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Biochemistry > Gluconeogenesis > Flashcards

Gluconeogenesis Flashcards

1
Q

Uses non-carbohydrates to produce glucose:

A

Lactate
Amino acids
Glycerol
Proprionyl CoA from Odd chain fatty acids

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2
Q

Gluconeogenesis occurs in

A

Liver 90%

Kidneys 10% major glucose producing organ in prolonged starvation

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3
Q

This pathway is important for

A

maintaining normal blood glucose levels

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4
Q

First step in gluconeogenesis is conversion of

by the enzyme

Happens in

A

Pyruvate -> oxaloacetate

Pyruvate carboxylase

Mitochondria of liver and kidney only kasi walang pyruvate carb sa muscle

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5
Q

Conversion of pyruvate from cytosol to oxaloacetate by pyruvate decarboxylase occurs in

A

mitochondria of liver and kidney

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6
Q

Pyruvate carboxylase in the mitochondria requires the coenzyme

A

Biotin B7

bound to lysine forming active biocytin

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7
Q

Pyruvate carboxylase is stimulated or regulated or allosterically regulated by

A

Inc levels of Acetyl CoA

Ex starvation and to replenish TCA
Inactive at low levels of acetyl coa and pyruvate is oxidized instead in TCA

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8
Q

During fasting, there is increased Acetyl Coa because fat is metabolized for energy

A

Fatty acids are metabolized by liver by beta oxidation with end product of Acetyl CoA

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9
Q

During starving, gluconeogenic amino acids and proprionyl coA (odd-chain fatty acids) can be shuttled to TCA to produce ATP

A

Inc ATP inhibits Kreb’s cycle and beta oxidation causing acetyl coA to rise hence activating pyruvate carboxylase

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10
Q

An experiment is performed on mice with knockout mutation resulting in inability to metabolize triglycerides.

After several days without food, how will the activity of the enzymes pyruvate carboxylase and glycerol kinase likely be altered in the knockout mice compared to healthy mice?

A

Decreased TAG metabolism leads to decreased fatty acid oxidation decreasing acetyl coA and decreasing pyruvate carboxyalse leading to decreased gluconeogenesis

Decreased TAG metabolism leads to dec glycerol leading to dec glycerol kinase

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11
Q

Decreased glycerol leads to a decrease in

A

DHAP with decreased activity Glycerol kinase

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12
Q

Second step:

Oxaloacetate from mitochondria is converted into this substrate to enter the cytosol

A

Malate by enzyme malate dehydrogenase

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13
Q

Oxaloacetate should be converted into Malate because in order for it to be shuttled to

A

cytosol because it cannot cross the mitochondrial membrane

Malate shuttle

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14
Q

NADH is generated each time malate is converted into oxaloacetate and is shunted by

A

Malate shuttle

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15
Q

Once in the cytoplasm, malate is convered back to

A

Oxaloacetate also generating

NADH

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16
Q

Third step: In the cytosol, oxaloacetate is converted to or decarboxylated and phosphorylated

by the enzyme

A

Phosphoenolpyruvate

Phosphoenolpyruvate carbokinase (PEPCK) 
pyruvate carboxylase

using up GTP to become GDP

Provides energetically favorable pathway from pyruvate to PEP

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17
Q

GTP utilized by PEPCK to convert Oxaloacetate to phosphoenolpyruvate comes from this reaction of TCA

A

Succinyl coa -> succinate by succinate synthase

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18
Q

Step 4: Phosphoenolpyruvate is converted to

By enzyme

A

Fructose 1,6 bisphosphate

Fructose 1,6 bisphosphatase bypasses the irreversible PFK1

*regulatory site of gluconeogenesis

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19
Q

Increase in fructose 1,6 bisphosphate allows conversion to frucose 6 phosphate. Fructose 6 phosphate is converted to glucose 6 phosphate.

Glucose 6 phosphate is converted to glucose by the enzyme

A

Glucose 6 phosphatase

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20
Q

Glucose 6 phosphate is converted to glucose in the

A

Liver and kidneys

21
Q

This upregulates or increases activity of glucose 6 phosphatase

A

Glucagon

22
Q

Deficiency of glucose 6 phosphatase is

A

Von Gierke’s

Type I GSD

23
Q

Lactate
Gluconeogenic amino acids

enter gluconeogenesis via

A

Pyruvate in cytosol

24
Q

Glycerol enters gluconeogenesis via

A

DHAP in cytoplasm

25
Q 
Gluconeogenic amino acids
Proprionyl CoA (from odd-chain fatty acids) enter gluconeogenesis via
A

TCA in matrix of mitochondria

26
Q

17/M
2 month history of weight loss, depression and a red blistering rash primarily affecting the leg

Two days ago, developed DVT

Rash consistent with necrolytic migratory erythema

Hyperglycemia

How will activity of fructose 1,6 bisphosphate and glucose 6 phosphatase likely be altered?

