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Biochemistry 316 : Metabolism > Topic 1 : Carbohydrate Biosynthesis and Metabolism > Flashcards

Topic 1 : Carbohydrate Biosynthesis and Metabolism Flashcards

1
Q

Metabolism is the sum of these 2 processes

A

Catabolism (breakdown)

Anabolism (synthesis)

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2
Q

Energy release of ATP hydrolysis

A

γ-β bond - 30.5 kJ / mol

β-α bond - 32.8 kJ / mol

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3
Q

Function of glycolysis

A

energy production

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4
Q

function of gluconeogenesis

A

glucose resynthesis

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5
Q

function of citric acid cycle

A

building blocks and energy

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6
Q

function of pentose phosphate pathway

A

NADPH and pentose synthysis

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7
Q

Brain uses this in well - fed state

A

glucose

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8
Q

storage of glycogen in this organ

A

liver

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9
Q

methods of enzyme regulation (general)

A 
enzyme activity modification (short term ie hours, minutes)
enzyme concentration (long term ie days, hours)
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10
Q

WHAT ARE THE ADVANTAGES OF USING A SINGLE ENERGY CURRENCY?

A

Easy to distribute energy. Reduces the number of necessary pathways to use energy
Can stock up on ATP without having to worry about converting to other forms

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11
Q

WHY DO CELLS LIKE MYOCYTES & NEURONS USE PHOSPHOCREATINE AS WELL AS ATP FOR ENERGY?

A

Phosphocreatine allows rapid regeneration of ATP from ADP. Cells like myocytes and neurons have to rapidly fire, and benefit from speedy recovery

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12
Q

IF ENZYMATIC STEPS ARE REVERSIBLE: WHY USE TWO PATHWAYS TO SYNTHESIZE AND BREAKDOWN COMMON CELLULAR COMPONENTS?

A

It makes it easier to regulate.
There are some steps that are virtually irreversible, the regulation of which aid in preventing the pathway from gong in both directions.

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13
Q

Sugar isomer used by mammals

A

D-isomers

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14
Q

Common aldoses (3)

A

D-glucose
D-galactose
D-mannose

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15
Q

Aldose

A

contains multiple alcohol groups and one carbonyl as an aldehyde

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16
Q

Ketose

A

contains multiple alcohol groups with one carbonyl as a ketone

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17
Q

Common Ketoses (2)

A

Fructose

Ribulose

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18
Q

anomeric carbon

A

hemiketal / hemiacetal carbon in a sugar
can be OH down (α)
or OH up (β)

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19
Q

What is unusual about the linkage between glucose and fructose in sucrose ?

A 
They are both attached on the reducing end 
Therefore:
Fru(2β-α1)Glc 
is the same as 
Glc (2β-α1) Fru
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20
Q

Reducing end

A

Hemiketal or hemiacetal end of a sugar (carbon 1)

or sugar chain

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21
Q

bonds of glycogen and amylopectin

A

α 1-6 linkages to create branches

α 1-4 linkages within branches

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22
Q

bonds between cellulose sugars

A

β 1-4 linkages

forms straight chains

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23
Q

n-linked glycoproteins use what aa for linkage to sugar ?

A

Asn

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24
Q

ARE DIGESTIVE ENZYMES GENERAL OR SPECIFIC FOR CERTAIN POLYSACCHARIDES OR GLYCOSIDIC LINKAGES?

A

Specific.

Amylases in the mouth are general

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25
Q

WHY DO ERYTHROCYTES (RED-BLOOD CELLS) DEPEND HEAVILY ON GLUCOSE FOR THEIR ENERGY?

A

There are no organelles,

most energy producing processes take place in the mitochondria

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26
Q

WHY DO WE NEED GLYCOPROTEINS, PROTEOGLYCANS AND MUCOPOLYSACCHARIDES ?

