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Carbohydrates 1 Flashcards

1
Q

Empirical formula of carbohydrate? what happens when n=1?

A

Cn(H2O)n or (CH2O)n

where n> or equal to 3

  • carb= hydrated carbon, saccharide of sugar n=1
  • > becomes H2C=O (formaldehyde), not considered a sugar
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2
Q

How does a plant make glucose from photosynthesis?

A

6CO2 + 6H2O + Energy -> C6H12O6 + 6O2

-uses energy from sun

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3
Q

What are the smallest and simplest sugars? (slide 5)

A

Trioses: smallest sugars

  1. Glyceraldehyde- contains an aldehyde, aldose group, 3 carbons, Carbon 2 is chiral
  2. Dihydroxyacetone- contains ketone, ketone group, 3 carbons
    - theses sugars are interchangeable
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4
Q

Enantiomers of Glyceraldehyde?

A
  • D and L enantiomers
  • chiral carbon- carries 4 different groups
  • forms non superimposable mirror images (hands)
  • most monosaccharides are D
  • most amino acids used for protein synthesis are L shape
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5
Q

what is the most popular dietary source and major energy source?

A
  • Glucose (C6H12O6)- 6 carbons and 6 waters
  • hexose
  • aldose- has an aldehyde group on C1
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6
Q

What are the different structures of glucose? (slide 8)

A
  • chain form
  • Ring form- more stable ring structure in water
  • C1 attacks C5
  • C6 not part of the ring
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7
Q

What are the two conformations of ringed glucose? (slide 9)

A

alpha- OH group on C1 angles down, different plane from C6, more stable b/c big groups point away from each other

beta- OH group on C1 angles up, same plane as C6

-these two conformations can interchange with each other by going through the linear form

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8
Q

Monosaccharides?

A
  • single sugars, monomers
  • glucose
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9
Q

Disaccharide? how it forms? (slide 10)

A
  • two glucose molecules can form a disaccharide (maltose) by condensation (eliminating a water molecule)
  • OH on C1 of alpha glucose combines with OH on C4 of beta glucose, water releases
  • glycosidic bond forms between C1 and C4 to form maltose (alpha 1, 4 glycosidic bond)
  • reducing end is the C1 b/c its electrons are pulled toward oxygen, it becomes oxidized and reduces other things
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10
Q

Lactose? (slide 11)

A
  • milk sugar
  • galactose and glucose
  • disaccharide
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11
Q

Sucrose? (slide 11)

A
  • table sugar
  • glucose and fructose
  • disaccharide
  • no free reducing group is available
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12
Q

Maltose? Maltotriose? Isomaltose? (slide 10)

A

Maltose: glucose(alpha 1, 4)-glucose

Maltotriose: glucose (alpha 1, 4) glucose (alpha 1, 4) gluc

Isomaltose: glucose (alpha 1, 6) glucose

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13
Q

Amylose? (slide 12)

A
  • condense to form oligosaccharide
  • only contains alpha 1, 4 glycosidic bonds
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14
Q

Amylopectin? (slide 12)

A
  • condense to form oligosaccharide
  • contains both alpha 1, 4 and alpha 1, 6 glycosidic bonds
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15
Q

What can Amylose and Amylopectin combine to form? (slide 12)

A
  • starch (plants) or glycogen (animals)- polysaccharides
  • sugars linked with alpha 1,4 (linear to form amylose) and alpha 1, 6 (branched to form amylopectin)
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16
Q

Difference between starch and glycogen? Same? (slide 12)

A
  • Starch is in plants
  • Glycogen is in animals
  • chemically they are the same
  • Glycogen is more branched and has higher molecular weight
  • they both have one reducing end (more chemically active) with many non reducing ends (metabolically more active especially in glycogen- can be cut off quickly to use glucose)
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17
Q

What is cellulose? how is it formed? (slide 13)

A
  • dietary fiber, indigestible carbohydrates
  • glucose molecules linked by beta 1, 4 glycosidic bonds
  • mulitple cellulose chains linked together in parallel by H bonds form strong fibrils, elastic, used by trees to form cell membranes
  • functions in smooth movement of bowels
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18
Q

Glycoproteins?

A
  • protein glycosylation to form a carb/protein mix
  • more protein than carbohydrate
  • membrane bound
  • secreted
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19
Q

Proteoglycans?