A

Glucagonoma (Dermatitis, Depression, Declining weight, DVTs)

Glucagon dec concentration of fructose 2,6 bisphosphate by increasing activity of fructose 2,6 bisphosphate

fructose 1,6 bisphosphatase activity is increased resulting in increased conversion of fructose 6 phosphate and increases glucose 6 phosphatase hence increased gluconeogenesis

27
Q

Liver glycogen can only sustain glucose in absence of carbohydrate intake within

A

10-18 hours

28
Q

4 alternate reactions that energetically favor synthesis of glucose

A

(Carboxylation of pyruvate)
pyruvate -> oxaloacetate

(Transport of oxaloacetate to cytosol)
Oxaloacetate -> phosphoenolpyruvate

(Decarboxylation of cytosolic oxaloacetate)

(Dephosphorylation of fructose 1,6 bisphosphate)
Fructose 1,6 -> fructose 6

Glucose 6 phosphate -> glucose

29
Q

Fructose 1,6 bisphosphatase is inhibited by

A

inc AMP signalling poor energy state

Fructose 2,6 bisphosphatase (allosteric) influenced by glucagon

30
Q

Fructose 1,6 bisphosphatase is stimulated by

A

ATP
Low AMP

stimulating gluconeogenesis

31
Q

Final step in gluconeogenesis

A

Glucose 6 phosphatase -> glucose by glucose 6 phosphatase

32
Q

Deficiency of enzyme on the last step of gluconeogenesis leads to

A

Von Gierke Type 1 Glucose 6 Phosphatase deficiency

33
Q 
Affects liver, kidney and intestine
Fasting hypoglycemia severe
Fatty liver and hepatomegaly 
Hyperlactiacidemia and hyperuricemia
Normal glycogen structure increased glycogen stored
A

Von Gierke’s Glucose 6 Phosphatase Deficiency

Type I

34
Q

Most important GLUCONEOGENIC precursors

A

Glycerol - from hydroysis of TAG

Lactate - from RBC and skeletal muscle ; from Cori cycle (blood glucose -> lactate by muscle)

Ketoacids (pyruvate, oxaloacetate and alpha-ketoglutarate) from glycogenic amino acids forming oxaloacetate

35
Q

Alpha keto acids from metabolism of glycogenic amino acids

A

Pyruvate
Oxaloacetate
a-ketoglutarate

36
Q

Ketogenic compounds like acetyl coa from acetoacetate and ketogenic amino acids cannot give rise to synthesis of glucose because

A

Pyruvate to Acetyl coa by Pyruvate dehydrogenase is irreversible

Instead they give rise to ketone bodies

37
Q

Hormone stimulating gluconeogenesis by

1) allosteric effect (low fructose 2,6 inc fructose 1,6 bisphosphatase and inhibition of PFK)?
2) covalent modification (inc cAMP and cAMP Protein kinase stimulates pyruvate kinase to inactive phosphorylated form) dec PEP to pyruvate

A

Glucagon

38
Q

Gluconeogenesis is regulated by

A

Glucagon

Substrate availability (glycerol, lactate, a-ketoacids)

Mobilization of amino acids from muscle protein and provide carbon skeletons for gluconeogenesis

Allosteric activation of pyruvate carboxylase by acetyl coa accumulation

39
Q

Glucogenic Amino acids

A 
Glycine
Serine
Valine
Histidine
Arginine
Cysteine
Proline
Alanine
Glutamate
Glutamine
Aspartate
Asparagine
Methionine
40
Q

Both glucogenic and ketogenic amino acids

A

Tryptophan
Tyrosine
Isoleucine
Phenylalanine

41
Q

Ketogenic amino acids

A

Leucine

Lysine

42
Q

Glycogen reserves drop after

A

12 hours

Inc gluconeogenesis

After 24 h, gluconeogesis is sole source

43
Q

Between meals, what happens to fatty acids

A

oxidation of fatty acids in liver -> acetyl coa accumulates -> pyruvate carboxylase converts pyruvate to oxaloacetate and conversion of lactate and alanine to acetyl coa prevented

44
Q

In the well fed state, what happens to acetyl coa

A

Acetyl coa accumulated is shuttled to cytoplasm for fatty acid synthesis from increased pyruvate formation (pyruvate dehydrogenase)

45
Q

Alcoholics are susceptible to hypoglycemia because of

A

the formation of high amounts of cytoplasmic NADH from alcohol dehydrogenase and acetaldehyde dehydrogenase

46
Q

Key central point of gluconeogenesis

Activated by ATP

A

Fructose 1,6 bisphosphate

47
Q

Fructose 1,6 bisphosphate is inhibited by

A

AMP

Fructose 2,6 bisphosphate

48
Q

Present in lumen of ER of liver
Glucose 6P is transported into ER and free glucose is transported back into cytoplasm
Absent in skeletal muscle accounting for the the fact that muscle glycogen cannot serve as source of blood glucose

A

Glucose-6 phosphatase

Biochemistry (32 decks)

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