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1. Foundations of Medicine PoNF > Carbohydrates > Flashcards

Carbohydrates Flashcards

1
Q

Carbohydrate and oxidisation

A

Highly oxidizable: sugar –> starch molecules have “high energy” H atom-associated electrons
This makes them a major energy source with carb catabolism being a major metabolic process for most organisms

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2
Q

What are carbs functions

A
  • To store potential energy:
    -starch (plants)
    -Glycogen (animals)
  • Structural/protective sunction in ECM
  • Contribut to cell-cell communication (ABO blood groups)
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3
Q

3 monosaccharides

A

hexoses 6-C sugars: Glucose, Galactose, Fructose

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4
Q

What are disaccharides

A

Formed from monomers linked by glycosidic bonds - covalent bond formed when OH group of one monosac reacts with anomeric carbon of other monosac

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5
Q

What is an anomeric carbon

A
  • Diff anomers = mirror images of each other (L/R)
  • C1 on glucose residue
  • stabilises structure of glucose
  • only residue that can be oxidised
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6
Q

3 disaccharides

A
  • Maltose
  • Lactose
  • Sucrose
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7
Q

Briefly explain maltose

A
  • Mostly break-down product of starch (not much from diet)
  • Anomeric C-1 is availabe for oxidation so maltose can be oxidised (termed a reducing sugar)
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8
Q

Briefly explain lactose

A
  • Main sugar in milk
  • Formed fromglycosidic bond between galactose and glucose
  • Anomeric C on the glucose available for oxidation (so it is termed reducing sugar)
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9
Q

briefly explain sucrose

A
  • “table” sugar
  • Does not have a free anomeric C-1 so there is no oxidation site, hence it is a non-reducing sugar
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10
Q

What are polysaccharides

A

Polymers of med-high molecular weight, and can be distinguished from each other in the:
* identity of recurring monosaccharide units
* length of their chains
* types of bonds linking monosaccharide units
* amount of branching they exhibit

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11
Q

What can polysaccharides be?

A
  • Homopolysaccharides - single monomeric species
  • Heteropolysaccharides - two or more monomer species
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12
Q

what is starch

A

2 typers of glucose polymer:
1. Amylose - D-glucose seridues in (a1->4) linkage and can hae thousands of glucose residues
2. Amylopectin - similar but branched. Glycosidic (a1->4) bonds join glucose in the chains but branches are (a1->6) and occur every 24 - 30 residues

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13
Q

what does starch have many of

A

Non-reducing ends (and few reducing ends)

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14
Q

Glycogen

A

Polymer of glucose (a1->4) linked sub-units with (a1-6) branches every 8 to 12 residues - makes it more extensively branched than starch - more dense and can pack more in

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15
Q

Where is glycogen found

A

90% in liver (replenishes blood glucose when fasting) and skeletal muscles (catabolism produces ATP for contraction)

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16
Q

Why do we store glucose as a polymer (glycogen)

A
  • Compactness
  • Amylopectin and glycogen have many non-reducing ends mening they can be readily synthesised and degraded to and from monomers
  • Polymers form hydrated gels and not “in solution”, making them osmotically inactive so doesn’t move out of cells etc
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17
Q

Glycoproteins

A

P with carbs covalently attached - most extracellular eukaryotic P have associated carboihydrate molecules

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18
Q

Glycoprotiens - what do carbs attached to proteins do

A
  • Inc P solubility
  • Inc P folding and conformation
  • Protect it from degredation
  • Act as communication between cells
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19
Q

Glycosamionglycans (GAG)

A

Un-branced polymers made from repeating units of hexuronicacid and an amino-sugar, which alternate through the chains

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20
Q

Function of GAG’s

A

in mucus and also synovial fluid around joints

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21
Q

Proteoglycans

A

GAGs covalently attching to Proteins. Are macromolecules found on the surface of cells/in ECM and part of many CT in body

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22
Q

What are proteoglycans similar to

A

Glycoproteins

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23
Q

Where are glycoproteins usually found

A

Outer plasma membrane and ECM - also in blood and within cells in secretory system

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24
Q

What does the disordered nature of glycoproteins mean they do?

