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MAD Exam 1 > Carb Metabolism > Flashcards

Carb Metabolism Flashcards

1
Q

salivary amylase

A

breaks down 1,4 linkages in complex carbs

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2
Q

pancreatic amylase

A

breaks down 1,6 linkages in complex carbs

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3
Q

sodium-dependent glucose transporter (SGLT1)

A

uses secondary active transport to move one Na+ and one glucose from the intestinal lumen into enterocytes

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4
Q

glucose transporter (GLUT 2)

A

transports glucose from enterocyte into blood by facilitated diffusion down its concentration gradient

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5
Q

sodium-potassium ATPase

A

actively transports 3 Na+ out of the cell (into blood) and 2 K+ into the cell to establish low intracellular Na+ concentration using ATP

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6
Q

hexokinase/glucokinase

A

make glucose-6-phosphate (in glycolysis)

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7
Q

phosphofructokinase

A

the first rate-controlling enzyme of glycolysis; produces the first committed metabolite (FRU-1,6-BP)

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8
Q

fructose-1,6-bisphosphate

A

the first committed metabolite in glycolysis; gets split into G3P and DHAP

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9
Q

stage 2 of glycolysis

A

uses G3P to create high energy phosphates on 3-C intermediates; these phosphates are then transferred to ADP (substrate-level phosphorylation)

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10
Q

substrate level phosphorylation

A

phosphoglycerate kinase and pyruvate kinase transfer a high-energy phosphate directly from one compound to ATP
*during stage 2 of glycolysis

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11
Q

glyceraldehyde-3-phosphate

A

the “parent” for the 3-carbon phosphorylated compounds that will support substrate-level phosphorylation of ADP to ATP

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12
Q

net effect of glycolytic pathway

A

2 NADH molecules and 2 ATP (we used 2 and made four so net = 2)

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13
Q

pyruvate kinase

A

converts PEP to pyruvate, in the process making ATP via substrate-level phosphorylation

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14
Q

glucokinase

A

found mainly in the liver and pancreas
-high Vmax
-larger Km (lower affinity for substrate)

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15
Q

hexokinase

A

found in all cells
-low Vmax (slower)
-smaller Km (high affinity for substrate)

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16
Q

negative regulators of PFK-1

A

ATP
citrate
low pH (lactic acid)

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17
Q

positive regulators of PFK-1

A

AMP
ADP
Pi
fructose-2,6-bisphosphate

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18
Q

positive regulators of pyruvate kinase

A

fructose-1,6-bisphosphate

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19
Q

negative regulators of pyruvate kinase

A

alanine
acetyl-CoA
ATP

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20
Q

how does cAMP/PKA affect pyruvate kinase?

A

phosphorylates pyruvate kinase, which INACTIVATES the enzyme

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21
Q

fate of pyruvate - anaerobic glycolysis

A

lactate dehydrogenase (LDH) converts pyruvate to lactate, oxidizing NADH to NAD+, in the absence of O2
-occurs in cytosol

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22
Q

fate of pyruvate - aerobic glycolysis

A

pyruvate is shuttled into the mitochondria, interacting with pyruvate dehydrogenase and coenzyme A to form Acetyl-CoA and NADH; requires thiamine

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23
Q

pyruvate dehydrogenase

A

3 subunits (E1, E2, E3); requires thiamine and makes 1 NADH molecule in the process of converting pyruvate to acetyl-CoA

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24
Q

citrate synthase (TCA cycle)

A

combines oxaloacetate and acetyl-CoA to make citrate

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25
Q

isocitrate dehydrogenase (TCA cycle)

A

converts isocitrate to a-ketoglutarate
*requires thiamine
*loses a CO2
*makes NADH

26
Q

a-ketoglutarate dehydrogenase (TCA cycle)

A

converts a-ketogluarate to succinyl-CoA
*requires thiamine
*makes NADH

27
Q

TCA cycle overview

A

uses acetyl-CoA to make 3 NADH and 1 FADH2, which will be used in the ETC to make ATP
-also makes GTP

28
Q

negative effectors of pyruvate dehydrogenase

A

-ATP
-acetyl-CoA
-NADH

29
Q

positive effectors of pyruvate dehydrogenase

A

-calcium
-ADP
-substrate levels

30
Q

TCA cycle is regulated by availability of

A

oxaloacetate and acetyl-CoA

31
Q

negative regulator molecules of citrate synthase (TCA cycle)

A

ATP, NADH, succinyl-CoA, citrate

32
Q

positive regulators of citrate synthase (TCA cycle)

A

ADP, oxaloacetate

33
Q

negative regulators of isocitrate dehydrogenase (TCA cycle)

A

ATP, NADH

34
Q

positive regulators of isocitrate dehydrogenase (TCA cycle)

A

Ca2+, ADP

35
Q

negative regulators of a-ketoglutarate dehydrogenase (TCA cycle)

A

succinyl-CoA, NADH

36
Q

positive regulators of a-ketoglutarate dehydrogenase (TCA cycle)

