Gluconeogensis Flashcards

1
Q

why is gluconeogenesis important?

A

helps the body maintain glucose levels during fasting

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2
Q

what does gluconeogenesis use to make glucose?

A

amino acids, lactate, and glycerol

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3
Q

where does gluconeogenesis occur?

A

mainly the liver (could also be epithelial cells in kidney or intestine

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4
Q

Fasting, where do we get glucose?

A

1) glycogen stores (12-24 hours) until we run out

2) gluconeogenesis (kicks in 12 hrs in as main provider of glucose)

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5
Q

gluconeogenesis

A

uses ATP to turn pyruvate into glucose

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6
Q

which glycolysis reactions are irreversible?

A

1, 3, and 10

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7
Q

sources of pyruvate for gluconeogenesis (1)

A

lactate (lactate dehydrogenase takes Hydrogen from lactate and makes it pyruvate while making NADH)

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8
Q

sources of pyruvate for gluconeogenesis (2)

A
amino acids (alanine)
alanine comes from breakdown of protein and skeletal muscle cells
alanine transaminase (vitamin B6 as a cofactor) removes amino from alanine and turns it to pyruvate
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9
Q

during fasting,

A

pancreas senses low glucose, releases glucagon

there is also low insulin, high epinephrine

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10
Q

gluconeogenesis step 1A

A

1) pyruvate enters mitochondria

2) pyruvate carboxylase adds a carbon to it creating oxaloacetate

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11
Q

carboxylase enzymes require what cofactors

A

ABC
ATP
Biotin
CO2

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12
Q

gluconeogenesis step 1B

A
  • we need oxaloacetate out of mitochondria and into the cytoplasm
    1) malate dehydrogenase adds Hydrogen to oxaloacetate making malate
    2) malate can exit mitochondria and get into cytoplasm where malate dehydrogenase converts it back into oxaloacetate
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13
Q

gluconeogenesis step 1C

A

oxaloacetate to phosphoenolpyruvate

enzyme: PEPCK removes a carbon and adds a phosphate
requires GTP

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14
Q

PEPCK regulation

A

stress hormones: glucagon, epinephrine, and cortisol enhance PEPCK by induction

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15
Q

gluconeogenesis 2nd roadblock

A

PEP to DHAP

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16
Q

using glycerol

A
  • glycerol can make DHAP
  • glycerol kinase adds phosphate from ATP to C3 on glycerol
  • makes glycerol-3-phosphate (G3P)
  • glycerol-3-phosphate dehydrogenase converts G3P to DHAP
17
Q

gluconeogenesis 3rd roadblock

A

PFK1 rxn

in gluconeogenesis, fructose 1,6 bisphosphatase removes phosphate from C1 of fructose-1,6-bisphosphate making fructose-6-phosphate

18
Q

rate limiting step of gluconeogenesis

A

fructose-1,6-bisphoshatase

19
Q

up-regulation of gluconeogenesis

A

when liver burns a lot of fat making a lot of ATP

high ATP = enhances fructose-1,6-bisphosphatase

20
Q

fructose-1,6-bisphosphatase regulation

A

glucagon activates, insulin inhibits

21
Q

final step of gluconeogenesis

A

glucose-6-phosphate to glucose

enzyme: glucose-6-phosphatase
- once phosphate is removed, glucose can enter bloodstream

22
Q

high levels of alcohol (ethanol)

A
  • processed in liver

- cause increase in NADH and ATP

23
Q

high NADH causes

A

lactate, malate, and G3P dehydrogenase enzymes in gluconeogenesis to go the reverse way

impairs gluconeogenesis!
causes low blood sugar when fasting