A
  • protein glycosylation to form a carb/protein mix
  • more carbohydrate than protein
  • mucins (mucus)
  • lectins (cell-cell interaction)
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20
Q

Protein glycosylation in blood type? (slide 14)

A
  • three genes encode different glycosyltransferases (A, B, O)
  • inherited from each parent (OO, OA, OB, AB)
  • backbone structure is the same but end is different
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21
Q

Process of digestion of dietary carbohydrates? (slide 16)

A
  1. dietary carbohydrates (starch, lactose, sucrose, glycogen) are digested to monosaccharides before absorption
  2. when in mouth, salivary alpha-amylase (endoglucosidase) hydrolyzes the internal alpha 1, 4 glycosidic bonds between glucose residues in starch which produces di and tri saccharides and starch alpha-dextrins (average 8 glucose units with one or more alpha 1, 6 glycosidic bond)
  3. action of salivary amylase stops at stomach
  4. in the lumen of small intestine, pancreatic alpha-amylase (endoglucosidase) continues digestion of starch dextrins to oligosaccharides, trisaccharides, and disaccharides, (maltose and isomaltose)
  5. Enzymes (maltase, isomaltase, sucrase, lactase) located in the brush border of small intestine digest oligo, tri, and disaccharides to generate monosaccharides
  6. Enzymes on brush border are present in complexes, these enzymes are on the membranes of intestinal epithelial cells with alpha helix transmembrane domains and longer extracellular domains, extending out from cells
  7. Glucose, Galactose, Fructose are transported into epithelial cells first, and then transported to the portal circulation that takes them to tissues
  8. undigested and indigestible carbs (cellulose) are excreted along with dietary fiber
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22
Q

What happens to people who have digestive enzyme deficiencies such as a lactase deficiency?

A
  • cannot digest carbs completely
  • the undigested carbs are then digested by bacteria in large intestine, which could generate large volumes of CO2 and H2, causing abdominal cramps, diarrhea, and flatulence
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23
Q

What are some factors that lead to lactase deficiency? treatments?

A
  • age dependent lactose intolerance- capacity to digest lactose decreases after infancy, adulthood lactase activity is genetically determined
  • intake of lactose has some effect on lactase expression
  • hereditary lactose intolerance- 25% of all adults in US, more common in Asians, African Americans, Natives
  • treatment- reduce or avoid dairy products, take lactase supplements with meal, take foods with live microorganisms (probiotics)
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24
Q

Why is brush border membrane of the small intestine folded?

A
  • like mitochondria, it increases surface area
  • allows more nutrients to be absorbed
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25
Q

What facilitates fructose transport in intestine? (slide 18)

A

GLUT 5

  • located on both luminal and basolateral sides of intestinal epithelial cells
  • facilitated diffusion- high to low concentration
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26
Q

What facilitates glucose transport in intestine? (slide 18)

A

GLUT 1

-facilitated diffusion (passive transport)

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27
Q

What is SGLT1? (slide 18)

A
  • Na+ glucose cotransporter (occurs in epithelial cells of intestines and renal tubule)
  • not facilitated diffusion, secondary active transporter
  • can bring galactose, glucose from the lumenal side to the bloodstream against the concentration gradient, low to high
  • Na+ moves into the cell down its gradient
  • coupled with Na+/K+ ATPase, involves use of energy
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28
Q

Process of Glucose and Galactose transport in epithelial cells of intestine? (slide 19)

A
  1. Glucose goes into luminal side (low glucose concentration) of the cell by facilitated diffusion by GLUT1
  2. Glucose and Galactose are transported against their gradient by SGLT1, and Na+ is transported down its gradient at the same time
  3. Glucose and Galactose is transported into the blood stream on the basolateral (high glucose concentration) side of the cell by facilitated diffusion by GLUT1
  4. Na+ is transported out of the cell against its gradient by Na+/K+ ATPase, while K+ is transported into the cell, ATP is used
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29
Q

Functions of GLUT1 and GLUT3?

A
  • present in many cell membranes
  • basal transporters of glucose at a constant rate into tissues that are metabolically dependent on glucose (brain, RBCs)
  • have lower Km (higher affinity) for glucose than GLUT2
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30
Q

Functions of GLUT2?