A

Ca2+

37
Q

purposes of malate-aspartate shuttle

A
  1. keeps conversion of glucose to pyruvate going by maintaining NAD+ levels
  2. provides some ATP via NADH to ETC
38
Q

glucose-6-phosphate dehydrogenase (G6PD)

A

rate-limiting enzyme for the pentose phosphate pathway

39
Q

pentose phosphate pathway

A

*yields NADPH!!
-also forms glycolytic intermediates (2 fructose-6-phosphates and 1 glyceraldehyde-3-phosphate)
RATE-LIMITING ENZYME = glucose-6-phosphate dehydrogenase (G6PD)

40
Q

NADPH is required for

A

*SYNTHESIS of fatty acids, cholesterol, neurotransmitters, and nucleotides
*DETOXIFICATION of oxidized glutathione and cytochrome P450 monooxygenases (protection against ROS)

41
Q

how does G6PD deficiency cause anemia?

A

in G6PD deficiency, we cannot make enough NADPH, which is necessary for producing reduced glutathione (GSH), which is necessary for glutathione peroxidase to convert hydrogen peroxide to water; this causes accumulation of ROS and damages RBC membranes, leading to hemolytic anemia

42
Q

stimulation of insulin secretion

A

increased levels of glucose, amino acids, and fatty acids (well-fed conditions) causes insulin release from beta cells in pancreas

43
Q

stimulation of glucagon secretion

A

LOW INSULIN levels trigger glucagon secretion
-low insulin levels occur in under-fed conditions

44
Q

disorders of glycogen metabolism

A
  1. Von Gierke (type I)
  2. Pompe (type II)
45
Q

Von Gierke disease

A

defective glucose-6-phosphatase or transport system (can’t get glycogen OUT of liver) -> enlarged liver, severe hypoglycemia, ketosis, hyperuricemia

46
Q

Pompe disease

A

defective 1,4-glucosidase (can’t BREAK glycosidic bonds) -> buildup of glycogen in lysosome -> cardiorespiratory failure causes death, usually before the age of 2

47
Q

glycogen structure

A

highly branched, with 1,4 and 1,6 linkages
-tens of thousands of glucose residues incorporated into a single glycogen molecule

48
Q

glycogen synthesis

A

1) glycogenin has built-in glycogen synthase, which makes the primer
2) glycogen synthase makes 1,4 glycosidic bonds and uses UDP-glucose; elongation of glycogen molecule
3) amylo-1,4-transglycosylase adds in the 1,6 branches

49
Q

glycogenolysis (breakdown of glycogen)

A

1) glycogen phosphorylase breaks 1,4 glycosidic bonds, making GLU-6-P
2) in the liver, GLU-6-P is acted on by glucose-6-phosphatase, which removes the phosphate and forms free glucose
3) debranching enzymes break the 1,6 branches
4) free glucose is transported into the blood to maintain euglycemia

50
Q

effect of glucagon on glycogen metabolism

A

glucagon turns on glycogen phosphorylase, causing BREAKDOWN of glycogen

51
Q

effect of insulin on glycogen metabolism

A

insulin stimulates glycogen synthase, causing FORMATION of glycogen

52
Q

what is the rate-limiting enzyme for gluconeogenesis

A

fructose-1,6-bisphosphate phosphatase (PEP-carboxykinase also important)

53
Q

how is the pyruvate kinase step of gluconeogenesis reversed

A

1) amino acids and lactate are converted to pyruvate
2) pyruvate carboxylase adds 1 CO2 and consumes 1 ATP to form oxaloacetate
3) PEP-carboxykinase removes a CO2 and uses GTP to add a phosphate and make PEP

54
Q

how is the phosphofructokinase 1 step reversed in gluconeogenesis

A

fructose-1,6-bisphosphate phosphatase converts FRU-1,6-BP to FRU-6-P

55
Q

how is the hexokinase step reversed in gluconeogenesis

A

glucose-6-phosphatase removes the phosphate from GLU-6-P to produce free glucose

56
Q

describe the structure of an N-linked glycoprotein

A

glucose linked to a protein by way of a nitrogen linkage (bound to asparagine)

57
Q

inclusion cell disease

A

a defect in glycoprotein carbohydrate recognition signals that there is a failure to phosphorylate mannose residues; the lysosome can’t function so it gets a buildup of material

58
Q

building N-linked glycoproteins

A

1) requires dolichol and adds monosaccharides to the dolichol carrier to create “high mannose content” chain
2) transfer high mannose oligosaccharide to a protein destined to be a mature N-linked glycoprotein
3) trim the oligosaccharide and add additional sugars to make a complex chain
4) completed N-linked protein

59
Q

mucopolysaccharidoses

A
  1. lysosomal storage disorder
  2. deficiency in GAG degradative enzymes
  3. lysosomal accumulation of GAG products cause dysfunction
    -s/s can include organomegaly, vision problems, etc
60
Q

degradation of proteoglycans

A
  1. extracellular proteases fragment in the proteoglycan and the fragments are gathered in coated pits
  2. enzymes cleave internal glycosidic bonds of GAG, creating smaller fragments
  3. GAG fragments are degraded to individual monosaccharides in lysosome

MAD Exam 1 (20 decks)

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