2012-11-26 1&2: Intro to Carbs; Glycolysis in RBCs Flashcards

1
Q

What f(x)s do carbs serve?

A

1) metab fuel, 2) protein components, 3) RNA/DNA components, 4) structure in plants, 4)

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2
Q

Which form of glucose is transported in the blood?

A

99% is cyclized; alpha-D-glucose is major (2/3) form

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3
Q

Is it glucose and oxidizing or reducing sugar? When is this important? What would the metab product be useful for?

A

it is a reducing sugar (i.e. it reduces other things will becoming OXIDATED itself); makes glucuronic acid which detoxifies things like heme by conjugating them

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4
Q

How does hyperglycemia cause neuro- and retin-opathy?

A
  1. Glucose—aldose reductase—>sorbitol
  2. lens, retina, kidney and nerve cells lack sorbitol DH
  3. sorbitol builds up—>cataracts, periph neurop, retinop, nephrop
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5
Q

Which of the following is NOT true regarding glucose?

a. It spontaneously forms a cyclic, hemiacetal in solution.
b. It is a diastereoisomer of ribulose.
c. It is the form in which carbohydrate is transported from the liver to skeletal muscle.
d. It reacts chemically to form a covalent bond! with hemoglogin.

A

B

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6
Q

What can glucose be metabolized to in humans?

A

lactate, CO2, pentoses or glycogen

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7
Q

What does the heart do with lactate?

A

sends it thru CAC to make ATP

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8
Q

What does liver do with lactate?

A

converts it to glucose via gluconeogenesis

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9
Q

What is made with the pentose phosphate pathway?

A

pentoses, NADPH, and ATP

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10
Q

Where does pentose phosphate pathway occur?

A

in RBCs

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11
Q

Which pathway(s) of glucose metab is(are) anaerobic?

A

glycolysis and pentose phosphate pathway

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12
Q

How can RBCs use glucose

A

glycolysis and pentose phosphate pathway ONLY

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13
Q

How and where do we make fructose?

A

glucose—reduced to alcohol—>sorbitol—oxidized—>fructose; occurs in seminal vesicles and liver

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14
Q

How is HbA1c formed?

A

glucose slowly reacts with NH2 groups on Hb

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15
Q

GAGs vs. proteoglycans

A

GAGs = glycosaminoglycans = polysaccs w/ carboxy, amino and sulfate groups (e.g. chondroitin, heparin, hyaluronic acid, keratan sulfate)

proteoglycans are proteins with GAGs added onto them; form joint lubes and c.t.

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16
Q

Which glycosidic linkages can humans digest? Not?

A

We can: α-1,4 glycosidic bond

We can’t digest: ß-1,4, glycosidic bonds (e.g. cellulose)

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17
Q

What is the first step glucose undergoes upon entering the cell?

A

glucose—>G6P

18
Q

What is the next step for G6P headed to glycolysis?

A

G6P—>F6P

19
Q

What is the next step for G6P headed to glycogen synthesis?

A

G6P—>G1P

20
Q

What is the next step for G6P headed to pentose phosphate pathway?

A

6-phosphogluconate

21
Q

Why phosphorylate glucose?

A

Phosphorylation of glucose lowers its intracellular concentration and promotes glucose influx.

22
Q

Why do RBCs need ATP?

A

to maintain membrane potential w/ Na/K ATPase

23
Q

How many ATP/glucose in glycolysis?

A

2

24
Q

Which enzymes regulate glycolysis?

A

hexokinase, phosphofructokinase-1 and pyruvate kinase

25
Q

What is the overall formula for anaerobic glycolysis in an RBC?

A

glucose + 2 ADP + 2Pi —> 2 lactate + 2 ATP

26
Q

Where is glucokinase present?

A

liver and pancreas

27
Q

Which has a higher Km, glucokinase or hexokinase? What does that mean?

A

Glucose kinase’s Km (10mM) is 100X higher than hexokinase; allows pancreatic ß cells to sense glucose amt AND high vMax allows it to allow liver to take up high amts of blood glucose

28
Q

What inhibits hexokinase?

A

G6P

29
Q

Draw glycolysis with important enzymes!

A
  1. glucose—gluco-/hexo-kinase—>G6P
  2. G-6-P—>F-6-P
  3. F-6-P—PFK-1—>F-1,6-BP
  4. F-1,6-BP—>G3P (and DHAP)
  5. G3P—>1,3-BPG
  6. 1,3,-BPG—>2-PG
  7. 2-PG—>3-PG
  8. 3-PG—>PEP
  9. PEP—>pyruvate kinase—>pyruvate
  10. pyruvate—LHD—>lactate
30
Q

What regulates PFK-1?

A

stimulated by: AMP, ADP, and F-2,6-BP

inhibited by: ATP, citrate

31
Q

What regulates pyruvate kinase?

A

inhibited by: glucagon, ATP

32
Q

How is glucokinase regulated?

A

It’s not? at least it’s not inhibited by G6P like hexokinase is

33
Q

What are the steps involved in insulin secretion?

A
  1. Glucose enters pancreatic ß cell via GLUT-2
  2. gluc—glucokinase—>G6P
  3. resultant higher ATP closes ATP-sensitive K+ channel
  4. K+ can no longer leak out, and the resulting depolarization opens Ca2+ channel
  5. incr intracell Ca causes exocytosis of insulin granules
34
Q

Which steps of glycolysis are NOT reversible?

A
  1. glucose—gluco- or hexo-kinase—>G6P
  2. F6P—PFK-1—>F1,6BP
  3. PEP—pyruvate kinase—>pyruvate
    (i. e. the steps w/ the important enzymes)
35
Q

What is the deal w/ PFK-2?

A

PFK-2 is bifunctional with kinase and phosphatase sides

kinase side does: F6P—>F-2,6-BP

F-2,6-P activates PFK-1

inhibited by glucagon (via cAMP via PKA)

36
Q

How does arsenic poisoning inhibit glycolysis?

A

arsenate subs for phosphate in G3P—>1,3-BPG

37
Q

Where/how much ATP is req’d in glyoclysis?

A

Two total:

  • 1 by the hexokinase rxn
  • 1 by F-6-P—>F-1,6-P
38
Q

What is 2,3-BPG?

A

made from 1,3-BPG

decr o2 affinity of hemoglobin

39
Q

What are the isozymes of LDH?

A
  • LDH is tetramer
  • h4 in heart: lactate—>pyruvate
  • m4 in SKM & liver: pyruvate—>lactate
40
Q

High plasma [H4-LDH] is indicative of what pathology?

A

acute M.I. (recall that H4 is heart-specific isozyme)

41
Q

In the conversion of glucose to lactate by glycolysis, how many of the enzymes involved exist as different “isozymes” in different tissues? 1, 2, 3 or 4?

A

3—pyruvate kinase, LDH and hexo-/gluco-kinase

42
Q

Why bother making lactate?

A

need to oxidize NADH—> to NAD+