A
  • present in liver and pancreatic beta cells
  • very high Km value for glucose, low affinity
  • glucose only enters these tissues when there are high concentrations in blood
  • pancreas senses glucose levels and adjusts the rate of insulin secretion
  • functional GLUT2 is needed for proper insulin secretion to remove glucose from blood for storage (glycogen, fat)
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31
Q

Summary of glucose transporters? (slide 20)

A
  • insulin dependent or insulin independent
  • several glucose transporter proteins mediate the thermodynamically downhill movement of glucose across plasma membranes
  • see chart
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32
Q

What is Km? (slide 21)

A
  • michaelis constant
  • a characteristic of transporters
  • Km is the concentration (molarity) when V= 1/2 Vmax
  • Km is inversely proportional to affinity for substrate
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33
Q

What is the Km of GLUT1 and GLUT3? what does that mean? (slide 22)

A
  • low Km (1 mM)= high affinity
  • glucose is relatively independent of extracellular glucose concentration
  • GLUT1= RBC -GLUT3= brain
  • these cells need glucose constantly so the change of V from low to high concentration is the same
34
Q

Km of GLUT2? what does that mean? (slide 22)

A
  • high Km= low affinity
  • GLUT2= liver transporter
  • almost proportional to extracellular glucose concentration
  • high Km allows glucose to rapidly enter liver cells in times when glucose is plenty in blood
35
Q

Functions of GLUT4? Km? (slide 23)

A
  • mediates insulin stimulated transport of glucose in muscle and adipose tissue
  • intermediate Km= 5 mM
  • amount of GLUT4 is present in muscle increase in response to endurance exercise
36
Q

Where is GLUT4 located in the absence of insulin? with insulin? GLUT4 defects? Vmax?(slide 23)

A
  • without insulin, it resides in the membrane enclosed intracellular vesicles
  • in the presence of insulin, there is a rapid increase in the number of GLUT4 on the plasma membrane to facilitate transport of glucose, they translocate with insulin stimulation
  • defects of GLUT4 can result in insulin resistance
  • low Vmax of cells in absence of insulin reflects low number of GLUT4 on cell surface, when insulin rises the Vmax also rises by increasing GLUT4 on the cell surface
37
Q

Distribution of glucose to various tissues? (slide 24)

A
  • consistent and relatively low levels of glucose are delivered to RBC by GLUT1 and brain by GLUT1 and GLUT3
  • absorption of glucose in adipose tissue and muscle is mediated by GLUT4 and is insulin dependent
  • liver glucose absorption and glycogen synthesis will not happen until blood glucose levels are even higher, this is the most efficient way to prevent too high levels of blood glucose, and glycogenolysis is main source in between meals
  • see chart
38
Q

Where does Glycolysis occur? what is it?

A
  • cytoplasm
  • Glycolysis is the degradation of 1 glucose to 2 pyruvate (3 C molecule) in a series of 10 reactions
  • substrate level phosphorylation
39
Q

Summary steps of Glycolysis? (slide 26, 29)

A
  1. Energy investment phase (steps 1-5), consume 2 ATP

Glucose -> 2-Glyceraldehyde-3-phosphate

  1. Energy generation phase (steps 6-10), generate 4 ATP and 2 NADH

2 (1, 3-Bisphosphate glycerate) -> 2 Pyruvates + 4ATP + 2NADH -net reaction: Glucose -> 2 Pyruvates + 2ATP + 2NADH

40
Q

Steps of Phase 1: Energy investment of Glycolysis? (slide 27)

A
  1. Glucose is phosphorylated by Glucokinase (liver) or hexokinase (most tissues) using one ATP to form Glucose-6-phosphate, irreversible step because ATP is used
  2. G6P is isomerize by Phosphohexose isomerase to become Fructose-6-Phosphate
  3. F6P is phosphorylated to Fructose 1, 6-Bisphosphate by Phosphofructokinase-1, using one ATP, this step is irreversible
  4. F1,6BP is broken down by Aldolase to become Glyceraldehyde-3-phosphate or Dihydroxyacetone phosphate (can serve backbone of fat synthesis)
  5. G3P and DHAP can be interchanged by triosephosphate isomerase
    - situation dependent and cell environment dependent
41
Q

Steps of Phase 2: Energy generation of Glycolysis? (slide 28)

