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Biochemistry > Carb metab > Flashcards

Carb metab Flashcards

1
Q

What are aldoses

A

Monosaccharide with aldehyde group at C-1

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2
Q

What are ketoses

A

Monosaccharide with ketone group at C-2

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3
Q

What is a monosaccharide

A

Basic sugar unit, e.g. glucose, galactose, fructose

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4
Q

What is a disaccharide

A

2 mono units linked via glycosidic bond (lactose and sucrose)

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5
Q

What is an oligosaccharide?

A

3-10 mono units

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6
Q

What is a polysaccharide?

A

Multiple mono units (starch)

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7
Q

What is alpha-amylase and where is it found

A

Random hydrolyses alpha-1,4 glycosidic bonds, except those that act as branch points (near alpha-1,6 linkage)

Found in saliva and pancreatic juice

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8
Q

What is sucrase-isomaltase complex?

A
  • Sucrase hydrolyses sucrose to form glucose and fructose
  • Maltase hydrolyses maltotriose and maltose
  • Isomaltase hydrolyses alpha-1,6 linkages
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9
Q

What is glucoamylase complex

A

Hydrolyses alpha-1,4 glycosyl units, starting from the non-reducing end of chains

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10
Q

How is sucrose digested

A

Hydrolysis of sucrose into glucose and fructose by sucrase

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11
Q

How is lactose digested

A

Hydrolysis by lactase.

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12
Q

What are the effects of lactase deficiency

A

No lactose absorption in lower intestine, bacterial fermentation of lactose producing lactic acid and gases, lactose and lactic acid is osmotically active, draws water into the lumen resulting in diarrhoea

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13
Q

Describe the absorption of glucose and fructose in intestines.

A

SGLT1 (active transport):

  • Na+ dependent cotransporter, works with Na+/K+ ATPase pump
  • energy from Na+ ionic conc gradient, secondary active transport
  • actively transports glucose and galactose into epithelial cells

GLUT 5:
Tansports fructose via facilitated diffusion- passive transport

Monosaccharides exit epithelial cells into bloodstream via GLUT2 (facilitated diffusion, passive)

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14
Q

Describe the transport of glucose in the liver and pancreatic beta cells

A

GLUT 2, low affinity transporter
in pancreas: regulate the secretion of insulin
in liver, remove excess glucose in the blood

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15
Q

Describe the transport of glucose in the brain and nerve tissues

A

GLUT3: high affinity transporter

Allows for basal glucose uptake

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16
Q

Describe the transport of glucose in the heart and skeletal muscles

A

GLUT 4, regulated by insulin, high affinity transporter-> in the presence of insulin, increase in translocation of GLUT4 to the cell surface

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17
Q

What is the glycaemic index

A

Describes blood glucose response after consumption of a carbs containing test food relative to a carbs containing reference food

High GI food-> blood glucose level increases rapidly after consumption

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18
Q

How does oral rehydration therapy function

A

ORS solution contains glucose, sodium chloride, potassium chloride and trisodium citrate

Solution retains fluid and salts within body via osmotic pressure, prevent excretion, replace lost fluid and salts

SGLT 1 cotransports glucose and sodium into epithelial cells, so when glucose is absorbed in the intestines, water and sodium is absorbed as well

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19
Q

What is the purpose of glycolysis in catabolism

A

Occurs when ATP is required, even in the absence of O2

Only source of ATP for cells without mitochondria (e.g. RBC)

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20
Q

Describe the action and regulation of hexokinase

A

Forms G6P from glucose using 1 ATP and giving 1 ADP

Inhibited by product, G6P

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21
Q

What is the difference between hexokinase and glucokinase

A

Glucokinase is a type of hexokinase only found in liver cells and beta pancreatic cells, has a higher Km value and thus lower affinity to glucose.

