Carbs I

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emmayarewhy
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237329
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Carbs I
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2013-09-27 08:41:51
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msbiochem
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msbiochem exam 1
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  1. 1. What % of total calories are carbs?
    2. What is IOM's recommended daily %? Daily g?
    3. What is a carb? What does this fail for? (3)
    4. What are simple carbs? (6)
    5. What are complex carbs? (6)
    6. What is an oligosaccharide? What is a polysaccharide?
    • 1. 50%
    • 2. 45-65%; 130 g
    • 3. Compounds containing C, H, O (1:2:1), oligo/polysaccharides + sugar alcohols
    • 4. Monosaccharides (glucose, fructose, galactose), trioses, tetroses, pentoses, oligosaccharides (3-10)
    • 5. Polysacchairdes (>10 monosaccharides), starch, glycogen, cellulose, pectin, gums
  2. 1. Examples of disaccharides? (3)
    2. How are carbons classified? (2)
    3. What do monosaccharides contain?
    4. Give defs and examples of enantiomers, epimers, anomers
    5. What are substituted sugars? 4
    • 1. Maltose, lactose, sucrose
    • 2. By # of carbons (pentose vs. hexose) and by carbonyl type (aldose vs. ketose)
    • 3. Enantiomers - mirror images of same chiral compounds (D vs. L); epimers - compounds w/ same chemical formula but differ with OH group at a chiral center (D-glucose vs. D-galactose); anomers - alpha-D-glucose vs. B-d-glucose. B=up, alpha = down at C1

    5. Sugars containing P, amino, sulfate, or N-acetyl groups
  3. 1. Homopolymers vs. heteropolymers?
    2. Purpose of polysaccharides (2)
    3. What is glycogen? Where is it stored?
    4. What is starch? Two types?
    5. What is cellulose? What is its major role? What type of linkages does it have? What do mammals lack?
    1. Homopolymers - all monosaccharides are the same; heteropolymers - monosaccharides are different.

    2. Energy storage and maintaining structural integrity (plants --> cellulose)

    3. Storage form of glucose in animals; muscle & liver
  4. 1. Where does main carb digestion take place?
    2. What is hydrolyzed less efficiently? Why?
    3. Can a-amylases break disaccharides into monosaccharides? Can they split branch points?
    4. What is found at brush border of small intestine? (2)

    5. Name disaccharidases and the bonds that are broken.
    6. What breaks branches?
    • 1. Small intestine (duodenum/jejunum)
    • 2. Whole grains bc enzyme cannot easily access a1,4 bond.
    • 3. No. No.
    • 4. Oligosaccharidases and disaccharidases (glycoproteins)

    • 5. Lactase (B-gal; B-1,4 bond)
    • Sucrase a-glucose, a,B1-2 bond
    • Maltase a1,4 bonds

    6. Isomaltase (a,1,6 bonds)
  5. 1. Which glycosidic bonds can't be hydrolyzed by human digestive enzymes? (2)
    2. Where are the above found?
    3. What is raffinose? What can break it down?
    4. Name types of fiber in the diet? (5)
    5. What can breakdown soluble fibers in humans? To what products? 2 What happens to one product?
    • 1. B1,4 bonds and a, galacosidic bonds
    • 2. Homopolymers of glucose (cellulose, pectins, gum) and oligosaccharides such as raffinose

    3. Trisaccharide: galactose-fructose-glucose goes to colon directly. Bacteria in colon

    4. Cellulose, hemicellulose, lignin, pectins, gums, mucilages

    5. Bacteria to short chain fatty acids and gases. short-chain fatty acids --> liver for caloric value 25-36 g/day fiber
  6. Describe absorption of monosaccharides

    1. Where does Na+ come from? (2)
    1. SGLT1: transports 2Na+/glucose or galactose symporter from lumen. Na+ comes from dietary intake and pancreatic secretions. (low IC Na+ drieves Na+ uptake, requiring glucose to be transported at same time). Na+ is then pumped out using Na+/K+ATPase.

    2. Facilitated diffusion - mostly glucose uptake into tissues. GLUT proteins transport hexose down concentration gradient (fructose)

    Then both use GLUT 2 to get out of cell.
  7. 1. What is the saturable amount of pure fructose absorption?
    2. How does fructose uptake compare to glucose uptake? (2)
    3. What enhances fructose entry into cell?

