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Science for Medicine > Carbohydrates 2 > Flashcards

Carbohydrates 2 Flashcards

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1
Q

What carbohydrates are there in our diets?

A
  • Starch
  • Glycogen
  • Cellulose and hemicellulose
  • Ogliosaccharides containing (a1-6) linked galactose
  • Lactose, sucrose, maltose
  • Glucose, fructose
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2
Q

Where in the body does carbohydrate digestion take place?

A
  • Mouth
  • Duodenum
  • Jejunum
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3
Q

Describe the digestion of carbohydrates in the mouth

A

Salivary amylase hydrolyses (a1-4) bonds of starch

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4
Q

Describe the digestion of carbohydrates in the duodenum.

A

Pancreatic amylase works as in the mouth

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5
Q

Describe the digestion of carbohydrates in the jejunum.

A

Final digestion by mucosal cell-surface enzymes:

  • Isomaltase: hydrolyses (a1-6) bonds
  • Glucoamylase: removes Glc sequentially from non-reducing end
  • Sucrase: hydrolyses sucrose
  • Lactase: hydrolyses lactose
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6
Q

What are the main products of carbohydrate digestion?

A
  • Glucose
  • Galactose
  • Fructose
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7
Q

How is glucose absorbed?

A
  • Through an indirect ATP-powered process
  • ATP driven Na pump maintains low cellular [Na] so glucose can continually be moved in to the epithelial cells
  • This system continues to work even if glucose has to be moved into the epithelial cells against its concentration gradient
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8
Q

How is galactose absorbed?

A

Similar mode of absorption to glucose utilising gradients to facilitate its transport

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9
Q

How is fructose absorbed?

A
  • Binds to the channel protein GLUT5

- Simply moves down its concentration gradient

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10
Q

What is the function of cellulose and hemicellulose?

A

-They cannot be digested by the gut so instead they increase faecal bulk and decrease transient time

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11
Q

When the polymers of cellulose/hemicellulose are broken down, what is yielded?

A
  • CH4

- H2

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12
Q

What can disaccharidase deficiencies result fro?

A
  • Genetic
  • Severe intestinal infection
  • Other inflammation of the gut lining
  • Drugs injuring the gut wall
  • Surgical removal of the intestine
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13
Q

What are disaccharidase deficiencies characterised by?

A

Abdominal distension and cramps

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14
Q

How are disaccharidase deficiencies diagnosed?

A
  • Enzyme tests of intestinal secretion

- Usually checking for lactase, maltase or sucrose activity

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15
Q

What is lactose intolerance?

A
  • Most common disaccharide defiency

- If lactase is lacking, then ingestion of milk will give disaccharidase deficiency symptoms

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16
Q

Why do symptoms of disaccharidase symmptoms occur in lactose intoerance

A
  • Undigested lactose is broken down by gut bacteria causing gas build up and irritant acids
  • Lactose is osmotically active, thus drawing water from the gut into the lumen causing diarrhoea
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17
Q

How can the symptoms of lactose intolerance be avoided?

A
  • Avoiding milk products
  • Using milk products treated with fungal lactase
  • Supplementing diet with lactase
18
Q

What happens to glucose after it is absorbed?

A
  • Glc diffuses through the intestinal epithelium cells into the portal blood and on to the liver
  • Glc is immediately phosphorylated into G-6-P by the hepatocytes
  • G-6-P cannot diffuse out of the cell because GLUT transporters won’t recognis eit
19
Q

What are the enzymes catalyst involved in the phosphorylation of glucose to G-6-P?

A
  • Gluokinase (liver)

- Hexokinase (other tissues

20
Q

What does high Vmax mean?

A

Efficient enzyme

21
Q

What does low Km mean?

A

High affinity for substrate

22
Q

What happens when blood Glc is normal?

A

The liver doesn’t (grab) all of the glucose so other tissue have it

23
Q

What happens when blood Glc is high?

A

-Liver ‘grabs’ the Glc

24
Q

What does high glucokinase Vmax mean?

A

It can phosphorylate all the Glc quickly thus most absorbed Glc is trapped by the liver

25
Q

What does hexokinase low Km mean?

A

Even al tow [Glc] tissues can grab Glc effectively

26
Q

What does hexokinase low Vmax mean?

A

Tissues are easily satisfied so don’t keep grabbing Glc

27
Q

What are the fates of G-6-P?

A

-Converted to Glc in the liver then transported through the blood to other tissues
-Glc acted on by hexokinase ot form G-6-P
G-6-P can then enter glycolysis, pentose phosphate pathway or be stored as glycogen

28
Q

Where is glycogen mainly found?

A

90% is in the liver and skeletal muscle

29
Q

What happens in the liver if [blood Glc] falls?

A

Glycogen is converted to G-6-P then transported as glucose in the blood

30
Q

What happens in skeletal muscle to glycogen?

A

G-1-P is converted to G-6-P which is acted on by substrate level phosphorylation in glycolysis to form lactate and ATP for muscle contraction

31
Q

How is glycogen synthesise?

A
  • Glycogenin begins the process by covalently binding Glc from uracil diphosphate glucose to form chains of approx. 8 Glc residues.
  • Then glycogen synthase takes over and extends the Glc chains
  • The chains formed by glycogen synthase are then broken by glycogen-branching enzyme and re-attached via (a1-6) bonds to give branch points
32
Q

How does the degradation of glycogen begin?

A

Glc monomers are removed one at a time from the non-reducing ends as G-1-P

33
Q

What happens after terminal Glc residues are removed to release G-1-P by glycogen phosphorylase from glycogen?

A

Glc near the branch is removed in a 2 step process by debranching enzyme.

34
Q

What roles does transferase play in the degradation of glycogen?

A

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

35
Q

What role does glucosidase play in the degradation of glycogen?

A

Glucosidase activity then removes the final Gls by breaking a (a1-6) linkage to release free Glc.

36
Q

What is the end product of the degradation of glycogen?

A

An unbranched chain which can be further degraded or built upon as needed

37
Q

What is Von Gierke’s disease?

A

Liver (kidney and intestine) Glucose-6-Phosphatase deficiency

38
Q

What are the symptoms of Von Gierkes’s disease?

A
  • High [liver glycogen]- maintains its normal structure
  • Low [blood Glc] - fasting hypoglycaemia because glycogen cannot be used as an energy source all Glc must come from dietary carbohydrate
  • High [blood lactate]- lacticacidaemia bacaue the lactate produced be skeletal muscle cannot be reconverted to Glc in the liver
39
Q

What is the treatmernt for Von Gierke’s disease?

A

Regular carbohydrate feeding- little and often

40
Q

What is McArdle’s disease?

A

Skeletal muscle phosphorylase deficiency

41
Q

What are the symptoms of McArdle’s disease?

A

-High [muscle glycogen]-maintains its correct structure
-Weakness and cramps after exercise
No increase in [blood Glc] after excercise

42
Q

What is the treatment for McArdle’s dsease?

A
  • Avoid strenuous activity

- Exercise briefly wait for the pain to subside, continue to excercise

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