Glucokinase only functional at high glucose levels, to slow down glycolysis in the liver, as glucose is used for glycogenesis to generate glycogen

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22
Q

Describe the action and regulation of phosphofructokinase-1

A

Reacts with F-6-P to form F-1,6-biphosphate

Uses 1 ATP and gives 1 ADP

Positive regulation

  • AMP
  • F26BP

Negative regulation

  • ATP
  • Citrate
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23
Q

Describe the action and regulation of glyceraldehyde 3-P dehydrogenase

A

Glyceraldehyde 3-phosphate—-> 1,3-Bisphosphoglycerate

Using 1 NAD-> NADH+H+ and 1 Pi

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24
Q

Describe the action and regulation of phosphoglycerate kinase

A

SUBSTRATE LEVEL PHOSPHORYLATION

Using 1 ADP to give 1 ATP

1,3-bisphosphglycerate-> 3-phosphoglycerate

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25
Q

Describe the action and regulation of pyruvate kinase

A

SUBSTRATE LEVEL PHOSPHORYLATION

Using 1 ADP to give 1 ATP

Phosphoenolpyruvate (PEP)-> Pyruvate

Negative regulators

  • alanine
  • ATP
  • Acetyl CoA
  • Phosphorylation of pyruvate kinase by protein kinase A (deactivates pyruvate kinase) in fasting state: glucagon

Positive regulators

  • F16BP
  • Dephosphorylation of pyruvate kinase by phosphatase in fed state: insulin
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26
Q

What is the net output of glycolysis

A

2 pyruvate
2 ATP
2 NADH

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27
Q

Describe the fate of pyruvate under aerobic conditions

A

Pyruvate produced in cytoplasm

Passes through impermeable mitochondria membrane via transporter

Converted to Acetyl CoA in mitochondria by Pyruvate dehydrogenase complex (PDC) and enters TCA cycle

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28
Q

Describe the reaction that pyruvate undergoes with PDC

A

Pyruvate+CoA+NAD+—-PDC—> CO2+ acetyl-CoA+ NADH

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29
Q

How many enzyme components are present in the PDC

A

3:
E1- Pyruvate dehydrogenase
E2- dihydrolipoyl transacetylase
E3- dihydrolipoyl dehydrogenase

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30
Q

How is PDC regulated?

A

Product inhibition by:

  • NADH
  • Acetyl CoA

Covalent modification:
Positive regulation:
- Phosphatase dephosphorylates E1 to activate PDC, activated by Ca2+ and Mg2+

Negative regulation:
- Kinase phosphorylates E1 to deactivate PDC
Inhibited by pyruvate, ADP and Ca2+
Activated by Acetyl-CoA and NADH

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31
Q

What are the effects of PDC deficiency

A

High pyruvate and lactate in blood, slightly low glucose

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32
Q

What are the possible treatments of PDC deficiency

A

Thiamine supplement: Part of PDC

High fat, low carb diet: FA metabolised into Acetyl-CoA without forming pyruvate

Oral sodium bicarbonate: to neutralise acidic environment caused by lactate

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33
Q

Describe the fate of pyruvate under anaerobic conditions

A

Pyruvate Lactate

NADH+H+—->NAD+

NAD returned to glycolysis

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34
Q

State the 2 paths for the fate of NADH under aerobic conditions

A

In the heart and liver: malate-aspartate shuttle

In the skeletal muscles and brain: Glycerophosphate shuttle

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35
Q

Describe the Malate-aspartate shuttle

A

NADH transported into mitochondria via malate-aspartate shuttle

  • NADH becomes NAD+ in cytosol when oxaloacetate becomes malate
  • Malate transported into mitochondria, forms NAD+ from NADH and becomes oxaloacetate

-e- transferred from malate to NAD+ in mitochondria to form NADH, NADH used in ETC

Oxaloacetate becomes aspartate, glutamate becomes alpha-kg

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36
Q

Describe the glycerphosphate shuttle

A

NADH transported to mitochondria via shuttle

electron transferred to dihydroxyacetone-P to form Glycerol 3-P, diffuses into the mitochondria

G3P donates electron to FAD to give FADH2.

FADH2 enters electron transport chain for more ATP generation

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37
Q

What is the function of the 2,3 bisphosphoglycerate (2,3BPG) shunt

A

RBC has no mitochondria, so anaerobic glycolysis is the only ATP source.

2,3 BPG is an allosteric regulator of Hb affinity for O2.

When conc. of 2,3BPG is high, oxygen is more readily released.

When low oxygen pressure at high altitudes, increase synthesis of 2,3BPG in RBCs, increased unloading of oxygen to tissues.

