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MEH > Carbs > Flashcards

Carbs Flashcards

1
Q

Stage 1 catabolism

A

From diet:
- protein —> amino acids
- carbs —> monosaccharides
- lipids —> glycerol and fatty acids
- alcohol —> alcohol

Complex molecules broken down to building blocks.
No energy produced.

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2
Q

Stage 2 catabolism

A

Amino acids —> NH4+ —> urea
—> alpha-keto acids
—> pyruvate

Monosaccharides —> pyruvate

Glycerol —> pyruvate

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3
Q

Stage 3 catabolism

A

Amino acids —> acetyl CoA —> TCA cycle
Alpha-keto acids —> TCA cycle

Pyruvate —> acetyl CoA —> TCA cycle

Fatty acids —> acetyl CoA —> TCA cycle

Alcohol —> acetyl CoA —> TCA cycle

Oxidative, some ATP produced.

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4
Q

Stage 4 catabolism

A

ETC and ATP synthesis

NADH and FAD2H reoxidised

O2 required

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5
Q

Glucose conc in blood

A

About 5 mM

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6
Q

Tissues with absolute requirement for glucose?

A

RBC
Neutrophils
Innermost cells of kidney medulla
Lens of eye
CNS (brain) - can however use ketone bodies for some energy requirements in times of starvation

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7
Q

What bonds do pancreatic amylase and isomaltase break?

A

Pancreatic - alpha 1,4 bonds

Iso - alpha 1,6 bonds

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8
Q

Types of lactose intolerance

A

Primary lactase deficiency

Secondary lactase deficiency

Congenital lactase deficiency

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9
Q

Primary lactase deficiency

A

Absence of lactase persistence allele.

Only occurs in adults.

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10
Q

Secondary lactase deficiency

A

Caused by injury to small intestine eg gastroenteritis, Crohn’s, coeliac, ulcerative colitis.

Occurs in both infants and adults.
Generally reversible (once epithelial cells have recovered).

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11
Q

Congenital lactase deficiency

A

Autosomal recessive defect in lactase gene.

Baby cannot digest breast milk.
Extremely rare

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12
Q

Symptoms of lactase deficiency

A

Bloating/cramps
Flatulence
Diarrhoea
Vomiting
Rumbling stomach

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13
Q

Absorption of monosaccharides

A

Active transport of sugar (glucose) into intestinal epithelial cells by sodium-dependent glucose transporter 1 (SGLT1).

Passive transport via GLUT2 into blood supply.
(Na+ pump to maintain gradient).

Transport via blood supply to target tissues.

Glucose uptake into cells via facilitated diffusion using transport proteins (GLUT1 - GLUT5).

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14
Q

Glycolysis

A

Glucose —> pyruvate (simply)
2 ATP net production
2 NADH made per glucose

Features:
Occurs in all tissues in cytoplasm
Exergonic, oxidative
Irreversible
Only pathway that can operate anaerobically with addition of LDH

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15
Q

Enzymes of glycolysis

A

Hexokinase (glucokinase in liver) - glucose to glucose-6-P

Phosphofructokinase-1 - fructose-6-P to fructose 1,6-bisphosphate
=> key control enzyme

Pyruvate kinase - final enzyme that produces pyruvate

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16
Q

Committing step in glycolysis

A

Step 3 - fructose-6-P to fructose 1,6-bisphosphate, catalysed by phosphofructokinase-1

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17
Q

Substrate level phosphorylation

A

Transfer Pi to ADP to give ATP, in the last four reactions of glycolysis.