A

stick

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25
Q

What is Mucopolysaccharidoses

A

group of genetic disorders caused by abence or malfunction of enzymes that are required for the breakdown of GAG. GAG build up. Damages cellular architecture/function. Causes dementia, heart problems, stunted bones, inflamed joints…

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26
Q

Examples of mucopolysaccharidoses

A

Hurler, scheie, hunter, sanfilippo syndromes

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27
Q

Where are carbs digested?

A
  1. Mouth - salivary amylase hydrolyses (a1->4) bonds of starch
  2. Stomach - no carb digestion
  3. Duodenum - pancreatic amylase works as in mouth
  4. Jejunum (small inntestine) - final digestion by mucosal cell-surface enzymes:
    * Isomaltase - hydrolyses a1->6 bonds
    * Glucoamylase - removes GLC sequentially from non-reducing ends
    * Suucrase - hydrolyses sucrose
    * Lactase - hydrolyses lactose
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28
Q

What are the main products of carb digestion

A

Glc, Gal, Fru

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29
Q

Briefly describe the absorption of glucose

A

sodium-glucose symporter pumps glucose into epithelial cells from the intestine against its conc grad. Glucose uniporter GLUT2 facilitates the efflux of glucose into the bloodstream

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30
Q

How is the absorption of galactose similar to that of glucose

A

Utilises gradients to facilitate its transport

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31
Q

How is the absorption of fructose different to that of glucose

A
  • Binds to the channel protien GLUT5
  • SImply moves down its conc grad (high in gut lumen, low in blood)
32
Q

How are cellulose and hemicellulose digested

A

Can’t be digested by gut but do have a use of inc feacal bulk (transit time): polymers are broken down by gut bacteria (yeilding CH4 and H2) - farts!

33
Q

What do disaccharidase deficiencise present as

A

Abdominal distension and cramps - enzyme tests of intestinal secretions needed (check lactase, maltase, sucrase activity)

34
Q

give an example of a disacchariidase deficiency

A

Lactose intolerance

35
Q

What then happens to Glucose once it is absorbed (dissused throug intestinal epithelium cells and into protal blood)?

A

Onto liver:
* Immediately phosphorylated into Glucose-6-phosphate by hepatocytes (or any other cell glucose enters)
* G6P cannot diffuse out of the cell because GLUT transporters won’t recognise it - traps glucose in cell
* Enzyme catalysts: Glucokinase (liver), hexokinase (other tissues)

36
Q

What does Vmax and Km mean?

A

High Vmax = efficient enzyme
Low Km = high affinity for substrate

37
Q

What are the Km and Vmax of glucokinase and hexokinase for glucose?

A

Glucokinase: Km-high, Vmax-high
Hexokinase: Km-low, Vmax-low

38
Q

What happens when blood [glucose] is normal

A

Liver doesn’t grab it all, so other tissues have it

39
Q

What happens when blood [glc] is high

A

Liver “grabs” the glc - high glucokinase Vmax means it can phosphorylate all that Glc quickly and trap it in the liver

40
Q

What happens when blood [glc] is low

A

hexokinase low Km means tissues can “grab” glc effectively, and low Vmax means tissues easiy “satisfied” so don’t keep grabbing it

41
Q

What are the fates of G6P

A
  • Glycolysis —> respiration (oxidative phosphorylation) Co2 +H20
  • Glycogen (skeleton muscle)
  • Pentose phosphate pathway
42
Q

What happens to glycogen in the liver (when [blood Glc] falls)?

A

Glc—>G6P—-G6Pase—> Glc into blood

Glucagon released to stimulate an inc in [blood glc]

43
Q

What happens in skeletal muscle with regards to glycogen

A

Glycogen—>G6P–(glycolysis)–>lactate

44
Q

Synthesis of glycogen (step 1)

A
  1. Glycogenin (enzyme) begins process by covelently binding Glc from uracil-diphosphate (UDP)-glucose to form chains of approx. 8 Glc residues
  2. Glycogen synthase takes over and extends the Glc chains
45
Q

Synthesis of glycogen (step 2)

A

Chains formed by glycogen synthase are then broken by glycogen-branching enzyme and re-attached via (a1->6) bonds to give branch points

