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Endocrine and Metabolism > Gluconeogenesis > Flashcards

Gluconeogenesis Flashcards

1
Q

Describe why glucose is classified as an aldose and a D-sugar

A

an aldose means that the last carbon on glucose is an aldehyde C=O

D glucose means that the bottom most OH group is on the right side.

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2
Q

Give the definition of gluconeogensis

A

its the opposite of glycolysis

also the formation of glucose from noncarbohydrate starting materials

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3
Q

Give the overall summary of gluconeogenesis including the number of ATPs GTPs and NADHs

A

4 ATP are spent
2 GTP spent
2 NADH’s spent

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4
Q

Where does gluconeogenesis take place?

A

liver and renal cortex cells

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5
Q

What is the purpose of gluconeogenesis

A

to make glucose for cells that can’t. for example, liver cells make glucose when fasting state and renal cortex cells make glucose for kidney. this is the only fuel that kidney cells get because there isn’t a good blood supply to the kidney.

keep blood sugar the same / for the brain / until we eat again. we need blood sugar at least at 65

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6
Q

Is gluconeogenesis an exact reversal of glycoclysis?

A

there are some irreversible steps in gluconeogenesis that are not the same as in glycolysis.

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7
Q

How does the use of fatty acids in the liver change during the fasting state?

A

during fed state, fatty acid producers use glucose to make fatty acids

in fasting state, the fatty acid users make glucose

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8
Q

How long after fasting does gluconeognesis kick in?

A

after half a day of fasting, gluconeogensis is the only source of blood sugar

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9
Q

Describe reaction catalyzed by pyruvate carboxylase. Where is it located. What cofactors are required? Products and reactants.

A

Pyruvate turns into oxaloacetate.

CO2 is required; ATP is required. as well as biotin

its allosterically activated by acetyl coA (coming from many places but also glucose in the fed state and fatty acids / beta oxidation in the fasting state).

in the mitochondrial matrix. its important for using glucose after high carb meal – making fatty acids, and now in the fasting state its important for gluconeogenesis

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10
Q

Describe the reaction catalyzed by phosphoenolphyruvate carboxykinase (PEPCK).
Products and reactants, location)

A

Oxaloacetate becomes phosphoenolpyruvate (PEP)

its a decarboxylation and a transfer of a phosphate. It happens in the cytosol. OAA is made in mitochondrial matrix and it cannot pass or go into the cytosol. It becomes 3 carbons and a phosphate (phosphoenolpyruvate).

Requires GTP. GTP is turned into GDP and a CO2 is lost. The phosphate is transferred to OAA.

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11
Q

Describe pathway to glucose from PEP.

A

Reversible step catalyzed by a kinase which costs an ATP going in the gluconeogenesis direction (phosphoglycerate kinase which happens twice).

Reversible step catalyzed by a dehydrogenase which costs an NADH going in the gluconeogensis direction (glyceraldehyde 3 phosphate dehydrogenase) happpens twice when 2 pyruvates become a glucose at the expense of 2 NADPH.

Irreversible step catalyzed by fructose 1,6 bisphosphatase (hydrolysis reaction works on phosphodiester bond)

Irreversible step catalyzed by glucose 6-phosphatase

isomerase (phosphoglucoisomerase)

then glucose 6 phosphate to glucose (removes a phosphate via phosphatase)

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12
Q

Which intracellular compartments of the liver are involved int he complete pathway from pyruvate to glucose?

A

pyruvate to glucose occurs in the matrix of mitochondria via pyruvate carboxylase.

then oxaloacetate in the cytosol (most of this happens here)

finally, the endoplasmic reticulum - glucose 6 phosphate to glucose

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13
Q

How are the cellular locations different for gluconeogenesis vs. glycolysis?

A

glycolysis only happens in the cytosol. there are 3 locations for gluconeogenesis

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14
Q

What are the two ways for oxaloacetate to be formed in the mitochondrial matrix to get into the cytosol?

A

1) change into a malate which requires malate dehydrogenase
2) OAA changes into aspartate that is released to oxaloacetate in a reaction where a transamination occurs. then it can change back into OAA once in cytosol.

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15
Q

Draw the chemical structure of malate. How is it the reduced form of oxaloacetate.

A

malate turns into oxaloacetate via malate dehydrogenase. NADH is the reducing agent.

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16
Q

Draw chemical structure of aspartate, how is it the alpha amino form of oxaloacetate?

A

alpha carbons are different. the alpha keto form is oxaloacetate and the alpha amino form is aspartate.

the reaction is a transamination one; the nitrogen comes from glutamate.

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17
Q

What is the alpha keto acid form of glutamate?

A

alpha ketoglutarate (5 carbons)

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18
Q

What is the alpha amino acid form of oxaloacetate?

A

asparate

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19
Q

what is the alpha amino acid form of pyruvate?

A

alanine

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20
Q

what is the alpha amino acid form of alpha ketoglutarate

A

glutamate

21
Q

What is the alpha keto acid form of alanine

A

pyruvate

22
Q

what is the alpha keto acid form of asparate?

