> phosphogluconolactone + NADPH).
Activated by insulin.
Allosterically inhibited by NADPH.
Saturated with inhibitor, starved for substrate (until it is needed).

130
Q

reactions that use NADPH

A

Synthesis of: FA, cholesterol, neurotransmitters, nucleotides.

Detoxification of: oxidized glutathione, cytochrome p450.

131
Q

NADPH vs NADH

A

Same function, different structure.

Allows enzymes to recognize structures, and keep ratios opposite for different reactions.

132
Q

myeloperoxidase

A

Can produce hypochlorous acid (bleach).
Kills bacteria and fungi.
Neutrophils.

133
Q

Chronic Granulomatous Disease (CGD)

A

Defect in NADPH oxidase.

Cannot form myeloperoxidase to kill bacteria.

134
Q

antioxidants

A

Get rid of free radicals.
Accept electron and decay without further damage.
Vitamins A, C, E.

135
Q

reduction of free radicals

A

Superoxide dismutase converts superoxide to hydrogen peroxide.
Glutathione peroxidase reduces peroxides using NADPH.

136
Q

effects of hypoglycemia

A

ADRENERGIC (autonomic):
Trembling, palpitations, sweating, anxiety, nausea, hunger, tingling.

NEUROGLYCOPENIC:
Headache, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness, tiredness.

137
Q

gluconeogenesis locations

A

Mainly in cytoplasm.
Pyruvate carboxylase is in mitochondria.
G6P’ase in ER.

90% liver
10% kidney

138
Q

Cori cycle

A

Lactate from RBC/muscle is shuttled thru blood to liver.
Gluconeogenesis converts lactate to glucose.
Glucose is returned to RBC/muscle for energy.

Spend 6 ATP, gain 2 ATP.

139
Q

Cahill Cycle

A

Alanine Cycle.
Pyruvate converted to alanine.
Alanine travels thru blood to liver.
Gluconeogenesis converts alanine to glucose.
Spend 6 ATP in liver, get 2 ATP in muscle/RBC.

140
Q

when is glycogen used as a main source of glucose?

A

4-16 hours after eating

141
Q

Faconi-Bickel Syndrome

A

GLUT2 deficiency.
Glucose transport is blocked.
Limited glucose uptake causes hypoglycemia.
Cannot export glucose from glycogen, so buildup of glycogen.

142
Q

limiting step of glycogen synthesis

A

Glycogen synthase.

Adds UDP-glucose 1 residue at a time.

143
Q

glycogen primer

A

Glycogenin.
Self-glycosylates.
Adds UDG-G to Tyr-194.

144
Q

branching enzyme

A

Transfers a block of residues from a terminal end.
Creates a 1-6 branch.
Must be 4+ residues away from an existing branch.

145
Q

debranching enzyme

A

Transfers 3 residues of a branching chain to a different chain, leaving 1 branched residue.
Cleaves remaining 1 residue via hydrolysis.

146
Q

Type I / von Gierke (glycogen storage disease)

A

G6P’ase deficiency (a).
Or defect in transport of G6P to ER (b).
Severe fasting hypoglycemia.
Unresponsive to glucagon, epinephrine.
Increased liver size due to excess glycogen.
Decreased gluconeogenesis causes lactic acidosis.
Treatment: cornstarch

147
Q

Type II / Pompe (glycogen storage disease)

A

Lysosomal acid maltase deficiency.
Inability to digest polysaccharides causes cell inclusions.
A type of LSD.

148
Q

Type III / Cori (glycogen storage disease)

A

Debranching enzyme deficiency.
Abnormal glycogen with short outer branches.
Growth retardation, hepatomegaly, hypoglycemia.
Not as severe as Type I bc gluconeogenesis still possible.

149
Q

Type IV / Anderson (glycogen storage disease)

A

Branching enzyme deficiency.
Abnormal glycogen with few branches.
Weird, long glycogen treated as a foreign body.
Death.

150
Q

Type V / McArdle (glycogen storage disease)

A

Muscle phosphorylase deficiency.
Muscle cramps during hard exercise.
No rise in lactate after exercise.
Myoglobinuria.

151
Q

Type VI / Hers (glycogen storage disease)

A

Liver phosphorylase or phosphorylase kinase deficiency.
Hypoglycemia.
Gluconeogenesis still possible, so not as severe.

152
Q

Type VII / Tauri (glycogen storage disease)

A

Muscle PFK deficiency.
Muscle glycogen content is increased.
Muscle cramps and exercise intolerance.
Helped by fructose (bypasses PFK step).

Exam 2 (5 decks)

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