A
  1. Glyceraldehyde-3-phosphate is changed by the enzyme G3P Dehydrogenase (GAPDH) into 1,3-Bisphosphoglycerate, the reducing equivalent NAD+ is used in this step, 2 H are given to form NADH + H+
  2. 1,3-BPG is dephosphorylated by phosphoglycerate kinase using ADP to form 3-phosphoglycerate and one ATP, reversible step
  3. 3-phosphoglycerate is changed to 2-phosphoglycerate by phosphoglycerate mutase, phosphate group moves from C3 to C2
  4. 2-phosphoglycerate is changed to phosphoenolpyruvate (PEP) by Enolase
  5. PEP is dephosphorylated by pyruvate kinase and ADP to form Pyruvate and one ATP
    - each of these steps happens twice
    - 4 ATP generated
    - 2 NADH generated -substrate level phosphorylation in cytoplasm
42
Q

2 levels of regulation of Glycolysis? (slide 31)

A
  • local
  • global
43
Q

3 enzymes involved in regulation of Glycolysis? (slide 32)

A
  1. Glucokinase (liver), hexokinase (other tissues)
  2. Phosphofructokinase-1 (rate limiting step)
  3. Pyruvate Kinase
44
Q

Role of Hexokinase in regulation of glycolysis? (slide 33)

A
  • Km= .05mM
  • constitutive, found in most other tissues besides liver
  • inhibited by its product, Glucose-6-phosphate (G6P)
  • high concentrations of G6P signal the cell that it no longer requires glucose for its energy purpose, glucose is left in blood
  • makes G6P for glycolysis
45
Q

Role of Glucokinase in regulation of glycolysis? (slide 33)

A
  • Km= 10mM
  • 100 fold lower affinity for glucose than hexokinase
  • is inducible by insulin in liver, when glucose levels high
  • found in liver and pancreatic beta cells
  • provides G6P for synthesis of glycogen of source of biosynthetic precursors
  • is inhibited by Fructose-6-phosphate (F6P)
46
Q

Kinetics of hexokinase vs glucokinase? (slide 34)

A

Km for hexokinase is much lower so has a much higher affinity for glucose and works for efficiently

47
Q

Regulation of Glucokinase activity? (slide 36)

A
  • F6P inhibits GK and enhances translocation of GK to nucleus
  • GK binds the RP and is inactivated
  • when glucose levels are again elevated, GK dissociates from RP and is translocated to cytoplasm to is activated again
48
Q

Role of Phosphofructokinase-1 in regulation glycolysis? (slide 38)

A
  • PFK-1 is rate limiting enzyme
  • catalyzes F6P to F1,6P
  • allosterically inhibited by ATP and Citrate
  • allosterically activated by AMP and F2,6P
49
Q

How does AMP and F2,6P allosterically activate PFK-1? (slide 38)

A
  • shifts curve left
  • lowers Km which raises affinity
50
Q

Role of F2,6P, PFK-2, and F2,6bisPase in regulation of glycolysis? (slide 40)

A
  • F2,6P is not an intermediate in glycolysis but plays important role in regulation of glycolysis by activating PFK-1
  • PFK-2 catalyzes reaction of F6P into F2,6P
  • PFK-2 and F2,6bisPase determine F2,6P levels
51
Q

What does F2,6P regulate in liver? adipose?

A
  • liver- regulates glycolysis and gluconeogenesis
  • adipose- regulates glycolysis
52
Q

Phosphorylated vs dephosphorylated regulation in PFK-2 and F2,6bisPase? (slide 41)

A
  • PFK-2:
  • increased insulin/glucagon
  • phosphorylated- inactive
  • dephosphorylated- active
  • F2,6bisPase:
  • decreased insulin/glucagon
  • phosphorylated- active
  • dephosphorylated- inactive
  • ratios of insulin/glucagon determine phosphorylation
53
Q

Why does ATP, AMP, and Citrate regulate glycolysis? (slide 39)

A
  • accumulation of ATP slows down glycolysis because already have enough energy
  • AMP leads to activation of glycolysis, want to make it into ATP
  • Citrate inhibits glycolysis because it is the first product of TCA cycle, high concentration of citrate it is transported from mitochondria to cytosol and bind PFK-1 and allosterically inhibits
54
Q

Regulation of Pyruvate Kinase in glycolysis? (slide 42)

A
  • Allosteric inhibitors:
  • Alanine
  • ATP
  • Allosteric activators:
  • F1,6P in a feed forward mechanism
55
Q

