metabolism Flashcards

(35 cards)

1
Q

gluconeogenesis what can be used

A

gluconeogenic amino acids, pyruvate, glycerol, lactate

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1
Q

gluconeogenesis where it occurs

A

only liver and kidneys
begins in mitochondria w oxaloactetate

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2
Q

amino acid (ketogenic)

A

turned into AcCoA

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3
Q

amino acid (glucogenic)

A

form glucose or enter the TCA cycle

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4
Q

how is nitrogen removed

A

converted to ammonia
buildup of ammonia is toxic -> has to be excreted
urea cycle occurs in liver
cytosol and mitochondria
2 nitrogen groups + CO2 -> urea and water
urea excreted in the urine

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5
Q

FA beta oxidation where does it occur

A

mitochondria

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6
Q

FA beta oxidation role of carnitine

A

shuttle FA into the mitochondria

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7
Q

FA beta ox metabolic products

A

2 C cleaved from FA chain -> Acetyl-CoA
NADH, H, FADH2

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8
Q

amino acid metabolism where

A

liver

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9
Q

amino acid metabolism requires what

A

deamination

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10
Q

AA can enter as

A

pyruvate, acetyl coa, tca cycle

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11
Q

carb’s role in beta ox

A

TCA needs oxaloacetate
cells can synthesize from pyruvate
carbs needed to create pyruvate

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12
Q

carb intake low

A

low oxaloacetate = low citric acid cycle
build up of acetyl coa
diverted into ketone production in liver
cells can use ketones (ketone -> acetyl coa-> TCA)

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13
Q

what gluconeogenesis requires

A

atp, biotin, riboflavin, niacin, b6

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14
Q

gluconeogenesis anabolic or catabolic

A

anabolic

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15
Q

low levels of insulin promote

A

gluconeogenesis, protein breakdown, lipolysis

16
Q

increased insulin promotes

A

glycogen, fat, protein synthesis

17
Q

feasting

A
  • metabolism favors fat formation
    FA -> triglycerides
    glucose -> glycogen or AceCoA -> FA
    AA -> Acetyl CoA -> FA
18
Q

hormones in initial fasting

A

Hormone sensitive lipase
triglycerides -> glycerol backbone + FA
increased by glucagon, growth hormone, and epu
decreased by insulin

19
Q

short term fasting

A
  • reliance on AA for glucose via gluconeogenesis
    2. increased ketone formation
    3. increased utilization of FA for energy
20
Q

prolonged fasting

A
  • increased formation of ketones
  • body tissue broken down to make glucose form gllucogenic amino acids
21
Q

adaptations to survive fasting

A
  • slow metabolic rate (reduce energy req, slow breakdown of lean body tissue for glucoeneogenesis)
  • allow nervous system to use more ketone bodies
22
Q

ketosis in semistarvation/fasting

A
  • glucose and insulin levels fall
  • FA flow into bloodstream and form ketone bodies in liver
  • SPARE PROTEINS from being used
  • heart, muscle, kidneys, and eventually the brain can use these for fuels
23
Q

glycolysis where

24
glycolysis starting products and ending products
atp nad glucose end = pyruvate, atp, nadh
25
anaerobic glycolysis converts
pyruvate into lactate gain some atp
26
cori cycle causes
lactate buildup and NAD+ regeneration lactate to liver -> convert to glucose
27
transition step products and factor
irreversible acetyl coa, nadh, co2
28
tca cycle products
co2, atp, nadh, fadh2
29
tca cycle where
mitochondrial matrix
30
cori cycle where
muscle rely on anaerobic cells
31
transition step where
mitochondrial matrix
32
oxidative phosphorylation where
inner mitochondrial membrane
33
oxidative phosp what goes in
nadh, h, fadh2
34
oxidative phosp products
water and atp