A

oxaloacetate

23
Q

Generalize about transamination reactions

A

they require PLP, occur in the cytosol

24
Q

Major way to get OAA out of the matrix?

A

Malate; its a major disguise for the mitchondria to get OAA out.

this is related to fatty acids for the major fuel in fasting state.

25
Q

What are the three most important noncarbohydrate precursors for the liver’s synthesis of glucose?

A

lactate, most familiar one - lactate dehydrogenase / lactate gets oxidized to pyruvate

alanine via the alanine aminotransferase becoming pyruvate

Glycerol turning into glycerol 3 phosphate and dihydroxyacetone phosphate

26
Q

how is pyruvate carboxylase activated?

A

allosterically activated by acetyl coA

27
Q

how is the pyruvate kinase reaction is inhibited

A

pyruvate kinase, pyruvate carboxylase, and pyruvate dehydrogenase are all inhibited by alanine. ATP also acts as an allosteric inhibitor. protein kinase A inhibits pyruvate kinase (phosphorylation)

28
Q

Which 3 enzymes of gluconeogenesis are inducible

A

phosphopyruvate carboxylase
fructose 1,6 bisphosphatase
glucose 6 phosphatse

29
Q

Describe reaction catalyzed by malate dehydrogenase

A

malate becoming oxaloacetate.

requires NADH

30
Q

Where does the malate dehydrogenase reaction happen?

A

mitochondrial matrix an in the cytosol.

31
Q

Describe reaction catalyzed by aspartate transaminase AST

A

reaction turns oxaloacetate to aspartate. the nitrogens come from glutamate.

32
Q

Where does the AST reaction occur?

A

In the cytosol

33
Q

What cofactor is required for the asparate transaminase reaction?

A

PLP (vitamin B6)

34
Q

Why is the liver’s major fuel during fasting state important for getting oxaloacetate out of the matrix?

A

malate dehydrogenase reaction requires NADH! lots of NADH during oxidation of fatty acids.

35
Q

What are the three precursors of glucose.

A

lactate (anaerobic cellular sources like RBC), amino acids (alanine), and glycerols

36
Q

Describe the conversion of glycerol to dihydroxyacetone phosphate DHAP

A

glycerol kinase followed by glycerol 3 phosphate dehydrogrenase

37
Q

Describe reaction catalyzed by glycerol 3 phosphate dehydrogenase

A

converts glycerol 3 phosphate into DHAP

38
Q

describe reaction catalyzed by glycerol kinase

A

adds a phosphate onto glycerol at position 3

39
Q

How does alanine become pyruvate?

A

alanine aminotransferase

40
Q

How is pyruvate dehydrogenase inhibited?

A

once carbons are made into an acetyl group it can’t be used as a glucose. don’t want the pyruvate dehydrogenase to happen bc then can’t create oxaloacetate (pyruvate carboxylase rxn).

NADH and acetyl coA inhibit pyruvate dehydrogenase

41
Q

how is pyruvate carboxylase activated?

A

allosterically activated by acetyl coA

during fasting state the acetyl coAs are coming from adipocytes releasing acetyl coA and fatty acids

42
Q

How is the pyruvate kinase reaction inhibited?

A

pyruvate kinase catalyzes the LAST STEP of glycolysis. its inhibited by alanine and ATP and really these happen when protein kinase A is involved and protein kinase A is let loose when there are glucagon signals (fasting state).

pyruvate kinase is important for glycolysis and we need it inhibited for gluconeogenesis.

43
Q

Describe the importance of the concentration of fructose 2,6 bisphosphate.

A

When there is a lot of it, its an allosteric activator for PFK1 for glycolysis and at the same time its an inhibitor of fructose 1,6 bisphposphatase

44
Q

When is there a lot of Fructose 2,6 bisophosphatase?

A

in the fed state - activates PFK1

45
Q

Describe glucagon signals and how that causes the concentration of fructose 2,6 bisphosphatase to decrease.

A

in the fasting state, glucagon activates protein kinase A which phosphorylates the PFK2 side of the bifunctional enzyme and inactivates it which causes the degradation of F26 BP into F6-P.

46
Q

Describe glucagon signals and how that causes a liver cell’s pyruvate kinase to be destroyed.

A

pyruvate kinase is the last step of glycolysis. so when glucagon signals this activates protein kinase A which activates phosphorylation of pyruvate kinase and therefore inactivates it.

47
Q

How does glucagon impact synthesis of PEPCK

A

PEPCK is an inducible enzyme, glucagon activates protein kinase A which causes phosphorylation of a response element –> therefore, protein kinase A goes into the nucleus and phosphorylates a transcription factor which leads to more gene expression and gluconeogenesis can go faster

48
Q

describe how cortisol cause synthesis of PEPCK

A

cortisol is a steroid hormone, the glucocorticoid receptor (GR) can dimerize and this acts as a transcription factor too. PEPCK is also expressed more. speeds up gluconeogenesis

49
Q

how are hepatic cells dependent on beta oxidation of fatty acids?

A

acetyl groups are worth ATP and beta oxidation creates NADH and FADH2 which is needed for gluconeogenesis

Endocrine and Metabolism (9 decks)

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