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SFM EXAM Real > Carb Metabolism > Flashcards

Carb Metabolism Flashcards

1
Q

Taruai Disease

A

PFK1 deficiency. No ATP. muscle weakness Hemolytic anemia from Na pumps requiring ATP.

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2
Q

Hemolytic anemia

A

most common from glycolytic enzyme defects, 95% time PK. Na pumps requiring ATP don’t function right. Na+ pulls water into cell lysing it.

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3
Q

PFK2 kinase active

A

Insulin. Dephosphorylated. Produces F2,6BP that activates PFK1

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4
Q

PFK2 phosphatase active

A

Glucagon. Phosphorylated. F2,6BP converted to F6P and sent to gluconeogenesis. glycolysis decreased.

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5
Q

gluconeogenesis location

A

Liver, kidney and small intestine

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6
Q

Malate dehydrogenase

A

Converts OAA to Malate oxidizing NADH in mitochondria of Gluconeogenesis. Converts Malate back to OAA reducing NAD+ in cytosol. COMMITMENT check for gluconeogenesis.

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7
Q

Pyruvate carboxylase and cofactor

A

Biotin cofactor. ATP dependent. Converts Pyruvate to OAA using ATP in mitochondria for gluconeogenesis. 1st irreversible glycolytic step bypassed.

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8
Q

PEP carboxylase

A

Converts OAA to PEP in cytosol of gluconeogenesis. 2nd glycolytic Step Bypassed.

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9
Q

Fructose 1,6 bisphopsphatase

A

Converts F1,6BP to F6P by removing a phosphate in gluconeogenesis. RATE LIMITING and 3rd glycolytic bypassed step.

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10
Q

Glucose 6 phosphatase function and name both pathways

A

converts G6P to Glucose by removing a phosphate. SKIPS HEXO/GLUCOKINASE

4th and last glycolytic step passed during gluconeogenesis.

Glycogenolysis - liver uses it to make glucose

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11
Q

glycolytic intermediates used in gluconeogenesis

A

PEP converted to pyruvate when ATP high/glucagon present.

F2,6BP converted to F6P when glucagon high

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12
Q

F1,6BP deficiency

A

Similar to tarui disease (PFK1 deficiency)(glycolysis). F1,6BP deficiency results inability to complete gluconeogenesis and results in hypoglycemia and lactic acid buildup from cori cycle.

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13
Q

Cori Cycle

A

oxygen cannot keep up with ATP need in muscle. Anerobic glycolysis produces ATP and lactate. Lactate sent from muscle to liver, recycled into glucose, and sent back to muscle. Unsustainable over time.

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14
Q

Gluconeogenesis precursors

A 
Fructose
Galactose
Glycogen - glycogenolysis
glycerol - FAs
Lactate - Cori Cycle
AA's - TCA intermediates converted to malate
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15
Q

Von Gierke disease (GSD1a) gluconeogenesis

A

G6P deficiency results in lack of glucose being produced from gluconeogenesis. hypoglycemia.

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16
Q

GLUT 1

A

High glucose affinity. brain

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17
Q

GLUT 3

A

high glucose affinity. neurons

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18
Q

Glut 4

A

Medium glucose affinity. Skeletal muscle. heart.

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19
Q

Glut 2

A

Low glucose affinity. liver pancrease.

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20
Q

Glucose + fructose

A

Sucrose

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21
Q

Galactose + glucose

A

Lactose

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22
Q

Fructose enterocyte absorption

A

GLUT5

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23
Q

Fructose basolateral transport protein into blood

A

GLUT2 and GLUT5

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24
Q

SGLT1

A

enterocyte membrane protein absorbs galactose and glucose

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25
Q

Fructose, galactose, and glucose transport protein from enterocyte basolateral membrane into blood

A

GLUT2

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26
Q

aldose reductase

A

reduces glucose to sorbitol

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27
Q

enzyme responsible for oxidizing sorbitol to fructose

A

sorbitol dehydrogenase

28
Q

Sorbitol dehydrogenase deficiency

A

sorbitol accumulation in liver, ovaries, seminal vesicles, and causes water influx

29
Q

Why is fructose metabolism faster

A

bypasses Rate limiting step of glycolysis (No PFK1 or PFK2 modulation)

30
Q

Product of fructose metabolism

A

TAGS

31
Q

Polyol pathway

A

Glucose to fructose. Sorbitol intermediate. Glucose reduced to sorbitol via aldose reductase (NAD+ produced), sorbitol oxidized to fructose via sorbitol dehydrogenase (NADH produced).

