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POM Exam 1 > L10: Glycolysis > Flashcards

L10: Glycolysis Flashcards

1
Q

lactose composed of

A
  • galactose

- glucose

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2
Q

sucrose composed of

A
  • glucose

- fructose

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3
Q

where are starches degraded?

A
  • salivary amylase in mouth first

- pancreatic amylase in small intestine

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4
Q

small saccharides are degraded by

A
  • glycosidases attached to the intestine

- sucrase, lactase

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5
Q

what happens to sugars like glucose, galactose, and fructose?

A
  • transported into intestinal cells

- then exported into the circulation

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6
Q

GLUT 1

A
  • present in most cell types, including fetal tissues
  • responsible for basal glucose transport in most cell types
  • Km lower than normal glucose levels
    • all cells can efficiently extract glucose from serum
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7
Q

GLUT 2

A
  • present in liver and pancreatic beta cells
  • transports only when glucose levels are high
  • Km is high
  • bidirectional transporter in liver
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8
Q

what does the liver usually use for energy?

A
  • fatty acid breakdown
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9
Q

GLUT 3

A
  • present mostly in neurons and the placenta
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10
Q

GLUT 4

A
  • present in muscle and fat cells
  • the number of transporters increases in presence of insulin
    • promotes ability of tissues like muscle to get glucose
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11
Q

is glucose anaerobic or aerobic?

A
  • facultatively anaerobic

- can run in presence or absence of oxygen

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12
Q

where does glycolysis occur?

A
  • cytoplasm
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13
Q

step 1 of glycolosis

A
  • glucose -> glucose-6-phosphate
  • via hexokinase
  • requires ATP
  • traps glucose in the cell because G-6-P cannot pass through membrane due to negative charge of phosphate tail
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14
Q

step 2 of glycolysis

A
  • glucose-6-phosphate -> fructose-6-phosphate

- via phosphoglucose isomerase

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15
Q

step 3 of glycolysis

A
  • fructose-6-phosphate -> frucose-1,6-bisphosphate
  • via PFK-1
  • requires ATP
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16
Q

step 4 of glycolysis

A
  • fructose-1,6-bisphosphate -> glyceraldehyde-3-phosphate and DHAP
  • via aldolase
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17
Q

step 5 of glycolysis

A
  • DHAP -> glyceraldehyde-3-phosphate
  • via triode phosphate isomerase
  • GAP can generate ATP but DHAP cannot
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18
Q

step 6 of glycolysis

A
  • GAP -> 1,3-bisphosphoglycerate
  • via glyceraldehyde-3-phosphate dehydrogenase
  • NAD+ reduced to NADH
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19
Q

step 7 of glycolysis

A
  • 1,3-bisphosphoglycerate -> 3-phosphoglycerate
  • via phosphoglcyerate kinase
  • ATP is formed
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20
Q

step 8 of glycolysis

A
  • 3-phosphoglycerate -> 2-phosphoglycerate

- via phosphoglyceromutase

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21
Q

NAD+ derived from

A
  • niacin or vitamin B3
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22
Q

FAD derived from

A
  • riboflavin or vitamin B2
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23
Q

step 1 of fructose metabolism

A
  • fructose -> fructose-1-P
  • by fructokinase
  • requires ATP
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24
Q

step 2 of fructose metabolism

A
  • fructose-1-P -> glyceraldehyde and DHAP

- via aldolase B

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25
Q

step 3 of fructose metabolism

A
  • glyceraldehyde -> glyceraldehyde-3-phosphate
  • via triose kinase
  • uses ATP
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26
Q

fructose intolerance cause

A
  • defect in aldolase B
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27
Q

result of fructose intolerance

A
  • fructose-1-phosphate accumulates in liver and kidney and cannot exit cell
  • depletes ATP pools since utilization of fructokinase requires ATP
  • also inhibits glycogen phosphorylase and glycogen breakdown
28
Q

reductions in aldolase B result in

A
  • decreased glucose
29
Q

symptoms of fructose intolerance

A
  • lactic acidosis
  • hypoglycemia
  • nausea
  • convulsions
  • jaundice
  • symptoms get worse with ingestion of honey, juice, fruit
30
Q

cause of essential fructosuria

A
  • defect in fructokinase
31
Q

symptoms of fructosuria

A
  • asymptomatic

- can compensate in other ways

32
Q

result of fructosuria

A
  • no accumulation of fructose in cells, since it can exit cell
  • unlike fructose-1-phosphate
33
Q

function of lactase

A
  • cleaves galactose from lactose
34
Q

where do we get most of our galactose?

