Carbohydrates 2

Question 1

What are the 2 main undigestible carbohydrates in our diet?

Answer 1

Cellulose and oligosaccharides (with alpha1->6 linked galactose)

Question 2

What are the 4 main diestible types of carbohydrates in our diet?

Answer 2

• Starch
• Glycogen (meat)
• Monosaccharides (glucose/fructose)
• disaccharides (lactose, sucrose, maltose)

Question 3

What carb digestion occurs in the mouth?

Answer 3

Salivary amylase hydrolyses (alpha1->4) bonds in starch

Question 4

What carb digestion occurs in the duodenum and where is it?

Answer 4

Duodenum is the first section of the small intestine

Pancreatic amylase hydrolyses (alpha1->4) bonds in starch

Question 5

Where is the Jejunum and what carb digestion occurs there?

Answer 5

The jejunum is the 2nd part of the small intestine

• Isomaltase hydrolses (alpha1->6) bonds
• Glucoamylase removes Glc from non-reducing ends of glycogen
• Sucrase hydrolyses sucrose
• Lactase hydrolyses Lactose

Question 6

What are the 3 main products of carbohydrate digestion in the small intestine?

Answer 6

Glucose, Galactose and Fructose (monosaccharides)

Question 7

Describe the first of 3 steps through which glucose passes form the gut lumen to the blood:

Answer 7

(1) Glucose passes from gut lumen to epithelial cell through the apical lamina using a Na+/glucose symporter (2 Na+ and 1 glucose pass through together). Na+ conc. gradient provides the energy for this meaning it can occur even when glucose is moving against its conc. gradient

Question 8

Describe the 2nd of 3 steps by which Glc passes from gut lumen to blood:

Answer 8

Na+K+ATPase pumps 3 Na+ from epithial tissue through basal lamina into the blood and 2K+ the opposite way. Driving the conc. gradient that moves glucose. This requires ATP therefore glucose moves by a Indirect ATP Powered Process.

Question 9

Describe the 3rd and last step by which Glc moves from the gut lumen to the bloodstream:

Answer 9

Glucose in the epitheial tissue move into the blood through the basal lamina via a glucose uniporter GLUT2 which facilliates downhill efflux.

Question 10

How do galactose and fructose absorbtion in the gut compare to Glc?

Answer 10

Galactose is very similar.
Fructose needs no sodium gradient and simply binds alone to channel protein GLUT5 moving down its conc. gradient to the blood.

Question 11

What happens to Indigestible Cellulose?

Answer 11

It increases faecal bulk and decreases transit time. Without it constipation can occur.

Question 12

What are the 5 possible reasons for dissacharidase deficiencies?

Answer 12

• Surgical removal of the intestine
• Genetics
• Inflammation of the gut wall
• Severe intestinal infection
• Drugs injuring the gut wall

Question 13

What are the symptoms of dissacharidase deficiencies?

Answer 13

Abdominal distention
Cramps from a build up of gasses released when gut bacteria break down dissacharides.
Others (see lactase deficiency)

Question 14

How are dissacharidase deficiencies diagnosed?

Answer 14

Testing for enzyme activity of common ones such as lactase, maltase and sucrase

Question 15

Explain lactose intolerance

Answer 15

In most humans (almost all non-whites) Lactase stops functioning after weaning.
Consumption of lactose after this results in gaseous build up from breakdown by gut bacteria
Lactose is osmotically active so it also drags water out of the blood into the lumen causing dehydration and diarrhoea

Question 16

What are the 3 treatments for Lactose intolerance?

Answer 16

Avoid milk products
Use milk products that are lacto-free, treated with fungal lactase.
Supplement diet with lactase. Unreliable as most is broken down in the stomach.

Question 17

What is the function of Hexokinase and Glucokinase?

Answer 17

They phosphorylate glucose to glucose-6-phosphate (g-6-P) in order to trap it in cells.

Question 18

Where aer hexo- and gluco- kinase found?

Answer 18

hexokinase in most tissue

Glucokinase in the liver

Question 19

What are the relative Km Vmax values for hexokinase and glucokinase?

Answer 19

Hexokinase has a low Km (high affinity) and a low Vmax

Glucokinase has a high Km (low affinity) and a high Vmax

Question 20

How do glucokinase and hexokinase work at a high blood [Glc]?

Answer 20

Hexokinase works at its max rate as normal converting all the glucose needed for the various tissues.
Glucokinase picks up all the slack, with its high Vmax it can convert a large amount of exces blood Glc very quickly and store it in the liver.

Question 21

How do glucokinase and hexokinase work at low blood [Glc]?

Answer 21

Hexokinase works at max rate (quite low) as it has a higher Km so has first dibs on blood glucose.
Glucokinase works at a low or non-existent rate, only picking up glucose that exceeds hexokinases Vmax.

Question 22

In short, what happens to G-6-P?

Answer 22

• Conveted to glycogen for storage in the liver and skeletal muscle
• Undergoes respiration for ATP
• In non-hepatic tissues converted to pentoses & NADPH.

Question 23

What is the fate of glycogen in liver and skeletal muscle?

Answer 23

Liver: when blood [Glc] is low = Glycogen -> G-6-P -> Glucose and released into bloodstream
Skeletal Muscle: No glucose-6-phosphatase so Glycogen->G-6-P->Lactate by glycolysis.

Question 24

Explain the 3 steps of glycogen synthesis:

Answer 24

(1) Glycogenin covalently bonds already stored glucose from carrier molecule UDP-glucose into ‘primers’ of 8 Glc residues
(2) lycogen synthase takes over and extends the Glc chains with dietary glucose
(3) Chains are broken by glycogen-branching enzyme and reattached with (alpha1->6) bonds to give branches.

Question 25

Explain the 3 steps of glycogen degradation:

Answer 25

(1) Glycogen phosphorylase removes Glc residues one by one form the nonreducing ends of the chain as G-1-P
(2) Transferase activity of a de-branchin enzyme removes 3 of the last 4 glucose residues on a branch and reattaches it to the nearest non-reducing end by (alpha1->4) bonds.
(3) Glucosidase breaks (alpha1->6) bonds, releasing final Glc on branch
One long Glycogen is produced that can be broken down further by glycogen phosphorylase.

Question 26

What is the cause of Von Gierkes Disease?

Answer 26

A Glucose-6-phosphatase deficiency.

Question 27

What does Von Gierkes disease cause?

Answer 27

Higher liver [glycogen]
low blood [Glc]
high blood [lactate]

Question 28

How is Von Gierkes disease treated?

Answer 28

3-4 hours a day of carb feeding.

Can be done through a tube but when it breaks or disconnects sudden death can occur

Question 29

What cause McArdles Disease?

Answer 29

Skeletal Muscle Glycogen Phosphorylase Deficiency

Question 30

What does McArdles disease do?

Answer 30

Causes:

• high muscle [glycogen]
• No increase in blood [Glc] after exercise
• Severe weakness/cramp upon exercise. At rest muscles use fatty acids and Glc from blood for energy

Question 31

How is McArdles disease treated?

Answer 31

Avoid strenuous exercise
Use 2nd wind. Brief exercise while body uses anaerobic resp, wait for pain to subside, body balances oxygen intake with resp and aerobic occurs making better use of glucose available.