32
Q

Physiological effect of excess fructose

A

increase glycerol and acetyl coa which increased Fatty acid. fatty liver disease

33
Q

Lactose intolerance

A

Deficiency in Lactase. inability to breakdown lactose to glucose and galactose

34
Q

deficiency of galactose 1-phosphate uridyl transferase (GALT)

A

Inability to do galactose metabolism. increased galactose and galactitol.

35
Q

Defective Galactose kinase

A

Increased galactose and galactitol inblood.

36
Q

PPP products

A

2 NADPH and Ribulose 5-phosphate

37
Q

Use of ribulose 5-phosphate

A

sugar backbone of DNA/RNA

38
Q

use of NADPH from ppp

A

reductive biosynthesis (FA and steroid synthesis) and reduction agent used to combat oxidative stress from infections and agents like h2O2.

39
Q

What pathways can the end products of the non-oxidative phase of PPP go into

A

F6P and G3P can enter glycolysis or gluconeogenesis

ribose 5-phosphate can enter nucleotide synthesis

40
Q

High ppp activity in which two cell types and why?

A

phagocytic because of need for NADPH in oxidative burst capabilities.

lactating mammary glands is fatty tissue and NADPH is needed for each FA.

41
Q

bond types in glycogen

A

a1,4 for elongationand a1,6 for branching

42
Q

glycogen is extended and degraded from which end

A

non-reducing end/terminal end

43
Q

glycogenin

A

reducing end of glycogen. acts as a primer to start glycogen chain

44
Q

How is glycogen stored

A

granules

45
Q

where is majority of glycogen stored

A

liver and muscle

46
Q

glycogen granules contain glycogen and …

A

enzymes needed for metabolism

47
Q

Regulates blood glucose levels

A

liver glycogen storage

48
Q

glucokinase/hexokinase role in glycogen synthesis

A

trapping glucose in the cell via phosphorylation. just like glycolysis

49
Q

phosphoglucomutase

A

glycogenesis. Converts G6P to G1P. SIMILAR TO GLYCOLYSIS. phosphoglucase isomerase normally converts G6P to F6P. its a mutase because not an isomer.

50
Q

UDP glucose pyrophosphorylase

A

activates G1P to UDP glucose to be added to glycogen chain

51
Q

glycogen synthase

A

Adds UDP glucose to non-reducing end of glycogen chain via 1,4

52
Q

glucosyl transferase

A

After 11 UDP glucose residues added to 1,4 chain it removes 7 of these and adds them as 1,6 branches

53
Q

rate limiting enzyme glycogenolysis

A

Glycogen phoshporylase

54
Q

Rate limiting enzyme of glycogenesis

A

Glycogen synthase

55
Q

Purpose of glycogen metabolism

A

blood sugar

energy to muscle

56
Q

phosphorylation status of active glycogen synthase

A

dephosphorylated

57
Q

phosphorylation status of active glycogen phosphorylase

A

phosphorylation active

58
Q

glycogenesis favored during which metabolic state

A

FED = high blood glucose, high insulin, high ATP

59
Q

Glycogenolysis favored during what physiological state

A 
fasting = low blood glucose, high glucagon, high AMP
Excercise = high cellular calcium in muscles
60
Q

Rate limiting step in PPP

A

G6P dehydrogenase. converts G6P to something not important

61
Q

Enzyme that converts galactose to Galactose 1-P in galactose metabolism

A

Galactokinase

62
Q

Rate limiting step/enzyme of galactose metabolism

A

GALT converting Galactose 1 P to G6P. G6p will then do reverse glycolysis and convert G6P to glucose by skipping hexokinase.

63
Q

ATP consuming steps of glycolysis

A

1 and 3. Hexokinase and PFK-1

64
Q

NADH producing step of glycolysis

A
  1. GAPDH converts G3P to 1,3 bpg.
65
Q

ATP producing steps of glycolysis

A
  1. phosphoglucose mutase converts 1,3 bpg to 3pg

8. Pyruvate kinase converts PEP to pyruvate

SFM EXAM Real (2 decks)

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