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BL Extras > energy production: carbs > Flashcards

energy production: carbs Flashcards

1
Q

what is the general formula for carbohydrate?

A

(CH2O)n

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2
Q

what are the different type of carbohydrates?

A
  • monosaccharide (1 sugar unit)
  • disaccharide (2 sugar unit)
  • oligosaccharide (3-12 sugar unit)
  • polysaccharide (10-1000’s sugar unit)
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3
Q

what are the three main dietary monosaccharides?

A
  • glucose
  • fructose
  • galactose
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4
Q

what does sucrose break down into?

A

glucose + fructose

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5
Q

what does lactose break down into?

A

galactose + glucose

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6
Q

what does maltose break down into?

A

2 glucose

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7
Q

what are the uses of glucose in the body?

A
  • used in respiration by all cells however some have an absolute requirement to meet e.g. red blood cells, lens of the eye, neutrophils
  • CNS prefers glucose as fuel (can use ketones in times of starvation but takes time to adapt)
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8
Q

what is the normal range of blood glucose concentration?

A

4-6 mmol/L

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9
Q

what is stage 1 in the catabolism of carbohydrates?

A

extracellular breakdown of carbohydrates in GI TRACT to produce building blocks

  1. amylase in saliva
  2. pancreatic amylase
  3. disaccharidases attached to membrane of epithelial cells
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10
Q

what is stage 2 in the catabolism of carbohydrates?

A
  • glycolysis forms pyruvate
  • reducing power (NADH) and some energy released
  • (intracellular)
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11
Q

what is stage 3 in the catabolism of carbohydrates?

A

Kreb’s cycle:

  • releasing of reducing power and some energy
  • Acetyl coA oxidised to CO2
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12
Q

what is stage 4 in the catabolism of carbohydrates?

A

oxidative phosphorylation:

  • conversion of reducing power into ATP
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13
Q

how are monosaccharides absorbed by tissues?

A
  1. active transport: from low to high conc into epithelial cells by sodium-dependent glucose transporter
  2. passive transport: high to low conc via GLUT2 and GLUT4
  3. transport via blood supply to tissues
  4. into target cells via facilitated diffusion using transport proteins
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14
Q

where are the transport proteins GLUT2 + GLUT4 functional?

A

GLUT2: kidney, liver, pancreatic beta cells

GLUT4: skeletal muscles, adipose tissues, striated muscles

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15
Q

where does glycolysis occur?

A

Cytosol

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16
Q

what happens in glycolysis?

A
  1. glucose (6C sugar) is oxidised to form 2 pyruvate (3C sugar) molecules
  2. 2 NADH are produced
  3. synthesis of ATP from ADP (net 2 ATP per glucose)
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17
Q

what is the rate limiting(control) enzyme in glycolysis?

A

phosphofructokinase-1
ADP molecule binds to the enzymes allosteric site increasing its activity

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18
Q

why are they so many steps/enzymes in glycolysis?

A
  1. efficient energy conversion
  2. allows for fine control
  3. chemistry easier in smaller stages
  4. gives versatility:
    * allows interconnections with other pathways
    * allows production of useful intermediates
    * allows part to be used in reverse
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19
Q

what is the importance of lactate synthesis in glycolysis?

A

in certain conditions pyruvate is reduced to lactate by lactate dehydrogenase

this is important because it means NADH is recycled producing NAD+ which ensures glycolysis can continue

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20
Q

how is lactate subsequently used by the body?

A
  1. circulated in blood and taken up by the heart + liver
  2. lactate converted to pyruvate by LDH
  3. pyruvate is catabolised by the heart
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21
Q

what intermediate of glycolysis is important in regulating the affinity of haemoglobin for oxygen?

A

2,3-biphosphoglycerate:

  • one BPG binds per haemoglobin and decreases its affinity for oxygen
  • so increased concentration = more readily oxygen dissociates
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22
Q

what is the TCA cycle also known as?

A

krebs cycle

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23
Q

where does the TCA cycle occur?

A

mitochondrial matrix

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24
Q

what happens in the TCA cycle?

A
  1. pyruvate transported from cytoplasm across mitochondrial membrane to the mitochondrial matrix
  2. pyruvate converted to acetyl CoA in the presence of pyruvate dehydrogenase enzyme (reaction is irreversible)
    pyruvate dehydrogenase is multi-enzyme complex, since they coenzymes rely on vitamin B the reaction is sensitive to vitamin B deficiency
  3. acetyl CoA is converted to 2CO2 (reaction is oxidative so relies on NAD+ and FAD) some energy is released as ATP
  4. NADH + FADH2 forms (reducing powers MEGA important)
25
Q

what is the function of the TCA cycle?

A
  • catabolic role- oxidise acetyl group of acetyl CoA to 2 CO2 molecules and the reduction of NAD+ + FAD to NADH + FADH2 which are reducing powers in oxidative phosphorylation
  • anabolic role- provide intermediates for the synthesis of various molecules e.g. fatty acids, glutamate and haem
26
Q

what is TCA cycle regulated by?

A

ATP/ADP ratio

NADH/NAD+ ratio

27
Q

what is pyruvate dehydrogenase activated by?

A
  • pyruvate
  • CoA
  • NAD+
  • ADP
  • insulin
28
Q

what is pyruvate dehydrogenase inhibited by?

A
  • acetyl-CoA
  • NADH
  • ATP
  • citrate
29
Q

what tissue is TCA cycle really important in?

A

CNS

the heart

30
Q

how are reducing powers involved in ATP synthesis?