    4. What does GLUT 2 do?
    - Where?
    - What does it transport?
    - Km/affinity?
    - Capacity (Vmax)?
    - Special job

    5. GLUT 4?
    - Where? - What does it transport?- Km/affinity?- Capacity?- Special job

    6. GLUT 5
    - Where? - What does it transport?-  Special job
    • 1. 5-50 g
    • 2. (1) fructose uptake is more rapid; in fact, glucose absorption enhances fructose entry into cell and (2) increased fructose absorption upregulates GLUT 5 expression

    3. Glucose absorption.

    4. GLUT 2: liver & pancreas; transports glucose, galactose, fructose;  low affinity/high Km; high capacity glucose transporter; serves as glucose sensor in b-cells results in insulin secretion; imports monosaccharides from enterocytes to blood

    GLUT 3 - brain; high affinity, low Km

    GLUT 4 - skeletal/cardiac muscle/adipocytes; glucose; low km/high affinity; low capacity; insulin-responsive glucose transporter

    GLUT 5 - small intestine/sperm; transports fructose, but not glucose/galactose
  8. 1. Why is it important that brain, kidney, and liver don't use GLUT 4?

    2. Why do liver and pancreas use GLUT 2 (low affinity) transporter? (2)

    3. Why do we want skeletal/cardiac muscle and adipocytes to have low Km?

    4. Where does most glucose go after a meal? What takes precedent?
    1. We don't want to wait for insulin for glucose uptake.

    • 2. Bc these systems will not easily saturate and allows systems to change its transport rate in response to glucose after a meal.

    • 3. Low Km --> high affinity --> low capacity. Because these places can store A LOT of glucose and we want glucose blood levels to be
    • maintained.

    4. 50% goes into storage (liver, muscle, fat) and 50% goes into energy synthesis (ATP). Brain.
  9. 1. What are the four important IC glucose central pathways?

    2. Is glucose metabolism the same in all tissues? How is it different?
    • 1. Glycogenesis vs. glycogenolysis
    • 2. Glycolysis vs. gluconeogenesis
    • 3. TCA
    • 4. ETC


    2. No, RBC: PPP but no TCA, ETC. Brain:Can do all basics (glycolysis, TCA, eTC); Muscle: basics + glycogenesis/glycogenolysis, but cannot export glucose. Liver: PPP, GNG, glycogen metabolism, and basics.
  10. 1. Why is it more favorable to store energy in fat? 3 In glycogen? 3
    1. (1) Fat - more calories/gram; doesn't require water - weight-efficient; unlimited stores (2) Glycogen is readily accessible (can be degraded from all termini)- quick source of energy, can be metabolized anaerobically, fat cannot be converted to glucose for secretion.
  11. Describe glycogen synthesis (5)
    1. Glucose activation (UDP-glucose pyrophosphrylase: G6P --> G1P + UTP --> UDP Glucose

    2. Synthesis initiation: Autocatalysis - Glycogenin + UDP-glucose --> glycogen initiation

    3. Elongation - glycogen synthase - UDP glucose + glycogen of at least residues ---> a1,4 bond --> glycogen elongation

    4. Branch formation -
    Branching enzyme - transfers 7 glucose molecules from chain of at least 11 residues and tacks on via a1,6 bond. Branch points are at least 4 residues apart

    5. Elongation + branch formation
    continues
  12. Describe glycogen breakdown (4)

    What are options for G6P? (3)
    1. Release of G1P - glycogen phosphorylase - cleaves glucose 1 by 1 until 4 left on branch.