A

Glycoproteins are used as cell markers
Proteoglycans are used for shock absorbing in cartilage
mucopolysaccharides are slippery (mucus)

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27
Q

3 main sources of sugars

A

Diet (plant / animal)
Glycogen storage
Individual sugars

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28
Q

1st step of glycolysis

A

Hexokinase is considered the first step, but is not always done

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29
Q

product of glycogen breakdown

A

glucose 1 phosphate (G1P)

later transformed into g6p

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30
Q

glucose transporter in liver

A

GLUT2

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31
Q

glucose transporter in muscle

A

GLUT4

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32
Q

insulin dependent glucose transporter

A

GLUT4

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33
Q

Difference between GLUT2 and GLUT4

A

GLUT2 (liver) has a high Km so it can absorb glucose when in excess
GLUT2(muscle) has lower Km, so it can take in glucose at physiological concentration

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34
Q

ATP producing steps of glycolysis

A

7 (phosphoglycerate kinase)
10 (pyruvate kinase)

Substrate level phosphorylation

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35
Q

Irreversible steps of glycolysis

A

1 (glucose -> G6P by hexokinase)

3 (fructose 6-phosphate -> fructose 1,6-biphosphate by phosphofurctokinase-1)

10 (phosphoenolpyruvate -> pyruvate by pyruvate kinase)

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36
Q

2 phases of glycolysis

A

preparatory

payoff

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37
Q

Purpose of lactate cycle

A

Remove pyruvate
and
revert NADH back to NAD+

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38
Q

WHY CAN’T HUMANS METABOLIZE CELLULOSE?

A

Do not have the proper enzymes to break linkages (β-1,4)

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39
Q

WHY DO WE NEED GLUTs?

A

Glucose does not diffuse fast enough through the membrane

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40
Q

WHAT HAPPENS TO EXCESS BLOOD GLUCOSE?

A

Insulin is released and it is absorbed into the tissues.
It is converted to glycogen in the liver
It may also be turned into fats

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41
Q

What is glucuconeogenesis ?

A

synthesis of glucose from non carbohydrate precursors

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42
Q

What non carbohydrate precursors can be used to make glucose ?

A

Lactate, glucogenic amino acids (alanine, etc), glycerol

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43
Q

Where does gluconeogenesis happen ?

A

Liver

Kidney (to a lesser extent)

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44
Q

Normal HbA1c ?

A

3.5 - 5.5 mM

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45
Q

What happens when HbA1c drops below normal ?

A

hypoglycaemic shock / coma

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46
Q

Gluconeogenesis

Catabolic or anabolic ?

A

Anabolic

Requires energy

47
Q

Irreversible steps of glucolysis (enzymes)

A

hexokinase,
phosphofructokinase-1,
pyruvate kinase

48
Q

irreversible steps in gluconeogenesis (enzymes)

A

glucose-6-phosphatase
fructose-1,6-bisphosphatase-1
pyruvate carboxylase

49
Q

Hexokinase in muscle

A

Hexokinase I and II

50
Q

Hexokinase in liver

A

Hexokinase IV (Glucokinase)

51
Q

Difference between hexokinase I and IV

A

Hexokinase IV / Gluclkinase (liver) has a higher Km so it will operate at a higher [glucose]
This is to process glucose more efficiently when in excess

52
Q

Which hexokinase is upregulated by insulin ?

A

Muscle (I)

53
Q

effect of G6P on hexokinase I?

A

Inhibition
(end product inhibition)

NB that Glucokinase is not inhibited by G6P

54
Q

Reaction catalyzed by PFK1

A

Phosphofructokinase - 1 catalyzes

Fructose 6-phosphate -> Fructose 1,6-biphosphate

55
Q

Activators and inhibitors of PFK1

A

Phosphofructokinase 1

Activators:
ADP, AMP, Fructose 1,6 bisP

Inhibitors:
ATP, citrate

56
Q

reaction catalysed by pyruvate carboxylase

A

pyruvate + bicarbonate -> oxaloacetate

57
Q

explain the role of fructose 2,6-bisphosphate in glucose control

A

In the presence of insulin, PFK-2 activates and creates fructose 2,6-BP, stimulating glycolysis

In the presence of glucagon, FBPase activates and creates fructose 6-phosphate, stimulating gluconeogenesis

58
Q

Why can liver and kidney export glucose from glycogen ?

A

Glycogen breakdown results in G6P.