A
  • e- on NADH and FADH2 transferred through series of carrier mol to O2 (e- transport chain) and each step releases energy
  • free energy from each step drives oxidative phosphorylation
31
Q

what happens in oxidative phosphorylation?

A
  1. e- transferred from NADH AND FADH2 through series of carrier mol to O2 which releases energy
  2. a H+ gradient forms across inner mitochondrial membrane = proton motive force (pmf)
  3. 30% energy used to move H+ out of mitochondrial matrix across inner membrane into intermembrane space
  4. H+ reenter mitochondrial matrix due to electrochemical potential, this can only occur in presence of ATP synthase
  5. oxidation of 2 moles NADH — synthesises 5 moles ATP and oxidation of 2 moles FADH2 — synthesis 3 moles ATP
32
Q

what is the relation between proton motive force (pmf) and ATP synthesised?

A

greater pmf = more ATP synthesised

33
Q

what is oxidative phosphorylation regulated by?

A

ATP/ADP
NADH/NAD+
FADH2/FAD

34
Q

what is oxidative phosphorylation inhibited by?

A

inhibitors block e- transport e.g. cyanide

35
Q

why is cyanide toxic to cells?

A
  • blocks the oxidation of NADH + FADH2 which stops the ETC
  • this prevents the generation of p.m.f and ATP synthesis
  • without ATP cell structure and function is compromised + cell dies
36
Q

what affect do uncouplers have on oxidative phosphorylation?

A
  1. uncouplers increase permeability of mitochondrial inner membrane to H+
  2. dissipate H+ gradient so reduced pmf
  3. reduced ATP synthesis
  4. e- transport continues energy is released as heat
37
Q

why happens to energy lost during oxidative phosphorylation?

A
  • lost as heat
  • brown adipose tissue ensures more heat generated
38
Q

where is brown adipose tissue found?

A
  • newborn babies: maintain heat around vital organs
  • hibernating animals: maintain body temp
39
Q

what effect does dinitrophenol have on oxidative phosphorylation?

A
  • acts as an uncoupler so there is increased inner mitochondrial membrane permeability to H+
  • this reduces PMF so reduces ATP synthesis
  • etc still occurs and all energy released as heat causing severe hyperhtermia
40
Q

why is cellulose not broken down by our digestive system?

A

our body doesnt have the enzymes to hydrolyse the beta glycosidic linkages

41
Q

how is fructose metabolised?

A

metabolised in the liver

broken down in presence of fructokinase to fructose-1 phosphate and further broken down by aldolase enzymes

42
Q

what is the clinical importance of fructose?

A
  1. essential fructosuria- occurs when fructokinase missing
    • fructose in urine
  2. fructose intolerance- occurs when aldolase missing
    • fructose-1-P accumulate in liver causing liver damage
    • managed by removing fructose and sucrose from diet
43
Q

how is galactose metabolised?

A

metabolised in the presence of enzymes:

  • galactokinase
  • uridyl transferase
  • UDP-galactose epimerase

If it isnt metabolised it causes galactosaemia

44
Q

what is galactosaemia?

A

disease in which person is unable to utilise galactose

causing galactose and galactose-1-P to accumulate

45
Q

what happens in galactokinase deficiency?

A

only galactose accumulates

this causes cataracts

46
Q

what happens in uridyl transferase deficiency?

A

galactose + galactose-1-P accumulate

causing kidney, liver and brain damage

also cataracts

47
Q

what happens when galactose accumulates in tissue?

A

galactose reduced to galactitol by enzyme aldose reductase which depletes NADPH levels and increases risk of oxidative damage

48
Q

how does galactose accumulation cause cataracts?

A

galactose is converted to galactitol by aldose reductase which depletes NADPH levels
increases cell risk of oxidative damage
crystalin proteins are denatured + oedema
results in cataracts

49
Q

what is the treatment of galactosaemia?

A

no lactose in diet

50
Q

what does glucose-6-phosphate do?

A

protects red blood cells from substances in blood that could cause them harm

51
Q

why is the pentose phosphate pathway important in some tissues?

A

important in fatty acid biosynthesis

important in steroid biosynthesis

important in glutathione regeneration

52
Q

what are the principles of G6PDH deficiency?

A

structural integrity + function of some proteins depends on -SH group (NADPH is one of them)

G6PDH deficiency is common inherited disease

53
Q

what is link between G6PDH deficiency and RBC?

A

in red blood cells:

  • decreased NADPH
  • cells at increased risk of oxidative damage since glutathione isn’t regenerated
  • so aggregated proteins form
  • causing haemolysis which leads to haemolytic anaemia
54
Q

what are the signs and symptoms of G6PDH deficiency?

A
  • paleness (in darker-skinned kids, paleness is sometimes best seen in the mouth, especially on the lips or tongue)
  • extreme tiredness or dizziness.
  • tachycardia
  • dyspnoea
  • jaundice (the skin and eyes look yellow)
  • splenomegaly
55
Q

what are the types of lactose intolerance?

A

Primary

Secondary

Congenital

56
Q

what is primary lactose deficiency caused by and whom does it affect?

A

caused by: absence of lactase persistence allele

affects: adults only

57
Q

what is secondary lactose deficiency caused by and whom does it affect?

A

caused by: injury to small intestine

  • Coeliac disease
  • Crohn’s disease

affects: infants and adults

generally reversible

58
Q

what is congenital lactose deficiency caused by?

A

caused by: VERY RARE autosomal recessive defect in lactase gene

59
Q

what are the symptoms of lactose intolerance?

A
  • bloating
  • diarrhoea
  • vomiting
  • rumbling stomach

BL Extras (4 decks)

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