    2. Remodeling: - transfers 3 residues to main branch for further degradation

    3. G1P --> G6P: phosphoglucomutase

    4. G6P --> Glucose (LIVER ONLY!!) glucose 6 phosphatase

    5. Debranching Enzyme: cleaves off last residue on branch and releases as free glucose (a1,6 glucosidase)

    Glycolysis, export to other tissues (G6Ptase) and PPP
  13. Glycogen storage disease

    Name, defective enzyme organ affected, glycogen in affected organ, clinical features

    1. Type I
    2. Type II
    3. Type III
    4. Type IV
    Type I "von Gierke" - G6Pase or transport system; kidney/liver; increased amount of glycogen but normal structure; enlargement of liver, failure to thrive, severe hypoglycemia, ketosis, hyperlipidemia


    Type II (Pompe's) - a1,4glucosidase; all organs; massive increase in amount, normal structure ; cardiorespiratory failure before age 2

    Type III (Cori disease) - debranching enzyme; muscle & liver; increased amount - short outer branches; like type I but milder

    Type IV (Andersen) Branching enzyme (a1,6);normal amount, long outer branches, progressive cirrhosis of liver --> liver failure
  14. Glycogen storage disease

    Name, defective enzyme organ affected, glycogen in affected organ, clinical feature

    Type V
    Type VI
    Type VII
    Type VIII
    Type V (McArdle) - p'lase - muscle - moderately increased,muscle; moderately increased amount/normal; limited ability to perform strenuous exercise bc of cramps

    Type VI (Hers disease) p'lase - liver - increased amount - like TYpe I but milder

    Type VII - PFK (muscle) - increaseda mount, normal structure. Like type V (cant exercise)

    Type VIII - PFK (liver) - increased amount, normal structure. Mild liver enlargement, mild hypoglycemia. Liek t ype I but milder
  15. Draw glycolysis (10 steps)

    Overall rxn?
    • Hexokinase/glucokinase, phosphohexose isomerase, PFK-1, aldolase, triose phosphate isomerase, glyceraldehyde-3-P dehydrogenase, phosphoglycerate kinase, phosphoglyceromutase, enolase, pyruvate kinase

    Glucose + 2 ATP + 2 ADP + 2 Pi ---> 2 pyruvate + 2H+ + 2 ATP + 2H2O

    Total possible ATP = 2 ATP + 4/6 ATP = 6-8 ATP
  16. 1. What happens to pyruvate after glycolysis in aerobic and anaerobic conditions?

    2. What else is glycolysis important for? (3)

    3. Draw the Cori cycle. What is it important for?
    1. Aerobic - pyruvate --> mitochondria for TCA: anaerobic: lactate dehydrogenase: pyruvate + NADH --> lactate + NAD+

    2. Triglyceride synthesis from G6P --> glycero P; 5 carbon sugar (DNA/RNA syn) from G6P; AA synthesis

    • 3.
    • Important for preventing lactic acidosis
  17. Draw fructose metabolism and where it intersects w glycolysis



    4 enzymes
  18. 1. What is missing in hereditary fructose intolerance?

    2. What happens?

    3. What is the result? 3

    4. What is the treatment?

    5. Can humans synthesize fructose? If so, in what pathway?
    1. Low aldolase B activity (in liver)

    2. Leads to accumulation of F1P --> inhibiting glycogen breakdown and GNG in liver

    3. Lactic acidosis

    4. Dietary treatment (no fructose)

    5. Yes from glucose --> fructose in polyol pathway.
  19. Describe galactose metabolism 3 steps
    1. Galactokinase: galactose --> gal-1-P

    2. Gal-1-P uridyl transferase: Gal-1-P + UDP-glucose --> UDP-galactose + GLUCOSE-1-P --> GLYCOLYSIS

    3. UDP-galactose-4-epimerase: UDP-galactose ---> UDP-glucose
  20. GNG

    1. What are non-carb precursors of glucose? (3)
    2. Is it a simple reversal of glycolysis?
    3. What is the abbreviated version? Name + description

    4. What organs are completely dependent on glucose for energy needs? (2)

    5. Where does GNG occur? (2)

    6. What is it stimulated by? (2) Inhibited by? (1)

    7. How much energy does it require? Where is this energy from?
  21. Draw GNG pathway

    What are the enzymes for the 3 irreversible rxns? What are their cofactors?




    1. Pyruvate carboxylase (pyruvate --> OAA in mit) Requires B7, Acetyl CoA = allosteric activator & PEPCK

    2. F1,BPtase (F1,6BP --> F6P)

    3. G6Ptase (bound in ER): G6P --> Glucose
  22. 1. What pathways require NADPH? 6

    2. Where? 7

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