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Science for Medicine > Carbohydrates 1 > Flashcards

Carbohydrates 1 Flashcards

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1
Q

What are the properties of carbohydrates?

A
  • Highly oxidizable
  • Function to store potential energy
  • Have structural and protective functions
  • Contribute to cell-cell communication
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2
Q

In what form are carbohydrates stored?

A
  • Starch in plants

- Glycogen in animals

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3
Q

Where do carbohydrates exhibit structural and protective functions?

A
  • In plant cell walls

- Extra cellular matrices of animal cells

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4
Q

How are carbohydrates highly oxidizable?

A

-Sugar and starch molecules have high energy H atom- associated electrons

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5
Q

What is another name for a monosaccharide?

A

Hexose

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6
Q

What are the 3 important hexoses?

A
  • Glucose (Glc)
  • Galactose (Gal)
  • Fructose (Fru)
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7
Q

How are disaccharides formed/

A
  • From monomers that are linked by glycosidic bonds

- Covalent bonds formed when hydroxyl group one monosaccharide reacts with anomeric carbon of another

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8
Q

What is an anomeric carbon/

A
  • Different anomers are mirror images of each other
  • It is carbon #1 on the glucose residue
  • It stabilises the structure of glucose
  • It is the only residue that can be oxidised
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9
Q

What are the 3 important disaccharides?

A
  • Maltose
  • Lactose
  • Sucrose
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10
Q

What is maltose?

A
  • Break down product of starch

- Found in beer and baby foods

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11
Q

Why is maltose a reducing sugar?

A

Anomeric C-1 is available for oxidation

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12
Q

What is lactose?

A

-Main sugar in milk

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13
Q

How is lactose formed?

A

From a glycosidic bond between galactose and glucose

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14
Q

Why is lactose a reducing sugar?

A

Anomeric carbon the glucose is available fro oxidation

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15
Q

What is sucrose?

A
  • Common sugar
  • Only made y plants
  • Sweetener in most processed foods
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16
Q

Why is sucrose not a reducing sugar?

A

It does not have a free anomeric C-1 so ther is no oxidation site

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17
Q

What are polysaccharides?

A

Polymers of medium to high molecular weight

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18
Q

How are polysaccharides distinguished from each other?

A
  • Identity of their recurring monosaccharide units
  • Length of their chain
  • Types of bond linking monosaccharide units
  • Amount of branching they exhibit
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19
Q

Homopolysaccharide

A

Single monomeric specie

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20
Q

Heteropolysaccharide

A

Have 2 or more monomer species

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21
Q

What 2 kind of glucose does starch contain?

A
  • Amylose

- Amylopectin

22
Q

Describe amylose.

A
  • Can have thousands of glucose residues

- D-glucose residues in (a1-4) linkage

23
Q

Describe amylopectin.

A
  • Similar structure as amylose but branched.

- Glycosidic (a1-4) bonds join glucose in the chains but branches are (a1-6) and occur every 24-30 residues

24
Q

Describe the structure of starch.

A

Has many non-reducing ends and very few reducing ends

25
Q

How are amylose and amylopectin arranged in starch?

A

They are believed to form alpha helices

26
Q

Describe the structure of glycogen.

A
  • Polymer of glucose (a1-4) linked to sub units with (a1-6) branches every 8-12 residues
  • This makes glycogen more extensively branched than starch
27
Q

Where is glycogen found in the body?

A

90% is in:

  • Liver (acts to replenish blood glucose when fasting)
  • Skeletal muscle (catabolism produces ATP for contraction)
28
Q

Why is glucose stored in polymers?

A
  • Compactness
  • Amylopectin and glycogen have many non-reducing ends
  • The polymers form hydrated gels and are not really in solution
29
Q

What does the many non-reducing ends of amylopectin and glycogen allow?

A

-Allows them to be synthesised and degraded to and from monomers respectively thus speeds up formation or degradation

30
Q

What is meant by ‘The polymers form hydrated gels and are not really in solution’?

A

-They are osmotically inactive
-If free glucose were in the cells then [Glc]inside&raquo_space; [Glc]outside
Either Glc would move out of the cell down the concentration gradient or the cell would use huge amounts of energy keeping it in the cell

31
Q

What are glycoproteins?

A

Proteins that have carbohydrate covalently attached

32
Q

Glycoproteins: What may the carbohydrates attached to the protein do?

A
  • Increases the protein solubility
  • Influence protein folding and conformation
  • Protect it from degradation
  • Act as a communication between cells
33
Q

What is the carbohydrate content of glycoproteins

A

1-80% by mass

34
Q

What is another name for glycosaminoglycans?

A

Mucopolysaccharides

35
Q

Where do GAGs function?

A

In mucus and also synovial fluid

36
Q

What are GAGs/

A

Un-branched polymers made from repeating units of hexuronic acid and an amino-sugar which alternate through the chains

37
Q

What are proteoglycans?

A
  • Macromolecules found on the surface of cells or in between cells in the ECM
  • Carbohydrate&raquo_space; Proteins
38
Q

How are proteoglycans formed?

A

From GAGs covalently attaching to proteins

39
Q

What do proteoglycans for part of?

A

Many connective tissues

40
Q

What are glycoproteins?

A

-Very similar to glycoproteins but protein» carbohydrate

41
Q

Where are glycoproteins usually found?

A

-On the outer plasma membrane and ECM but also in the blood and within cells in the secretory system

42
Q

What are exampled of glycoproteins?

A

Some cytoplasmic and nuclear proteins

43
Q

What are mucopolysaccharidoses?

A

Group of genetic disorders caused by the absence or malfunction of enzymes that are required for the breakdown of GAGs

44
Q

How does mucopolysaccharidoses occur?

A
  • Over time GAGS build up in connective tissue, blood and other somatic cells
  • The build up damages cellular architecture and function
45
Q

What can mucopolysaccharidoses cause?

A

?-Severe dementia

  • Heart problems
  • Build up of GAGs between endothelial cells causing damage
  • Stunted bones
  • Inflammed joints
46
Q

What are examples of mucopolysaccharidoses

A
  • Hurler Syndrome
  • Scheie Syndrome
  • Hunter Syndrome
  • Sanfilippo Syndrome
47
Q

What are the characteristics of Hurler Syndrome?

A
  • Severe developmental delays
  • Clouding and degradation of the cornea
  • Areterial wall thickening
  • Dementia
48
Q

What is the dementia in Hurler syndrome caused by?

A
  • Build up of CSF

- Enlarged vermicular spaces

49
Q

What are the sever developmental delays seen in Hurler syndrome?

A
  • Stop developing at around 4yo

- Death at around 10yo

50
Q

What experimental therapies currently exist for Hurler syndrome?

A
  • Gene therapy

- Enzyme replacement therapies

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