46
Q

Another word for “degredation” of glycogen

A

mobilisation

47
Q

Give process of degredation of glycogen

A
  • Glc monomers removed 1 at a time from the non-reducing ends as G-1-P
  • Following removal of terminal Glc residues to release G-1-P, by glycogen phosphorylase, Glc near the branch is removed in a 2-step process b de-branching enzyme
  • Transferase activity of de-branching enzyme removes a set of 3 Glc residues and attaches them to the nearest non-reducing end via a (a1->4) bond
  • Glucoidase activity then removes the final Glc by breaking a (a1->6) linkage to release free Glc
  • Leaves an unbranched chain, which can be further degraded orbuilt upon as needed
48
Q

What happens to this (degraded) glycogen

A

G-1-P —> G-6-P—or—> Glc (to blood) Sub level phosphorylation (ATP of muscle contraction) and glycolysis (lactate)

49
Q

What happens to this (degraded) glycogen

A

G-1-P —> G-6-P—or—> Glc (to blood) Sub level phosphorylation (ATP of muscle contraction) and glycolysis (lactate)

50
Q

Give a quick summary of Glycolysis (overview not process)

A

Catabolic pathway that saves some Ep from glucose/G6P by forming ATP through substrate level phosphorylation. Only way energy can be made when cells lack oxygen.

51
Q

Where does glycolysis occur

A

Cytosol (no organelles/mitochondria required)

52
Q

How many phases does glycolysis have?

A

2: preparatory and payoff phase

53
Q

Summarise what is used and released in glycolysis?

A
  • 2 ATP used in preparatoy phase but 4 released in payoff phase - Net gain of 2 ATP per Glc molecule
  • 2 molecules of G3P formed to enter payoff phase
  • 2 NADH (e carrier) gained
54
Q

Give the steps of glycolysis

A
  1. Phosphorylation of glucose to Glucose-6-Phosphate (G6P) - hexokinase but uses 1 ATP
  2. Conversion of G6P to Fructose-6-Phosphate (F6P) - phosphpohexose isomerase
  3. Phosphorlation of F6P to F-1,6-bisP Phosphofructokinase-1 (PFK-1) - uses 1 ATP and is irreversible and 1st committed step (as F6P could be used for other processes)
  4. Cleavage of F-1,6-bisP aldolase and reaction reversiable - splitting part: 1 Glc (6C) to 2 different 3C triose sugars (dihydroxyacetone phosphate + G3P)
  5. Interconversion of triose sugars of dihydroxyacetone phosphate to G3P using triose phosphate isomerase - thus have 2 G3P from 1 Glc
  6. oxidation of G3P to 1,3-bisPG - glyceraldehyde 3-phosphate dehydrogenase and 2 NADH’s produced so start of payoff phase
  7. P transfer from 1,3-bisPG too ADP forming ATP + 3-PG - phosphoglycerate kinase - generates 2 ATP, free-floating E in cytoplasm interact with intermediates to form ATP
  8. Conversion fo 3-PG to 2-PG - phosphoglycerate mutase
  9. Dehydration of 2-PG to PEP, releasing H20 - enolase
  10. transfer of P from PEP to ADP - pyruvate kinase, produces 2 ATP and pyruvate
55
Q

What happens if we don’t have NAD+

A

No glycolysis will occur

56
Q

What must the fates of pyruvate all have in common?

A

They must all produce NAD+ to replenish the NAD+ required for reduction of various intermediate metabolites - redox balance

57
Q

What can happen to pyruvate after glycolysis

A
  • Aerobic conditions: 2Acetyl-CoA —> 4CO2 and 4H20
  • Anaerobic conditions: 2 Lactate (still regenerates NAD+)
  • Ethanol in plants n shit
58
Q

Give brief summary of C numbers as go through respiration

A
  • Glucose - 6C
  • 2 Pyruvate - 3C
  • 2 Acetyl-CoA - 2C 2C02 released
  • CO2 - 4C
59
Q

When will pyruvate be converted to lactate and how does this work? - give key enzyme involved

A

In cells lacking O2 - exercising muscle/RBC’s (lack mitochondria)
Pyruvate reduced to lactate via fermentation: oxidation of NADH allows for this reduction and replenishes NAD+ store for further glycolysis - lactate dehydrogenase

60
Q

Cori cycle

A

ATP made via substrate-level phosphorylation, producing lactate which is the converted to Glc in the liver through gluconeogensis - interaction between liver/muscle=cori cycle

Liver: Lactate–>Pyruvate-6P-> Glucose
Through blood
Muscle: glucose –2P->Pyruvate–>lactate
through blood…

61
Q

What happens in cells with access to O2 after pyruvate is made?