How does Alanine regulate pyruvate kinase? (slide 42)

A
  • pyruvate can be turned into Alanine by alanine aminotransferase
  • accumulation of alanine tells pathway to stop
56
Q

How does F1,6P regulate pyruvate kinase? (slide 42)

A
  • F1,6P is before it in the path so it activates the path to move forward
  • this is why PFK-1 is the rate limiting enzyme because it regulates F1,6P
57
Q

Hormonal regulation of pyruvate kinase? (slide 43)

A
  • liver pyruvate kinase is insulin inducible
  • hormonally regulated by covalent modification (phosphorylation)
  • high glucose leads to high insulin which leads to dephosphorylation of pyruvate kinase, more active
  • low glucose leads to low insulin, high glucagon which leads to phosphorylation of pyruvate kinase, inactive
58
Q

Summary of enzyme regulation of glycolysis? (slide 44)

A

explain pic

59
Q

Summary of hormonal regulation of glycolysis? (slide 44)

A

explain pic

60
Q

What are anaerobic conditions? what happens to pyruvate under these conditions? (slide 45)

A
  • lack mitochondria
  • lack O2
  • strenuous exercise
  • RBCs
  • pyruvate is reduced to lactate in cytosol by lactate dehydrogenase (LDH) using reducing equivalents NADH, it is turned back to NAD+
  • NAD+ being freed is important because it can be used in other reactions of glycolysis
  • under anaerobic glycolysis, 2 ATP are generated for every one mole of glucose degrading into 2 moles of lactate
61
Q

What are the 4 metabolic fates of pyruvate? (slide 42)

A
  1. decarboxylation to form acetyl CoA which can be used for ATP synthesis or fatty acid synthesis
  2. formation of amino acid, Alanine, and connecting to protein synthesis
  3. carboxylation and formation of oxaloacetate for gluconeogenesis
  4. formation of lactate which can be reversibly oxidized to pyruvate (used for gluconeogenesis in liver) or entering cori cycle
62
Q

What happens to pyruvate under aerobic conditions? steps? (slide 46)

A
  • conditions: enough oxygen, mitochondria, and low ATP/ADP
    1. pyruvate enters mitochondria through monocarboxylate transporter (anti porter) with exchange of OH
    2. inside mitochondria, pyruvate is decarboxylated into acetyl CoA catalyzed by pyruvate dehydrogenase (PDH), highly regulated step
    3. acetyl CoA is oxidized to CO2 and H2O through the TCA cycle to generate ATP
    4. reducing equivalent (NADH, FADH2) generated in cytoplasm and mitochondria will be transferred to mitochondrial matrix through shuttle systems to be used for ATP synthesis
63
Q

Steps of TCA cycle? (slide 47)

A
  1. Acetyl CoA is turned into Citrate by citrate synthase
  2. Citrate is turned into Isocitrate by aconitase
  3. Isocitrate is turned into alpha-ketoglutarate by isocitrate dehydrogenase, CO2 released, NADH generated
  4. alpha-ketoglutarate is turned into Succinyl CoA by alpha-ketoglutarate dehydrogenase, CO2 released, NADH generated
  5. Succinyl CoA is turned into Succinate by succinate thiokinase, GTP produced (substrate level phosphorylation)
  6. Succinate is turned into Fumarate by succinate dehydrogenase (complex 2), FADH2 produced
  7. Fumarate is turned into Malate by fumarase
  8. Malate is turned into Oxaloacetate by malate dehydrogenase, NADH produced
    - summary:
    - 4 carbon OAA + 2 carbon acetyl CoA = 6C Citrate
    - 2 carbon atoms in acetyl CoA become 2 CO2
    - 4 major oxidation/reduction steps, H atoms turned into reducing equivalents in forms of NADH and FADH2 to be used for ATP synthesis
    - 3 NADH = 7.5 ATP, 1 FADH2= 1.5 ATP
    - 1 GTP molecule is made by substrate level phosphorylation (high energy Succinyl CoA)
    - TCA cycle connects metabolisms of carbs, proteins, lipids
64
Q

What adjusts the rate of the TCA cycle? (slide 49)

A
  • oxidation of acetyl CoA in the TCA cycle can only go as fast as electrons from NADH and FADH2 enter the electron transport chain
  • so the rate of TCA is adjusted to the rate of oxidative phosphorylation
  • availability of substrates (acetyl CoA and OAA) for citrate synthase sometimes limits rate of citrate formation
65
Q