Only the liver and kidneys have G6Pase to create glucose for transport

59
Q

WHAT HAPPENS IF YOUR BLOOD GLUCOSE FALLS <3.5 mM?

A

Hypoglycaemic shock / coma / death

60
Q

WHY DO WE NEED TWO SEPARATE PATHWAYS IN GLYCOLYSIS AND GLUCONEOGENESIS TO BREAKDOWN & RESYNTHESIZE GLUCOSE?

A

These two pathways are opposing, so only one should be happening at a time.
Having separate pathways allows for regulation

61
Q

WHAT IS THE CONSEQUENCE OF TISSUES (eg MUSCLE) LACKING THE ENZYME, GLUCOSE-6-PHOSPHATASE?

A

G6P cannot be dephosphorylated to glucose, and therefore cannot be transported outside the cell

62
Q

Difference between glycogen and amylopectin

A

Amylopectin has a α1-6 branch every 24-30 residues

Glycogen has α1-6 branches every 12-14 residues

63
Q

what is glycogenenin ?

A

glycogenin is the core around which glycogen is fomed

64
Q

Amino acid glycogenin uses to attach to glucose

A

Tyr 194

65
Q

Compare glycogen and fat

A

Glycogen is stored with water (hydrated), which makes it less dense, but easier to access

66
Q

Type of chemical reaction used in glycogen breakdown

A

phorylysis (NOT hydrolysis)

results in G6P

67
Q

enzyme that converts G1P to G6P

A

phosphoglucomutase

68
Q

HOW DOES AMYLASE DIFFER FROM GLYCOGEN PHOSPHORYLASE? (BOTH HYDROLYZE GLUCOSE POLYMERS SUCH AS GLYCOGEN)

A

Amylase is hydrolytic and acts in the gut,
whereas glycogen phosphorylase is phospholytic to maintain the high energy phosphate bond and acts in the cell
Both cleave at the alpha 1-4 link

69
Q

WHY IS TRIGLYCERIDE A BETTER LONG-TERM STORAGE FORM?

A

It is more energy dense (more energy per bond), and is kept in an anaqueous environment.
This makes it good for storing lots of energy in a small space, but its hard for the enzymes to access

70
Q

WHAT IS THE CONSEQUENCE IF THERE IS A GENETIC DEFECT IN GLYCOGEN STORAGE

A

Mostly death

71
Q

Steps to glycogen synthesis

A
  • 1) GLYCOGENIN FORMS 8-Glu CORE OF THE GLYCOGEN PARTICLE
  • 2) GLYCOGEN BRANCHING ENZYME INSERTS (α1->6) LINKAGES
  • 3) GLYCOGEN SYNTHASE USING UDP-GLUCOSE COUPLES GLUCOSE UNITS JOINED BY (α1->4) LINKAGES
  • 4) REPEATS OF STEPS 2) AND 3) TO PRODUCE MULTIPLE (12) TIERS FOUND IN HIGHLY BRANCHED GLYCOGEN STRUCTURE
72
Q

INSULIN IS A GLUCOSE-ABUNDANCE HORMONE? GLUCAGON IS A GLUCOSE-SHORTAGE HORMONE? WHAT TYPE OF BIO-MOLECULES ARE THEY?

A

Yes
Yes
Protein

Prof’s answer:
Peptide hormones (Lectures 25,27,29) that work through completely different signal
transduction processes: insulin via receptor-tyrosine kinase-mediated pathway
(Lecture 27); glucagon via cAMP and protein kinase A mediated pathway (Lecture 29)

73
Q

WHAT IS GLYCOGENIN AND WHAT DOES IT DO?

A

It is a protein that acts as the core in glycogen synthesis

It makes the 8-glucose primer before glycogen synthase takes over

74
Q

WHAT ARE THE ANSWERS TO THE FOLLOWING FACTUAL QUESTIONS REGARDING GLYCOGENIN?

a) HOW MANY GLUCOSE UNITS COMPRISE THE PRIMER ON GLYCOGENIN?
b) HOW BIG IS GLYCOGENIN?
c) WHICH AMINO ACID RESIDUE IS ATTACHED TO THE PRIMER?
d) TO WHICH END OF THE PRIMER CHAIN ARE NEW GLU RESIDUES ADDED?