High 2,3BPG in chronic obstructive airway disease

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38
Q

Describe mechanism of 2,3BPG shunt

A

1,3BPG — BPG mutase —> 2,3 BPG — 2,3 BPG phosphatase —> 3PG

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39
Q

Describe fructose metabolism in liver, kidney and small intestine

A

Mainly in liver, kidney and small intestine:
fructose—fructokinase —> fructose-1-P— Fructose-1-phosphate aldolase (aldolase B) —> glyceraldehyde—triose kinase—>glyceraldehyde-3-P

ATP consumed in first and third step

Second step produces dihydroxyacetone-P which can change into glyceraldehyde-3-P

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40
Q

Describe fructose metabolism in muscles

A

Fructose—hexokinase—> Fructose-6-P

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41
Q

What is essential fructosuria?

A

Fructokinase deficiency

Fructose excreted in urine, no accumulation of toxic metabolites, benign

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42
Q

What is hereditary fructose deficiency

A

F1P aldolase (aldolase B) deficiency

cellular accumulation of F1P, inhibits glycogenolysis and gluconeogenesis!!

Avoid fructose (treatment)

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43
Q

Describe metabolism of galactose

A

Galactose—galactokinase—> galactose 1P—galactose 1-phosphate uridylyltransferase—> glucose-1-phosphate—>glucose 6-phosphate

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44
Q

How does galactose 1-phosphate uridylyltransferase work?

A

Substitutes galactose in galactose-1-phosphate with glucose from UDP-glucose to give UDP-galactose.

UDP-glucose is regenerated by epimerase to form UDP-galactose

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45
Q

What causes type 1 (classical) galactosemia?

A

No galactose-1P uridylyltransferase activity

  • galactosemia
  • galactouria
  • galactose-1P accumulation

mental retardation, cataract formation, liver damage, kidney failure

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46
Q

What is type II (nonclassical) galactosemia?

A

Mutation in galactokinase

  • galactosemia
  • galactouria

cataract formation

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47
Q

What is type III galactosemia

A

Epimerase mutation

  • benign form no symptoms
  • severe form, UDP glucose not regenerated, type I symptoms
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48
Q

Where does TCA take place

A

in the mitochondria matrix

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49
Q

What enzyme catalyses the reaction of oxaloacetate to form citrate?

A

citrate synthase

Acetyl CoA—> Coenzyme A

Acetyl group donated to form citrate

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50
Q

What regulates citrate synthase

A

Citrate inhibits citrate synthase (product inhibition)

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51
Q

What enzyme catalyses the reaction of isocitrate to form alpha-kg

A

Isocitrate dehydrogenase

(oxidative decarboxylation)

NAD+—> CO2+NADH+H+

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52
Q

What regulates isocitrate dehydrogenase

A

Positive regulators:

  • ADP
  • Ca2+

Negative regulators:
-NADH

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53
Q

What enzyme catalyses the reaction of alpha-kg to form succinyl-CoA

A

Alpha-kg dehydrogenase

(oxidative decarboxylation)

CoA-SH+NAD+—>CO2+NADH+H+

54
Q

What regulates alhpa-kg dehydrogenase

A

Positive regulator:
-Ca2+

Negative regulator:
-NADH

55
Q

Which enzyme catalyses the reaction of succinate to form fumarate?

A

succinate dehydrogenase

FAD—>FADH2

56
Q

Which enzyme catalyses the reaction of L-Malate to form oxaloacetate?

A

malate dehydrogenase

NAD+—>NADH+H+

57
Q

What regulates malate dehydrogenase?

A

NADH is an inhibitor

58
Q

Which step of TCA involves substrate level phosphorylation?

A

Succinyl-CoA—succinate thiokinase—>succinate

GDP+Pi—> GTP+CoA

59
Q

Name the enzyme complex that allows for the link between glycolysis and TCA cycle via acetyl CoA

A

PDC

Pyruvate—PDC—> acetyl coA

60
Q

Why is TCA cycle amphibolic

A

Catabolic: oxidation of fuel molecules converge at TCA cycle, contributes e carriers for ATP production

Anabolic: intermediates used for synthesis of other molecules

61
Q

What are the anabolic substrates in the TCA

A

Citrate: FA synthesis
alphakg and OAA: amino acid
Succinyl-CoA: heme
Malate: gluconeogenesis

62
Q

What are anaplerotic reactions

A

Reactions to replenish intermediates removed for biosynthesis

63
Q

Name one example of an anaplerotic reaction

A

Conversion of pyruvate to OAA by pyruvate carboxylase

Activated by acetyl-CoA and requires biotin

Biotin is a vitamin synthesised by intestinal bacteria, required in small amounts in humans

