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endocrine biochem > Gluconeogenesis > Flashcards

Gluconeogenesis Flashcards

1
Q

net equation for gluconeogenesis

A

2 pyruvates + 4 ATP + 2 GTP + 2 NADH —-> 1 glucose + 4 ADP + 2 GDP + 6 Pi+ 2 NAD+

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2
Q

location for gluconeogenesis

A

liver cells & renal cortex cells

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3
Q

why are renal medulla largely anaerobic? what fuel do they use?

A

they don’t get good blood supply (blood delivers O2). glucose. renal medulla cells are always making a lot of lactate

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4
Q

when does gluconeogenesis in the liver increase?

A
  1. the fasting state

2. in a high protein meal

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5
Q

why is it important that gluconeogenesis and glycolysis aren’t exact reversals of one another?

A

it gives the cell tremendous control to be a glucose user in the fed state (glycolysis) and a glucose producer in the fasting state (gluconeogenesis)

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6
Q

where is blood sugar coming from in the fed state?

A

your meal (mostly)

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7
Q

where is blood sugar coming from in the fasting state?

A

First, hepatic gycogenolysis (for about 1.5 days)
Not long after glycogenolysis begins contributing, so does gluconeogenesis
Gluconeogenesis becomes the sole provider until the person eats again (up to about 40 days)

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8
Q

name the enzyme that catalyzes the rxn from pyruvate to oxaloacetate

A

pyruvate carboxylase

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9
Q

what cells have pyruvate carboxylase

A

liver cells and adipocytes

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10
Q

catalytic cofactor for pyruvate carboxylase

A

biotin

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11
Q

location for the pyruvate carboxylase rxn

A

mitochondrial matrix

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12
Q

pyruvate carboxylase is allosterically activated by __________

A

acetyl coA (coming from glucose in the fed state and beta-oxidation of fatty acids in the fasting state)

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13
Q

liver cell’s favorite fuel

A

fatty acids (carried from adipocytes by albumin)

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14
Q

name the enzyme that catalyzes the rxn from oxaloacetate to PEP

A

Phosphoenolpyruvate carboxykinase (PEPCK)

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15
Q

why is the PEPCK rxn improtant

A

changes OAA into something that can get out of the mitochondrial matrix (PEP

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16
Q

high energy phosphate donor in the PEPCK rxn

A

GTP

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17
Q

location for the PEPCK rxn

A

cytosol

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18
Q

name the enzyme that turns PEP ——> 2-phosphoglycerate

A

enolase

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19
Q

name the enzyme that turns 2-phosphoglycerate ——> 3-phosphoglycerate

A

phosphoglyceromutase

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20
Q

name the enzyme that turns 3-phosphoglycerate ——> 1,3-bisphosphoglycerate

A

phsophoglycerate kinase

21
Q

what enzyme catalyzes the rxn from 1,3 bisphosphoglycerate ——–> glyceraldehyde-3-phosphate?
what does it cost?
how many times does it happen?

A

glyceraldehyde-3-phosphate dehydrogenase

  • costs NADH
  • happens twice
22
Q

name the fate of the two glyceraldehyde-3-phosphate molecules produced in gluconeogenesis

A

1 gets converted to DHAP (dihydroxyacetone phosphate) using triose phosphate isomerase
1 gets converted to fructose-1,6-phosphate using aldolase

23
Q

what enzyme catalyzes the rxn from fructose-1,6-bisphosphate —-> fructose-6-phosphate?

A

fructose-1,6-bisphosphatase

  • only happens once
  • irreversible
  • hydrolysis of a phosphoester bond
24
Q

what enzyme catalyzes the rxn from fructose-6-phosphate —-> glucose-6-phosphate?

A

phosphoglucose isomerase

- change from a ketose to an aldose

25
Q

what enzyme catalyzes rxn from glucose-6-phosphate —-> glucose?

A

glucose-6-phosphatase

  • hydrolysis rxn
  • allows liver cells to have exportable glucose
26
Q

location for the glucose-6-phosphatase rxn

A

endoplasmic reticulum

27
Q

how does oxaloacetate formed in the mitochondrial matrix get into the cytosol for continuation of gluconeogenesis?

A
  1. can change to malate via the malate dehydrogenase rxn (the major option)
  2. can change to aspartate via an amino transferase rxn
28
Q

what’s the major rxn in the conversion of OAA into something that can go into the cytosol for gluconeogenesis? why?

A

malate dehydrogenase rxn
b/c the liver’s fave fuel is fatty acids, beta-oxidation of fatty acids in the fasting state produces a lot of NADH which pushes the malate dehydrogenase rxn further towards the direction where OAA (ketone) —> malate (secondary alcohol)

29
Q

locations for the malate dehydrogenase rxns

A

mitochondrial matrix & cytosol

30
Q

reducing agent for the malate dehydrogenase rxn

A

NADH

31
Q

name the enzyme:

oxaloacetate + glutamate ——–> aspartate + alpha-KG

A

aspartate transaminase rxn (AST)

32
Q

catalytic cofactor for transaminases?