A

a) 8
b) 37K
c) Tyr
d) non-reducing

75
Q

Overall purpose of the citric acid cycle

A
  • convert acetyl coA into CO2
  • Trap reducing power as NADH, FADH2, GTP
  • generate useful building blocks
76
Q

Where does the TCA cycle take place ?

A

Inside the mitochondrial matrix

77
Q

How many subunits does the pyruvate dehydrogenase complex have ?

A

3

E1, E2, E3

78
Q

3 parts of pyruvate dehydrogenase (names)

A

E1 : Pyruvate dehydrogenase

E2 : Dihydrolipoyl transacetylase Dihydrolipoyl dehydrogenase

79
Q

Citric acid cycle intermediates

A 
citrate
isocitrate
α-ketogluterate
succinyl-CoA
succinate
fumerate
malate
80
Q

of steps in TCA cycle

A

8

81
Q

enzymes in TCA cycle that give reducing agents

A

NADH:

  • isocitrate dehydrogenase
  • α-ketogluterate dehydrogenase complex
  • malate dehydrogenase

FADH2:
-succinate dehydrogenase

GTP:
-succinyl coA synthetase

82
Q

H+ to ATP generation ration

A

~4H+ to make 1 ATP

83
Q

ATP generated from NADH

A

gives 10H+ (2.5 ATP)

84
Q

ATP generated from FADH2

A

gives 6H+ (1.5ATP)

85
Q

Net total ATP produced from 1 glucose

A

30 - 32

86
Q

Citric acid cycle regulation molecules

A

Activators:
AMP, CoA, ADP, Ca2+

Inhibitors:
ATP, NADH, fatty acids, succinyl CoA

87
Q

Anapleurotic steps

A

PEP to Oxaloacetate

Pyruvate to malate

88
Q

WHY DO EITHER THIAMIN DEFICIENCY OR LOSS-OF-FUNCTION MUTATIONS
OF PYRUVATE DEHYDROGENASE PRIMARILY AFFECT BRAIN?

A

The brain uses glucose and ketones exclusively

89
Q

WHY ARE MAMMALS UNABLE TO CONVERT FATTY ACIDS OR ACETYL CoA TO
GLUCOSE? WHAT DOES THIS TELL US ABOUT PYRUVATE DEHYDROGENASE?

A

1) TCA does not occur at the same time as gluconeogenesis in the liver
2) Acetyl CoA (product of fatty acid breakdown) is not converted totally to oxaloacetate
3) Pyruvate dehydrogenase is irreversible and inhibited by Acetyl CoA

90
Q

IF GLYCOLYSIS ENDS IN PYRUVATE & IS CYTOSOLIC AND PYRUVATE
DEHYDROGENASE OCCURS IN MITOCHONDRION THEN HOW DOES PYRUVATE
GET INTO THE MITOCHONDRION.

A

Pyruvate translocase transports it across inner mitochondrial membrane

91
Q

steps of Glyoxylate cycle

A 
citrate
isocitrate
succinate
malate
oxaloacetate
92
Q

Glyoxylate cycle differences compared to TCA (4)

A

5 steps (vs 8)
2 acetyl coA added
glyoxylate
2 new enzymes (isocytrate lyase and malate synthase)

93
Q

Glyoxosome found in what type of cell ?

A

Plant cells only

94
Q

Regulation of TCA vs Glyoxylate is controlled by (enzyme):

A

isocitrate dehydrogenase

95
Q

Glyoxylate cycle is preferred over TCA under in circumstance ?