64
Q

Where does ETC take place

A

On inner mitochondria membrane

65
Q

What is Complex I

A

NADH-CoQ reductase

66
Q

What is complex II

A

Succinate-Co Q reductase

67
Q

What are the two mobile electron carriers in the ETC

A

Coenzyme Q (CoQ) ubiquinone

Cytochrome C (complex III to IV)

68
Q

What is Complex III

A

Co Q-cytochrome c reductase

69
Q

What is complex IV

A

Cytochrome c oxidase

70
Q

Complex V

A

ATP synthase

71
Q

How are electrons transported

A

Through prosthetic groups

  • FMN Flavin mononucleotide (Complex I)
  • Iron-sulfur clusters (FeS) (Complex I and III)
  • Heme (containing Fe) within the cytochromes (Complex III and IV)
  • Cu (complex IV)
72
Q

How does Fe in heme and FeS accept and release e-

A

Charge varies between +2 and +3

73
Q

What is the net output of the TCA

A

6 NADH, 2 FADH2, 2GTP for each glucose molecule–> 2 acetyl CoA molecules

74
Q

Where does NADH and FADH2 enter the ETC

A

NADH enters at complex I (NADH-CoQ reductase)

FADH2 enters at complex II (succinate CoQ dehydrogenase)

75
Q

Where is H+ pumped out of matrix across inner mitochondria membrane?

A 
Complex I (4H+)
Complex III (4H+)
Complex IV (2H+)
76
Q

How many ATPs are produced by NADH and FADH2

A

NADH: 2.5 ATPs
FADH2: 1.5 ATPs

77
Q

What 2 transport systems are used to transport ADP and Pi into mitochondria matrix

A

1) Pi-H+symport, both ions transported in together, driven by proton gradient.
2) ADP-ATP translocase- export ATP and import ADP

78
Q

How does complex V (ATP synthase) work

A

Rotation of c-ring due to passage of protons from inter-membrane space through F0 pore to the matrix mechanically induces conformational changes in the F1 headpiece that synthesizes ATP from ADP and Pi

79
Q

What are uncoupling proteins

A

They form channels in the inner mitochondria membrane to conduct protons back into the mitochondrial matrix, disrupts proton gradient while releasing heat without ATP production.

80
Q

Where is thermogenin found

A

In brown adipose tissue, allows for non-shivering thermogenesis in babies especially

81
Q

What is dinitrophenol?

A

Carries H+ across inner mitochondria membrane to dissipate H+ gradient-> no energy to drive ATP synthesis, electron transport continues, but energy from H+ gradient lost as heat

82
Q

What is Leigh’s syndrome?

A

Nerodegenerative disorder

  • Complex mutation
  • Pyruvate carboxylase mutation-> pyruvate not converted to OAA (anaplerotic reaction) TCA breakdown
  • PDC mutation, pyruvate not converted to Acetyl CoA-> accumulation of pyruvate, converted to lactate

LEADS to
High pyruvate and lactate in blood

83
Q

Where does pentose phosphate pathway (HMP shunt) take place

A

In the cytoplasm

84
Q

What is the function of the HMP shunt

A

Provides Ribose-5-phosphate for nucleotide and nucleic acid synthesis

Provides NADPH for:

  • biosynthesis
  • counter oxidative stress
  • detox reactions by CYP450
  • generation of superoxide/nitric oxide to counter bacteria infection in cells
85
Q

What are the products of the oxidative phase of PPP/HMP shunt

A

NADPH and 5C sugars

When R5P and NADPH is balanced, no non-oxidative phase takes place.

G6P—G6PD—>6phosphogluconolactone
NADP+—> NADPH+H+

6-phosphogluconate—6-phosphogluconate dehydrogenase—>R5P
NADP+—>NADPH+H+ +CO2

86
Q

What is the purpose of non-oxidative reaction in HMP

A

When NADPH is needed, less/no need for R5P

R5P converted to glycolytic intermediates

87
Q

What happens if R5P is needed and NADPH not needed

A

Oxidative phase inhibited and glycolytic intermediates converted back to R5P via reversible non-oxidative reactions

88
Q

What is glutathione? oxidising or reducing agent

A

Reducing agent, and antioxidant

89
Q

How does glutathione eliminate oxidants like H2O2

A

reduced glutathione (GSH) is oxidised by H2O2 to form oxidised glutathione (GSSG) under action of glutathione peroxidase

90
Q

How is PPP related to GSH

A

GSSG is converted back to GSH by NADPH

GSSG+NADPH+H+—> 2GSH+NADP+

91
Q

Effects of G6PD deficiency?

