Flashcards in Carbohydrates 2 Deck (31):
What are the 2 main undigestible carbohydrates in our diet?
Cellulose and oligosaccharides (with alpha1->6 linked galactose)
What are the 4 main diestible types of carbohydrates in our diet?
- Glycogen (meat)
- Monosaccharides (glucose/fructose)
- disaccharides (lactose, sucrose, maltose)
What carb digestion occurs in the mouth?
Salivary amylase hydrolyses (alpha1->4) bonds in starch
What carb digestion occurs in the duodenum and where is it?
Duodenum is the first section of the small intestine
Pancreatic amylase hydrolyses (alpha1->4) bonds in starch
Where is the Jejunum and what carb digestion occurs there?
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
What are the 3 main products of carbohydrate digestion in the small intestine?
Glucose, Galactose and Fructose (monosaccharides)
Describe the first of 3 steps through which glucose passes form the gut lumen to the blood:
(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
Describe the 2nd of 3 steps by which Glc passes from gut lumen to blood:
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.
Describe the 3rd and last step by which Glc moves from the gut lumen to the bloodstream:
Glucose in the epitheial tissue move into the blood through the basal lamina via a glucose uniporter GLUT2 which facilliates downhill efflux.
How do galactose and fructose absorbtion in the gut compare to Glc?
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.
What happens to Indigestible Cellulose?
It increases faecal bulk and decreases transit time. Without it constipation can occur.
What are the 5 possible reasons for dissacharidase deficiencies?
- Surgical removal of the intestine
- Inflammation of the gut wall
- Severe intestinal infection
- Drugs injuring the gut wall
What are the symptoms of dissacharidase deficiencies?
Cramps from a build up of gasses released when gut bacteria break down dissacharides.
Others (see lactase deficiency)
How are dissacharidase deficiencies diagnosed?
Testing for enzyme activity of common ones such as lactase, maltase and sucrase
Explain lactose intolerance
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
What are the 3 treatments for Lactose intolerance?
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.
What is the function of Hexokinase and Glucokinase?
They phosphorylate glucose to glucose-6-phosphate (g-6-P) in order to trap it in cells.
Where aer hexo- and gluco- kinase found?
hexokinase in most tissue
Glucokinase in the liver
What are the relative Km Vmax values for hexokinase and glucokinase?
Hexokinase has a low Km (high affinity) and a low Vmax
Glucokinase has a high Km (low affinity) and a high Vmax
How do glucokinase and hexokinase work at a high blood [Glc]?
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.
How do glucokinase and hexokinase work at low blood [Glc]?
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.
In short, what happens to G-6-P?
- Conveted to glycogen for storage in the liver and skeletal muscle
- Undergoes respiration for ATP
- In non-hepatic tissues converted to pentoses & NADPH.
What is the fate of glycogen in liver and skeletal muscle?
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.
Explain the 3 steps of glycogen synthesis:
(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.
Explain the 3 steps of glycogen degradation:
(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.
What is the cause of Von Gierkes Disease?
A Glucose-6-phosphatase deficiency.
What does Von Gierkes disease cause?
Higher liver [glycogen]
low blood [Glc]
high blood [lactate]
How is Von Gierkes disease treated?
3-4 hours a day of carb feeding.
Can be done through a tube but when it breaks or disconnects sudden death can occur
What cause McArdles Disease?
Skeletal Muscle Glycogen Phosphorylase Deficiency
What does McArdles disease do?
- 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