A
  • from dairy products in the form of lactose
35
Q

galactose metabolism overview

A
  • galactose broken down into glucose

- uses ATP

36
Q

classical galactosemia cause

A
  • defect in galactose-1-phosphate uridyltransferase

- second step of galactose metabolism

37
Q

classical galactosemia result

A
  • accumulate galactose-1-phosphate and galactose
38
Q

classical galactosemia symptoms

A
  • intellectual disability
  • cataracts
  • liver disease
39
Q

classical galactosemia treatment

A
  • reduce lactose consumption
40
Q

nonclassical galactosemia cause

A
  • defect in galactokinase
41
Q

non classical galactosemia result

A
  • accumulates galactose only
42
Q

non classical galactosemia symptoms

A
  • mild

- cataracts

43
Q

low levels of lactase

A
  • or intestinal injury

- result in abdominal pain, bloating, nausea, flatulence, and diarrhea when consuming lactose-containing products

44
Q

western Northern Europeans and tribes of subsaharan Africa

A
  • maintain high levels of lactase as adults

- lactose tolerant

45
Q

congenital lactase deficiency

A
  • rare

- results in severe lactose intolerance in adults

46
Q

NAD+ regeneration under hypoxic conditions

A
  • pyruvate can oxidize NADH to produce lactate and NAD+
  • via lactate dehydrogenase
  • unable to form acetyl CoA and generate energy
  • results in reduced blood pH and lactic acidosis
  • glycolysis still sustained because you donโ€™t have a buildup of pyruvate
47
Q

NAD+ regeneration under normoxic conditions

A
  • shuttle systems used for transferring reducing equivalents between cytoplasm and mitochondria
48
Q

chronic alcoholism

A
  • buildup of NADH
  • pyruvate will go into lactate instead of TCA
  • why alcoholics are often lethargic
49
Q

cori cycle

A
  • glucose produced in liver taken up by other cells and is converted to lactate and released back into the blood
  • lactate taken up and converted back to glucose through gluconeogenesis
50
Q

glycerol-3-phosphate shuttle

A
  • cytoplasmic glycerol 3-P dehydrogenase transfers electrons from NADH to DHAP โ†’ glycerol 3-P and NAD+
  • Glycerol 3-P diffuses into the mitochondrial membrane where a mitochondrial glycerol 3-P dehydrogenase donates the electrons to FAD to form FADH2
  • CoQ accepts electrons from FADH2 during oxidative phosphorylation
51
Q

malate aspartate shuttle

A
  • Cytosolic malate dehydrogenase transfers electrons from NADH to oxaloacetate to form malate
    • Occurs in the cytosol
    • Regenerates NAD+
  • Malate is transferred across mitochondrial membrane in exchange for ๐›ผ-ketoglutarate being transported into the cytosol
  • In the mitochondria, malate is oxidized to oxaloacetate, generating NADH โ†’ donates electrons for oxidative phosphorylation
  • Oxaloacetate is transaminated (TA) to aspartate, which is transported to the cytoplasm and transaminated back to oxaloacetate
52
Q

inhibition of hexokinase

A
  • inhibited by glucose-6-phosphate
53
Q

inhibition of PFK-1

A
  • inhibited by high levels of ATP (binds at regulatory site)
  • inhibited by citrate from TCA cycle, and low pH
    • makes sense because these are both products
54
Q

stimulation of PFK-1

A
  • stimulated by AMP
  • stimulation by fructose-2,6-bisphosphate
    • AMP indicates low energy status so need more glycolysis
55
Q

regulation of the cycle by fructose-2,6-phosphate

A
  • stimulates PFK-1 when glucose levels are high

- inhibits fructose-1,6-bisphosphatase

56
Q

insulin secreted by

A
  • pancreatic beta cells
  • in response to high glucose
  • insulin receptor binding triggers signal transduction cascade
57
Q

glucagon secreted by

A
  • pancreatic alpha cells and epinephrine

- binding to GCPRs stimulates a protein kinase A signal transduction pathway

58
Q

regulation of fructose-2,6-bisphosphate

A
  • regulated by PFK-2
  • kinase
  • phosphatase
59
Q

PFK-2 kinase

A
  • phosphorylates F-6-P to form F-2,6-BP

- stimulates glycolysis

60
Q

PFK2 phosphatase

A
  • dephosphorylates F-2,6-BP to form F-6-P

- inhibits glycolysis

61
Q

high glucose levels, insulin, PFK2

A
  • glucose high
  • insulin activates phosphoprotein phosphatase
  • removes phosphate from PFK2 kinase domain
  • increases F-2,6-BP from F-6-P -> glycolysis predominates
62
Q

pyruvate kinase inhibition

A
  • inhibition by ATP (allosterically)
  • inhibited by glucagon
    • results in phosphorylation of pyruvate kinase, reducing it
63
Q

pyruvate kinase stimulation

A
  • stimulated by F-1-6-BP

- insulin stimulates phosphatases dephosphoryate PK and it becomes more active

64
Q

mature red blood cells

A
  • require glycolysis for ATP

- cannot do anything else

65
Q

genetic reduction of pyruvate kinase activity

A
  • glycolytic enzyme mutation
  • results in death and lysis of red blood cells
  • anemia
  • tissues with mitochondria are okay because they can generate ATP by oxidative phosphorylation
66
Q

step 9 of glycolysis

A
  • 2-phosphoglycerate -> phosphoenolpyruvate

- via enolase

67
Q

step 10 of glycolysis

A
  • phosphoenolpyruvate -> pyruvate

- via pyruvate kinase

POM Exam 1 (16 decks)

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