A

G6PD deficiency, no NADPH produced, less GSSG converted back to GSH, less GSH to remove harmful peroxides, proteins and lipids in RBC oxidised, impairs cell membrane RBC lysis

antimalaria drug (primaquine), fava beans stimulate peroxide formation

92
Q

What is the difference between the function of hepatic and muscle glycogen

A

Hepatic glycogen:
- store of glucose for fasting situations to maintain blood glucose levels

Muscle glycogen:
-store of glucose which can be rapidly mobilised and metabolised via glycolysis under anaerobic conditions

93
Q

What is the difference between the fate of glucose-6P from hepatic and muscle glycogen

A

Muscle: Glucose-6P enters glycolysis, no glucose-6P phosphatase present in muscles

Hepatic: glucose-6P—Glucose-6P phosphatase—> glucose enters bloodstream

94
Q

What is the key enzyme for glycogenolysis

A

Glycogen phosphorylase

Glycogen(n) +Pi—-> glycogen (n-1)+G-1P

95
Q

What enzyme produces G6P from G1P and vice versa

A

Phosphoglucomutase

96
Q

What is a limit branch?

A

Branch of about 4 glucose, where glycogen phosphorylase can no longer act

97
Q

What are the 2 functions of debranching enzyme

A
  1. Transglycosylase
    Transfers alpha1->4 linked tri/quartrosaccharid unit from limit branch to nonreducing end of another branch
  2. Hydrolyse last remaining alpha 1->6 linked glycosyl residue in the branch to yield GLUCOSE
98
Q

What is the key enzyme for glycogenesis

A

Glycogen synthase

UDP-glucose+PPi+glycogen (n)—Glycogen synthase—> glycogen (n+1) + UDP

glycosyl residues added from UDP-glucose to non-reducing ends of glycogen chain via alpha,1->4 linkages

99
Q

What does UDP-glucose pyrophosphorylase do?

A

Glucose-1P+UTP—-UDP-glucose pyrophosphorylase—> UDP-glucose+PPi

100
Q

What happens when chains reach 11 residues

A

Branching enzyme cleaves 6-8 residue piece and reattached to another glycosyl unit by alpha-1,6 glycosidic bond

Glycogen is highly-branched molecule

101
Q

How is muscle glycogen synthase regulated

A

+ Glucose-6-phosphate

102
Q

How is muscle glycogen phosphorylase regulated

A

+ AMP, Ca2+

- ATP, Glucose-6-phosphate

103
Q

How is liver glycogen phosphorylase regulated?

A

-ve glucose

104
Q

What is the effect of glucagon on glycogen

A

Activate glycogen breakdown in LIVER to maintain blood glucose levels during fasting

Activates phosphorylase kinase to phosphorylate (activate) glycogen phosphorylase and various kinases to phsophorylate (deactivate) glycogen synthase

105
Q

What is the effect of insulin on glycogen

A

Activate glycogen storage in LIVER AND MUSCLE during fed state

Activates phosphoprotein phosphotase I (PPI) which removes phosphate group from both glycogen synthase (activates) and glycogen kinase (deactivates)

106
Q

What is the effect of epinephrine on glycogen

A

Activate glycogen breakdown in liver (to maintain blood glucose levels) and muscle (to provide energy for muscle movement)

Activates phosphorylase kinase to phosphorylate (activate) glycogen phosphorylase and various kinases to phsophorylate (deactivate) glycogen synthase

107
Q

What is an allosteric activator of hepatic PP1?

A

Glucose

108
Q

Why is phosphofructokinase deficiency considered a glycogen storage disease?

A

PFK deficiency results in F6P not being converted to F16BP, so glycolysis cannot take place. Thus there is no need for Glucose-6P and glycogenolysis will not take place.

109
Q

What is gluconeogenesis?

A

Synthesis of glucose from non-carb sources (even chain fatty acids {metabolised to acetyl CoA} and acetyl CoA {cannot be converted back to pyruvate} not precursors)

110
Q

What is the purpose of gluconeogenesis?

A

To maintain blood glucose especially in fasting state/ especially for tissues with little/ no mitochondria (brain, lens of eye, rbc)

111
Q

Where does gluconeogenesis take place?

