Carbohydrates 2 Flashcards Preview

Carbohydrates > Carbohydrates 2 > Flashcards

Flashcards in Carbohydrates 2 Deck (36):
1

What carbohydrates are found in our diet?

Starch
Glycogen
Cellulose and hemicellulose
ogliosaccharides containing (a1-6) linked galactose
Lactose, sucrose, maltose
Glucose, fructose

2

Describe the digestion of carbohydrates in the mouth

Salivary amylase hydrolyses (a1-4) bonds of starch.

3

Describe the digestion of carbohydrates in the duodenum.

Pancreatic amylase works as in the mouth.

4

Describe the digestion of carbohydrates in the jejunum.

Final digestion by mucosal cell-surface enzymes
1. Ismaltase- hydrolyses (a1-6) bonds
2. Glucoamylase- removes Glc sequentially from non-reducing ends.
3. Sucrase- hydrolyses sucrose
Lactase- hydrolyses lactose

5

What are the main products of carbohydrate digestion?

Glc
Gal
Fru

6

What process allows for the absorption of glucose?

Glucose is absorbed 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 it’s concentration gradient (i.e. When blood glucose is high)
Galactose has a similar mode of absorption as glucose, utilising gradients to facilitate it’s transport

7

How is fructose absorbed?

Fructose binds to the channel protein GLUT5. Simply moves down its concentration gradient (high in gut lumen, low in blood)

8

What are cellulose and hemicellulose used for?

Increase faecal bulk and decrease transit time.

9

What can a lack of ogliosaccharides in the diet lead to?

Poor health

10

Polymers are broken down by the gut to yield what?

CH4
H2

11

What can disaccharidase deficiencies result from?

It may be genetic
Severe intestinal infection
Other inflammation of the gut lining
Drugs injuring the gut wall
Surgical removal of the intestine.

12

What are disaccharidase deficiencies characterised by?

abdominal distension and cramps

13

How are disaccharidasse deficiencies diagnosed?

Requires enzyme tests of intestinal secretions. Usually checking for lactase , maltase or sucrose activity.

14

Why does the ingestion of milk give disaccharidase deficiency if lactase is lacking?

Undigested lactose is broken down by the gut bacteria causing gas build up an irritant acids.
Lactose is osmotically active, thus drawing water from the gut into the lumen causing diarrhoea.

15

How can symptoms of lactose intolerance be avoided?

Avoiding milk products
Using milk products treated with fungal lactase.
Supplementing diet with lactase.

16

What is the fate of absorbed glucose?

Glc diffuses through the intestinal epithelium cells into the portal blood and on to the liver
Glc is immediately phosphorylated into glucose 6-phosphate by the hepatocytes (or any other cell glucose enters)

17

How does glucose get trapped in the cell?

Glucose 6-phosphate cannot diffuse out of the cell because GLUT transporters wont recognise it

18

What are the enzyme catalysts involved in the fate of absorbed glucose?

Glucokinase (liver)
Hexokinase (other tissues)

19

glucokinase/ hexokinase

10

20

Where is 90% of glycogen found?

The liver and skeletal muscle

21

What happens when blood glucose levels fall in the liver?

glycogen >G-6-P>(using glucose 6 phosphatase) Glc into the blood

22

What happens when blood glucose levels fall in the skeletal muscle?

In skeletal muscle: there is no glucose 6-phosphatase so G-6-P straight to lactate

23

What does the process of glycogenin involve?

Glycogen does not form directly from Glc monomers
Glycogenin begins the process by covalently binding Glc from uracil-diphosphate (UDP)-glucose to form chains of approx. 8 Glc residues

24

What process extends the glucose chains?

Glycogen synthase takes over and extends the Glc chains.

25

What happens the chains formed during glycogen synthase?

The chains formed by glycogen synthase are then broken by glycogen-branching enzyme and re-attached via (α1→6) bonds to give branch points

26

Where are glucose monomers removed from during the degradation of glycogen?

The non-reducing ends as G-1-P.

27

What happens after the removeal of glucose monomers?

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 by de-branching enzyme

28

What does transferase do in the degradation of glycogen?

Transferase activity of de-branching enzyme removes a set of 3 Glc residues and attaches them to the nearest non-reducing end via a (α1→4) bond

29

What does glucosidase do in the degradation of glycogen?

Glucosidase activity then removes the final Glc by breaking a (α1→6) linkage to release free Glc
This leaves an unbranched chain, which can be further degraded or built upon as needed

30

What is Von Gierkes' disease?

Liver (and kidney, intestine) glucose 6-phosphatase deficiency.

31

What are the symptoms of Von Gierke's disease?

high [liver glycogen] – maintains it’s normal structure
low [blood Glc] – fasting hypoglycaemia
This is because glycogen cannot be used as an energy source – all Glc must come from dietary carbohydrate
high [blood lactate] – lacticacidaemia
Because the lactate produced by skeletal muscle cannot be reconverted to Glc in the liver

32

What is the treatment for Von Gierke's disease?

Regular carbohydrate feeding – little and often
Every 3-4 hours throughout the day and night
Can be administered through a nasogastric tube and pump, but sudden death has occurred when the pump fails or the tube disconnects

33

What is McArdles's disease?

Skeletal muscle phosphorylase deficiency

34

What are the symptoms of McArdle's disease?

High [muscle glycogen] – maintains it’s correct structure
Weakness and cramps after exercise
No increase in [blood glucose] after exercise

35

When is McArdle's disease seen?

Most symptoms are not apparent in resting state, when muscles will use other energy sources (Glc and fatty acids from the blood)
Usually becomes apparent in 20-30 year olds
Children do suffer the disease but may remember pain during adolescence and childhood

36

What is the treatment for McArdle's disease?

Avoid strenuous activity
Make use of your “second wind”
Exercise briefly (anaerobically), wait for the pain to subside, continue to exercise (aerobically using oxidative phosphorylation of fatty acids)