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18
Q

2,3-bisphosphoglycerate

A

Produced in RBC

Regulator of Hb O2 affinity (promotes release)

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19
Q

Clinical application of glycolysis

A

Rate of glycolysis up to 200x greater in cancer - can be seen with PET scan (positron emission tomography)

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20
Q

Glycerol 3-phosphate dehydrogenase???
Bisphospoglycerate mutase???
***

A

Produces glycerol phosphate

Produces 2,3-bisphosphoglycerate

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21
Q

Regulation of glycolysis

A

Irreversible steps

Feedback inhibition - where increased conc. of product inhibits an earlier enzyme, so less product is made

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22
Q

Allosteric site

A

Other site

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23
Q

Regulation of phosphofructokinase

A

Allosteric regulation
Inhibited by
- high ATP
- high citrate
Stimulated by
- high AMP
- high F2,6BP

Hormonal regulation
Inhibited by
- glucagon
Stimulated by
- insulin

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24
Q

Lactate dehydrogenase (LDH)

A

Catalyses reaction converting pyruvate to lactate and back, producing either NAD+ or NADH + H.

This occurs when there is an inability to use NADH for ox. phos.

Important to recycle NAD+/NADH.

25
Q

Lactate - what increases its conc. in the blood?

A

Produced from glucose via pyruvate.

Increased in blood by strenuous exercise, but this will return to normal by 90 mins.

Also increased by pathological situations eg shock, congestive heart failure (stroke, MI).

Normal conc. in blood is <1mM.

26
Q

Hyperlactaemia

A

2-5 mM
Below renal threshold
No change in blood pH - buffer system

27
Q

Lactic acidosis

A

Above 5mM
Above renal threshold => excreted by kidneys
Blood pH lowered, as buffer system in blood can no longer adapt to maintain pH levels.
—> alter protein shape/function
—> loss of circulatory control and heart

28
Q

Fructokinase - where is it metabolised?

Associated enzymes in its metabolysis?

A

Metabolised in liver.

Fructokinase - catalyses fructose to fructose-1-P
Aldolase - catalyses fructose-1-P

29
Q

Essential fructosuria - what is missing?
Symptoms?

A

Fructokinase missing.

Fructose in urine; no clinical symptoms.

30
Q

Fructose intolerance - what is missing?
Symptoms?

A

Aldolase missing.

Fructose-1-P accumulates in liver, leading to liver damage and possibly death.
Managed by removing fructose and sucrose from diet.

31
Q

Fructose-1-P

A

Produced from phosphorylation of fructose; catalysed by fructokinase.

Accumulation in liver leads to liver damage and death eg in patients with fructose intolerance.

32
Q

Galactose metabolism

A

Broken down into galactose-1-P, then glucose-1-P, then glucose-6-P which feeds into glycolysis.

Enzymes: galactokinase (1st reaction), uridyl transferase (2nd reaction).

UDP-galactose epimerase catalyses galactose-1-P into UDP-galactose which then gets made into glycogen.

33
Q

Galactokinase

A

Catalyses galactose into galactose-1-P.

34
Q

Uridyl transferase

A

Catalyses galactose-1-P into glucose-1-P.

35
Q

UDP-galactose epimerase

A

Catalyses galactose-1-P into UDP-galactose.

36
Q

Galactosaemia - what is it?
Symptoms?
Treatment?

A

Unable to utilise glucose.

Galactokinase deficiency (rare) - galactose accumulates.
Transferase deficiency (common) - galactose and galactose-1-P accumulate.

=> galactose enters other pathways
galactose -> galactitol (catalysed by aldose reductase)

Galactitol:
- depletes lens of NADPH - can’t protect against ROS - damage causing cataracts

Galactose-1-P:
- affects kidney, liver, brain (mechanism unclear)

Treatment:
No lactose in diet

37
Q

Galactitol

A

Produced from galactose entering other pathways as it can’t be utilised.
- causes cataracts in lens of eye, as it depletes them of NADPH - can’t regenerate GSSG (glutathione) so can’t protect against ROS - cataracts

38
Q

Aldose reductase

A

Catalyses galactose to galactitol.

39
Q

PPP (pentose phosphate pathway) - what does it do?
What does it generate (aside from final product)?

A

Glucose -> pyruvate; also generates ribose-5-P — needed for nucleotides, DNA, RNA, coenzymes

Generates NADPH - needed to regenerate glutathione to protect against ox. stress.