A

90% in liver, 10% in kidney, where there is glucose-6-phosphatase (glucose-6P—> glucose)

Takes place mainly in cytosol, minority in mitochondria

112
Q

Is gluconeogenesis a reversal of glycolysis?

A

No. Different key enzymes.

113
Q

Name the key enzyme of gluconeogenesis that converts Glucose 6-phosphate to glucose

A

Glucose-6-phosphatase

114
Q

Name the key enzyme of gluconeogenesis that converts fructose 1,6 bisphosphatase to fructose 6-phosphatase

A

Fructose-1,6-bisphosphatase

115
Q

Name the key enzyme of gluconeogenesis that converts OAA to Phosphoenolpyruvate (PEP)

A

Phosphoenolpyruvate carboxykinase

116
Q

Describe the mechanism by which pyruvate enters gluconeogenesis pathway

A

Pyruvate formed in cytosol, transported to mitochondria

Pyruvate—pyruvate carboxylase—>OAA

OAA transported to cytosol through malate-aspartate shuttle

OAA—> PEP—> Glucose

117
Q

Name the precursors for gluconeogenesis

A

Glycerol

Lactate

Glucogenic amino acids

118
Q

Where is glycerol from, and how does it enter gluconeogenesis pathway

A

TG in adipocytes broken down during lipolysis-> release FA and glycerol-> transported to liver

glycerol—glycerol kinase—> Glycerol 3-P—>dihydroxy acetone phosphate

phosphate provided by ATP

Glycerol 3-P converted to DHAP by NAD

119
Q

Where is lactate from, and how does it enter gluconeogenesis pathway

A

Lactate is produced by anaerobic glycolysis via lactate dehydrogenase from pyruvate.

Lactate—lactate dehydrogenase—> pyruvate,
producing NADH

pyruvate—pyruvate carboxylase—> OAA

120
Q

When does the cori cycle take place?

A

When ATP demand at tissues is greater than capacity of mitochondria’s oxidative phosphorylation.

Anaerobic glycolysis takes place in skeletal muscle/RBC, lactate transported to liver for gluconeogenesis, glucose produced transported back to muscles

121
Q

Where are glucogenic amino acids from, and how does it enter gluconeogenesis pathway

A

During prolonged fasting, proteolysis occurs.

Glucogenic amino acids enter TCA cycle at different points, converted to OAA

122
Q

How is alanine converted to pyruvate?

A

By alanine aminotransferase (ALT) via transamination.

alpha kg converted to glutamate via transamination catalysed by ALT at the same time

123
Q

Name one key allosteric regulator of both glycolysis and gluconeogenesis in the liver

A

Fructose-2,6-bisphosphate

124
Q

What is the effect of insulin on fructose-2,6-bisphosphate levels?

A

When insulin is produced in wellfed state, activates phosphatase, dephosphorylates and activates PFK2, F6P—> F26BP

125
Q

What is the effect of glucagon on F26BP levels

A

When glucagon is produced in starving state, activates kinase, phosphorylates and activates fructobisphosphatase 2, converts F2,6BP to F6P, lower F26BP

126
Q

How does F26BP regulate FBPase and phosphofructokinase (PFK)

A

It is an inhibitor of FBPase and an activator for PFK

127
Q

What are the inhibitors for FBPase

A
  • AMP

- F26BP

128
Q

What are the activators for phosphofructokinase?

A
  • AMP

- F26BP

129
Q

What are the inhibitors for phosphofructokinase?

A
  • ATP

- Citrate

130
Q

What is type 1 glycogen storage disease?

A

Von Gierke’s disease, Glucose-6 phosphatase deficiency.

G6P cannot be converted to Glucose

Gluconeogenesis impaired, low glucose levels, hypoglycemia

Glycogenolysis impaired, liver glycogen phosphorylase activated by glucagon, but Pi trapped within G6P

131
Q

What does fructose bisphosphatase deficiency cause?

A

F16BP cannot be converted to Fructose 6 Phosphate.

Gluconeogenesis cannot take place.

Hypoglycemia, metabolic acidosis upon fasting. Lactate and pyruvate accumulation

132
Q

What does pyruvate carboxylase deficiency cause?

A

Pyruvate cannot be converted into OAA for gluconeogenesis, OAA obtained only from amino acids

Hypoglycemia.

Anaplerotic reaction breakdown, TCA disrupted

Pyruvate undergo anaerobic glycolysis, lactate, lactic acidosis

Biochemistry (3 decks)

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