Where does it occur?

A

Pyruvate oxidised to form acetyl CoA + CO2 - mitochondria
NADH formed in this reaction gives up Hydride ion (H-) in Electron transport chain

62
Q

If we need more glucose (sugar) how can we get it?

A

Glucose made from other non-carb moleules- normally controlled in liver in response to hormonal controls

63
Q

What is Gluconeogenesis not a reverse of and why

A

Glycolysis - although 7/10 reactions are reversiable, large -#G prevents 3 from being reversiable - cell bypasses these with enzymes that catalyse a **seperate set of irreversible reactions **

64
Q

Give a brief summary of the 4 bypass reactions sidesteeping the 3 irreversible reactions of glycolysis - gluconeogenesis

A

Can be used to regulate the pathway
A) 10. Pyruvate -> PEP, releasing ATP: but here (mitochondria) Pyruvate—> oxaloacetate - pyruvate carboxylase
B) 10. Oxaloacetate –malate dehydrogenase (m)–> matate (leave mitochondria) –malate dehydrogenase (c)– oxaloacetate –PEP carboxykinase (c) –> PEP
C) 3. F6P + ADP–> F1,6BP: Control point for glucogenesis as irreversiable under cellular conditions. fructose1,6-biphosphatase catalyses hydrolysis of F16BP + H2O to F6P + Pi
D) Guucose + ADP–>G6P: Dephosphorylation of G6P to glucose, hydroplysis: G6P + H2O –> Glucose - G6Pase

65
Q

In C) and D) why are they not reversiable

A

require phosphoryl group transfer from G6P/F-1,6-bisP to ADP which is energetically unfavourable

66
Q

What happens with glalctose and fructose metabolism?

A

Can enter glycolysis at various points, most fructose metabolised by the liver

67
Q

What happens when ur pished

A

Dec glucogenesis: liver needs NAD+ but drinking inhibits this, causing lacticacidemia (inc [blood lactate]) and hypoglycaemia —> confusion, loss of consciousness—> death

68
Q

Main differences between hexoinase and glucokinase

A

The main difference between hexokinase and glucokinase is that the hexokinase is an enzyme present in all cells whereas the glucokinase is an enzyme only present in the liver. Furthermore, hexokinase has a high affinity towards glucose while glucokinase has a low affinity towards glucose

69
Q

main differnece in fucntion of glycogen stored in skeletal musces and the liver

A

Liver glycogen primarily maintains blood glucose levels, while skeletal muscle glycogen is utilized during high-intensity exertion,

70
Q

What does pyruvate dehydrogenase do (brief)

A

converts pyruvate to acetyl-coA, and thereby increases the influx of acetyl-coA from glycolysis into the TCA cycle.

71
Q

What is the fate of blood lactate

A

Lactate circulating in the bloodstream is transported to the liver, where it is reconverted by the processes of gluconeogenesis/glyconeogenesis into glucose or glycogen, respectively.

72
Q

What is the function of glucogenesis

A

Gluconeogenesis refers to synthesis of new glucose from noncarbohydrate precursors, provides glucose when dietary intake is insufficient or absent. It also is essential in the regulation of acid-base balance, amino acid metabolism, and synthesis of carbohydrate derived structural components. the biochemical pathway in which glycogen breaks down into glucose-1-phosphate and glucose.

73
Q

Where does gluconeogenesis take place

A

the hepatocytes and the myocytes - in the mitochondria in the liver

74
Q

What 2 key enzymes is gluconeogenesis under the regulation of

A

phosphorylase kinase and glycogen phosphorylase????

2nd one not inc in notes/presentations

75
Q

Fate of absorbed galactose

A

Galactose is primarily converted into glucose and stored as glycogen.

76
Q

Fate of absorbed fructose

A

Fructose is largely extracted by splanchnic organs (gut and liver), where it is essentially converted into glucose, lactate and fatty acid, which can subsequently be used as an energy substrate by extrahepatic cells.

77
Q

What is substrate-level phosphorylation?

A

Substrate-level phosphorylation refers to the formation of ATP from ADP and a phosphorylated intermediate, rather than from ADP and inorganic phosphate, Pi, as is done in oxidative phosphorylation. The amount of ATP that is generated by glycolysis is relatively low.

1. Foundations of Medicine PoNF (22 decks)

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