G6PDH catalyses glucose-6-P, generating NADPH. (=> G6PDH deficiency causes oxidative damage).

40
Q

G6PDH

A

Catalyses glucose-6-P into intermediate, generating NADPH.

41
Q

G6PDH deficiency

A

NADPH not generated, so glutathione is not regenerated (reduced back to GSH reduced form), so body can’t protect against oxidative damage from ROS, so proteins/lipids etc damaged.

  • causes cataracts
42
Q

Pyruvate dehydrogenase

A

Complex of 5 enzymes that converts pyruvate into acetyl CoA.

Key site of regulation of entry into TCA cycle (acetyl CoA) - irreversible reaction.

Sensitive to vit B1 deficiency as many coenzymes needed, and B-vitamins provide the factors needed to make these.

43
Q

What deficiency can affect CoA?
*

A

Vit. B

44
Q

What deficiency is PDH (pyruvate dehydrogenase) sensitive to?

A

Vit. B1.

45
Q

PDH regulation

A

Activated by:
Pyruvate
CoA
NAD+
ADP
Insulin

Inhibited by:
Acetyl-CoA
NADH
ATP
Citrate (downstream product of TCA cycle)

46
Q

What do kinase enzymes do?

A

Phosphorylation

47
Q

What do phosphatase enzymes do?

A

Dephosphorylation

48
Q

TCA cycle - what does it do?

A

Acetyl CoA converted to 2 CO2.
Produces some ATP.
Oxidative => requires NAD+, FAD

49
Q

Regulation of TCA cycle

A

Regulated by energy availability; ATP/ADP ratio, NADH/NAD+ ratio.

50
Q

Isocitrate dehydrogenase

A

Enzyme in TCA cycle that is allosterically regulated by ATP:ADP ratio (increased ATP inhibits).

51
Q

Alpha-ketoglutarate dehydrogenase

A

Enzyme in TCA cycle that is regulated by the ratio of its products, succinyl CoA and NADH, as well as ATP.

Succinyl CoA and NADH inhibit.
ATP:ADP - increase in ratio will inhibit (more ATP)

52
Q

Stage 4 catabolism

A

ETC and ATP synthesis in mitochondrion
NADH and FADH2 reoxidised
O2 reduced to H2O - oxygen is final electron acceptor.
Large amounts of ATP produced.

53
Q

ETC

A

Electrons of NADH and FADH2 are transferred through a series of carrier molecules to O2; releases energy in steps.

Builds up H+ electrochemical gradient in intermenbranous space.
- generates proton motive force (pmf)

54
Q

Oxidative phosphorylation

A

Free energy released and used to drive ATP synthesis.

Regulated by conc.s of ATP and ADP.

55
Q

ATP synthase

A

Enzyme complex through which H+ pass through down their electrochemical gradient, generating energy to drive production of ATP from ADP and Pi.

56
Q

Inhibition of ox. phos.

A

Inhibitors eg cyanide block electron transport, which prevents acceptance of e- by O2. CO also binds to final complex like CN-.

57
Q

Uncoupling of ox. phos.

A

Uncouples increase permeability of inner mito. membrane to H+ ions, this dissipates the proton gradient, therefore reducing p.m.f. => no drive for ATP synthesis
The energy is lost as heat.

eg dinitrophenol (DNP), dinitrocresol, fatty acids

58
Q

Where/when does uncoupling occurring naturally in the body?

A

Can occur naturally in body in brown adipose tissue, where the degree of coupling is controlled by fatty acids, allowing extra heat generation.

In hibernating animals
In babies - called non-shivering thermogenesis.

59
Q

How does brown adipose tissue respond to cold?

A

Contains thermogenin (UCP1) - a naturally occurring uncoupling protein.

When cold, noradrenaline activates:
1. Lipase, which release FA from triglycerides
2. FA oxidation -> NADH/FADH2 -> e- transport
3. FA activate UCP1
4. UCP1 transports H+ back into mito.

=> ETC uncoupled from ATP synthesis; energy of p.m.f released as extra heat

MEH (14 decks)

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