A

Well - fed state.
TCA produces more NADH and FADH2

Glyoxylate allows for gluconeogenesis

96
Q

2 options of the pentose phosphate pathway

A

Oxidative and non-oxidative phase

97
Q

Difference between 2 pathways of pentose phosphate pathway

A

Oxidative:
Irreversible
produces NADPH from NADP

Non oxidative:
The opposite of that

98
Q

purpose of pentose phosphate pathway:

A

changes G6P to ribulose 5-phosphate, then to ribose 5-phosphate for use in DNA, nucleotides, conezymes, RNA

99
Q

Things that cause free radicals

A

Electron transport chain

Chemotherapy

100
Q

Key points of the nonoxidative pentose phosphate pathway (3)

A
  • six 5C sugars converted to five 6C sugars (or the other way)
  • Enzymes involved are transketolase (2x) and transaldolase
  • Energy supplied by thiamine pyrophosphate at transketolase steps
101
Q

Regulating factor of pentose phosphate pathway

A

NADPH

102
Q

PENTOSE PHOSPHATE PATHWAY PROVIDES: NADPH & RIBOSE-5-P WHAT IF A CELL HAS SUFFICIENT NADPH & A HIGH [NADPH]/[NADP] RATIO BUT STILL NEEDS RIBOSE-5-P FOR NUCLEOTIDE SYNTHESIS?

HOW DOES A CELL MAKE RIBOSE-5-P IF G-6-P-D IS INHIBITED?

A

It will use the nonoxidative pathway, (which is reversible)

103
Q

WHAT IS NAPDH USED FOR? WHICH TISSUES NEED A RICH SUPPLY?

A

All tissues involved in fat production (liver, adipose, mammary gland)
or steroid production (adrenal)

104
Q

IT IS ESTIMATED THAT 400 MILLION PEOPLE HAVE G-6-P-D DEFICIENCY. HOW WOULD YOU EXPECT THESE INDIVIDUALS TO BE AFFECTED?

A

Antioxidant pathways require NADPH.
Drugs and other dietary methods are used to regulate this
The cell most vulnerable is the RBC, and this condition may induce haemolysis.

105
Q

Definition of vitamin

A

Essential substance not synthesized, and must be ingested in diet
(Sometimes converted a bit, but the important part is that its not created de novo)

106
Q

When are vitamins converted to active form and why ?

A

They are converted near the time of use because it improves specificity and regulates

(“You dont want coenzymes floating around and fucking shit up”)

107
Q

Biotin is a prosthetic group of what 4 enzymes ?

A

Pyruvate carboxylase
Acetyl-CoA carboxylase
Propionyl-CoA carboxlase
3-methylcrotonyl-CoA carboxylase

Starred enzymes important to know

108
Q

Biotin containing enzymes have these three parts :

A

1) biotin carrying protein
2) biotin carbozylase
3) Transcarboxylase

109
Q

How carboxylases work (details of the 3 parts)

A

1) Biotin carrying protein
carries biotin and moves it between parts 2 and 3

2) Biotin carboxylase
Adds COO- group to biotin (activates biotin, requires ATP)

3) Transcarboxylase
Transfers carboxyl group to substrate

110
Q

Substance blocks biotin absorption

A

Avidin (found in egg white)

(Biotin and avidin are used in antibody studies because it binds so tightly

111
Q

Reasons for biotin deficiency (or any vitamin deficiency, really) (3)

A

Biotin supply
dietary, gut flora, absorption issues

Biotin enzyme error
If the enzyme is not properly handling biotin, its effects will present as a deficiency

Biotin recycling efficiency (biotinidase)
If it is not properly being reused, it will run out

112
Q

WHAT WOULD BE THE CLINICAL OUTCOME IF THERE WAS A MUTATION OF THE
BIOTIN CARRIER PROTEIN (1) SUBUNIT?

A

Death

The patient would not be able to add biotin to the enzyme, non-functional enzyme

113
Q 
WHAT WOULD BE THE CLINICAL OUTCOME IF THERE WAS A MUTATION OF THE
BIOTIN CARBOXYLASE (2) SUBUNIT?
A

Death

The patient would not be able to carboxylate the biotin and therefore the enzyme would be non-functional

114
Q

WHAT WOULD BE THE CLINICAL OUTCOME IF THERE WAS A MUTATION OF THE
TRANSCARBOXYLASE (3) SUBUNIT OF ANY ONE OF THE CARBOXYLASES?

A

That particular pathway would be inhibited, but the patient may be able to survive if the pathway blocked is non-critical and the diet is changed to accommodate.

Biochemistry 316 : Metabolism (7 decks)

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