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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
step 3 of fructose metabolism
- glyceraldehyde -> glyceraldehyde-3-phosphate - via triose kinase - uses ATP
26
fructose intolerance cause
- defect in aldolase B
27
result of fructose intolerance
- 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
reductions in aldolase B result in
- decreased glucose
29
symptoms of fructose intolerance
- lactic acidosis - hypoglycemia - nausea - convulsions - jaundice - symptoms get worse with ingestion of honey, juice, fruit
30
cause of essential fructosuria
- defect in fructokinase
31
symptoms of fructosuria
- asymptomatic | - can compensate in other ways
32
result of fructosuria
- no accumulation of fructose in cells, since it can exit cell - unlike fructose-1-phosphate
33
function of lactase
- cleaves galactose from lactose
34
where do we get most of our galactose?
- from dairy products in the form of lactose
35
galactose metabolism overview
- galactose broken down into glucose | - uses ATP
36
classical galactosemia cause
- defect in galactose-1-phosphate uridyltransferase | - second step of galactose metabolism
37
classical galactosemia result
- accumulate galactose-1-phosphate and galactose
38
classical galactosemia symptoms
- intellectual disability - cataracts - liver disease
39
classical galactosemia treatment
- reduce lactose consumption
40
nonclassical galactosemia cause
- defect in galactokinase
41
non classical galactosemia result
- accumulates galactose only
42
non classical galactosemia symptoms
- mild | - cataracts
43
low levels of lactase
- or intestinal injury | - result in abdominal pain, bloating, nausea, flatulence, and diarrhea when consuming lactose-containing products
44
western Northern Europeans and tribes of subsaharan Africa
- maintain high levels of lactase as adults | - lactose tolerant
45
congenital lactase deficiency
- rare | - results in severe lactose intolerance in adults
46
NAD+ regeneration under hypoxic conditions
- 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 don't have a buildup of pyruvate
47
NAD+ regeneration under normoxic conditions
- shuttle systems used for transferring reducing equivalents between cytoplasm and mitochondria
48
chronic alcoholism
- buildup of NADH - pyruvate will go into lactate instead of TCA - why alcoholics are often lethargic
49
cori cycle
- 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
glycerol-3-phosphate shuttle
- cytoplasmic glycerol 3-P dehydrogenase transfers electrons from NADH to DHAP → 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
malate aspartate shuttle
- 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 𝛼-ketoglutarate being transported into the cytosol - In the mitochondria, malate is oxidized to oxaloacetate, generating NADH → donates electrons for oxidative phosphorylation - Oxaloacetate is transaminated (TA) to aspartate, which is transported to the cytoplasm and transaminated back to oxaloacetate
52
inhibition of hexokinase
- inhibited by glucose-6-phosphate
53
inhibition of PFK-1
- 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
stimulation of PFK-1
- stimulated by AMP - stimulation by fructose-2,6-bisphosphate - AMP indicates low energy status so need more glycolysis
55
regulation of the cycle by fructose-2,6-phosphate
- stimulates PFK-1 when glucose levels are high | - inhibits fructose-1,6-bisphosphatase
56
insulin secreted by
- pancreatic beta cells - in response to high glucose - insulin receptor binding triggers signal transduction cascade
57
glucagon secreted by
- pancreatic alpha cells and epinephrine | - binding to GCPRs stimulates a protein kinase A signal transduction pathway
58
regulation of fructose-2,6-bisphosphate
- regulated by PFK-2 - kinase - phosphatase
59
PFK-2 kinase
- phosphorylates F-6-P to form F-2,6-BP | - stimulates glycolysis
60
PFK2 phosphatase
- dephosphorylates F-2,6-BP to form F-6-P | - inhibits glycolysis
61
high glucose levels, insulin, PFK2
- glucose high - insulin activates phosphoprotein phosphatase - removes phosphate from PFK2 kinase domain - increases F-2,6-BP from F-6-P -> glycolysis predominates
62
pyruvate kinase inhibition
- inhibition by ATP (allosterically) - inhibited by glucagon - results in phosphorylation of pyruvate kinase, reducing it
63
pyruvate kinase stimulation
- stimulated by F-1-6-BP | - insulin stimulates phosphatases dephosphoryate PK and it becomes more active
64
mature red blood cells
- require glycolysis for ATP | - cannot do anything else
65
genetic reduction of pyruvate kinase activity
- 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
step 9 of glycolysis
- 2-phosphoglycerate -> phosphoenolpyruvate | - via enolase
67
step 10 of glycolysis
- phosphoenolpyruvate -> pyruvate | - via pyruvate kinase

POM Exam 1 (16 decks)

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