A

pyridoxal phosphate (PLP), derived from vitamin B6 (pyroxin)

33
Q

what does it mean if ALT or AST levels are too high in a pt’s tests?

A

sign of liver disease

34
Q

non-carbohydrate precursors for the liver’s synthesis of glucose

A

alanines
glycerol
lactate

35
Q

what enzyme catalyzes the rxn from lactate ——> pyruvate?
oxidizing agent?
reactants?
products?

A

lactate dehydrogenase rxn
oxidizing agent: NAD+
reactants: lactate + NAD+
products: pyruvate + NADH + H+

36
Q

name the enzyme:

alanine + alpha-KG <—–> pyruvate + glutamate

A

alanine transaminase rxn

37
Q

name the enzyme:
glycerol ——-> glycerol-3-phosphate

what does it require?

A

glycerol kinase

- requires ATP

38
Q

what cells have glycerol kinase & why?

A

liver cells; to be able to use glycerol where other cells can’t (to make glucose)

39
Q

name the enzyme:
glycerol-3-phosphate —-> dihydroxyacetone phosphate (DHAP)

what is required?

A

glycerol-3-phosphate dehydrogenase

- NAD+ required

40
Q

name the enzyme:

pyruvate ——-> acetyl group of acetyl CoA

A

pyruvate dehydrogenase

- unfavorable for gluconeogenesis

41
Q

inhibitors of the pyruvate dehydrogenase rxn

A

enzyme action: pyruvate —-> acetyl group of acetyl coA

acetyl CoA & NADH
- activate PDC-kinase which turns off PDC by catalyzing its phosphorylation

42
Q

activator of pyruvate carboxylase rxn

A

enzyme action: pyruvate —-> OAA

acetyl CoA (comes from beta-oxidation of fatty acids from adipocytes carried by albumin)

43
Q

inhibitors of the pyruvate kinase rxn

A

action: PEP —-> pyruvate

alanines
ATP
protein kinase A (catalyzes phosphorylation of pyruvate kinase)

44
Q

what enzymes of gluconeogenesis are inducible?

A

PEPCK
fructose-1,6-bisphosphatase
glucose-6-phosphatase

45
Q

what factors reciprocally control PFK-1 and fructose-1,6-bisphosphatase?

A

concentration of fructose-2,6-bisphosphate

  • activator of PFK-1 for glycolysis (from fructose-6-phosphate —–> fructose-1,6-bisphosphate)
  • inhibitor of fructose-1,6-bisphosphatase for gluconeogenesis (from fructose-1,6-bisphosphate —–> fructose-6-P)
46
Q

how do glucagon signal lead to phosphorylation of pyruvate kinase?

A

  1. glucagon binds to glucagon receptor on outside of liver cell
  2. receptor changes shape
  3. heterotrimeric G-protein feels shape change
  4. alpha subunit drops a GDP and picks up a GTP
  5. shape change activates adenylate cyclase
  6. cAMP concentration increases and becomes second messenger
  7. activates protein kinase A
  8. catalyzes phosphorylation of pyruvate kinase
47
Q

how do glucagon signals lead to increased PEPCK synthesis?

A
  1. glucagon binds to glucagon receptor on outside of liver cell
  2. receptor changes shape
  3. heterotrimeric G-protein feels shape change
  4. alpha-subunit drops GDP and picks up GTP
  5. shape change activates adenylate cyclase
  6. cAMP concentration increases, becomes second messenger
  7. activates protein kinase A
  8. protein kinase A catalyzes phosphorylation of CRE (cAMP response element) binding protein
  9. transcription factor changes shape
  10. increases transcription of gene which codes for PEPCK
48
Q

how do glucocorticoid signals for cortisol stimulate PEPCK synthesis?

A
  1. cortisol binds to intracellular glucocorticoid receptor in the cytosol
  2. GR begins to dimerize
  3. GRs go into nucleus and bind to gene that code for PEPCK in the glucocorticoid response element (GRE)
  4. gene that codes for PEPCK gets transcribed more
49
Q

why is gluconeogenesis dependent on beta-oxidation of fatty acids?

A

beta oxidation of fatty acids from adipocytes carried by albumin to liver cells produces:

  1. NADH
  2. FADH2
  3. Acetyl CoA

While fatty acids are not a source of carbons for gluconeogenesis, they’re still important because…

  • liver cells need ATP (from acetyl Coa and from the electrons being sent to the ETC by the FAD2H and NADH)
  • NADH inhibits pyruvate dehydrogenase rxn and converts OAA –> malate in the mito matrix
  • acetyl CoA is worth ATP, inhibits pyruvate dehydrogenase, and activates pyruvate carboxylase

endocrine biochem (7 decks)

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