What are the major regulatory enzymes of TCA cycle? (slide 49)

A
  • Citrate synthase (step 1)
  • isocitrate dehydrogenase (step 3)
  • alpha ketoglutarate dehydrogenase (step 4)
66
Q

Inhibitors and activators of citrate synthase in TCA? (49)

A
  • inhibitors: citrate, succinyl CoA
  • activators: OAA, acetyl CoA
67
Q

Inhibitors and activators of isocitrate dehydrogenase in TCA? (49)

A
  • inhibitors: NADH
  • activators: ADP, calcium
68
Q

Inhibitors and activators of alpha ketoglutarate dehydrogenase in TCA? (49)

A
  • inhibitors: NADH, succinyl CoA, GTP
  • activators: ADP, Calcium released from SR
69
Q

What is the primary regulator of TCA? (49)

A

ratios:

  • ATP/ADP
  • NADH/NAD+
  • ATP and NADH are inhibitory
  • ADP and NAD+ are stimulatory
70
Q

How does the NADH/NAD+ ratio regulate TCA? (49)

A

-NADH, generated in isocitrate and alpha ketoglutarate oxidation, accumulates when TCA slows down so a high NADH/NAD+ ratio inhibits both dehydrogenases

71
Q

Howe does calcium regulate TCA? (49)

A

-in muscle, calcium signals for contraction and for increase of demand of ATP, this activates isocitrate dehydrogenase and alpha ketoglutarate dehydrogenase, and PDH complex

72
Q

How is the TCA cycle an open system? (51)

A
  • anaplerosis- synthesizing and replenishing the intermediates of the TCA cycle
  • cataplerosis- intermediates escaping from the TCA cycle and synthesizing other molecules
73
Q

What is the Warburg effect? (52)

A
  • increased aerobic glycolysis in cancer cells
  • more intermediary molecules for anabolism and cell growth
  • acidity helps cancer cells invasion and escape from immune system
  • administer FDG therapy- tumor in liver shrinks, FDG goes to kidney and is secreted in urine
74
Q

What other simple sugars can be converted into intermediates in glycolysis? (53)

A
  • mannose
  • galactose
  • fructose
75
Q

How does mannose turn into an intermediate of glycolysis? (53)

A

-hexokinase converts mannose to mannose-6-P -mannose-6-P can be converted to fructose-6-P by an isomerase

76
Q

How does Fructose turn into an intermediate of glycolysis (53)

A
  • fructokinase converts fructose into fructose-1-P -aldolase B cleaves the 6C sugar into two 3C sugars, DHAP and glyceraldehyde
  • glyceraldehyde kinase converts glyceraldehyde into G3P
77
Q

What happens if too much fructose is consumed? (54)

A
  • leads to fatty liver or hyperglycemia
  • overweight and obesity (high fructose corn syrup)
  • fructose bypasses rate limiting step of glycolysis (PFK-1), less regulated
  • fructose can only be used as energy or stored as fatty acid, which cannot be reversed to be used as energy (cannot be stored as glycogen)
  • glucose can be used as energy, stored and glycogen and then reversed to be used as energy
78
Q

Fructokinase deficiency?

A
  • autosomal recessive
  • fructosuria- high fructose in blood, secreted in urine
79
Q

Aldolase B deficiency?

A
  • autosomal recessive
  • fructose intolerance
  • F1P accumulation
  • low phosphate availability
  • inhibition of glycolysis and gluconeogenesis
  • decreased ATP/ADP
  • liver damage
80
Q

How does Galactose turn into an intermediate of glycolysis? (53)

A
  • galactokinase converts galactose to galactose-1-P
  • transferase utilizes a high energy form of glucose (UDP-glucose) to exchange galactose for glucose
  • epimerase converts UDP-galactose to UDP-glucose
81
Q

Why is too much glucose bad? (55)

A
  • no enzymatic glycosylation (formation of Hb-a1c)
  • conversion to fructose (high fructose toxicity)
  • leads to accumulation of sorbitol in tissues (Schwann cells, lens, retina, kidneys and these tissues lack sorbitol dehydrogenase) and causes cataracts, retinopathy, peripheral neuropathy
82
Q

Energy cycle? (56)

A

see pic

MBM (24 decks)

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