Carbohydrates 2 Flashcards
What carbohydrates are there in our diets?
- Starch
- Glycogen
- Cellulose and hemicellulose
- Ogliosaccharides containing (a1-6) linked galactose
- Lactose, sucrose, maltose
- Glucose, fructose
Where in the body does carbohydrate digestion take place?
- Mouth
- Duodenum
- Jejunum
Describe the digestion of carbohydrates in the mouth
Salivary amylase hydrolyses (a1-4) bonds of starch
Describe the digestion of carbohydrates in the duodenum.
Pancreatic amylase works as in the mouth
Describe the digestion of carbohydrates in the jejunum.
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
What are the main products of carbohydrate digestion?
- Glucose
- Galactose
- Fructose
How is glucose 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 its concentration gradient
How is galactose absorbed?
Similar mode of absorption to glucose utilising gradients to facilitate its transport
How is fructose absorbed?
- Binds to the channel protein GLUT5
- Simply moves down its concentration gradient
What is the function of cellulose and hemicellulose?
-They cannot be digested by the gut so instead they increase faecal bulk and decrease transient time
When the polymers of cellulose/hemicellulose are broken down, what is yielded?
- CH4
- H2
What can disaccharidase deficiencies result fro?
- Genetic
- Severe intestinal infection
- Other inflammation of the gut lining
- Drugs injuring the gut wall
- Surgical removal of the intestine
What are disaccharidase deficiencies characterised by?
Abdominal distension and cramps
How are disaccharidase deficiencies diagnosed?
- Enzyme tests of intestinal secretion
- Usually checking for lactase, maltase or sucrose activity
What is lactose intolerance?
- Most common disaccharide defiency
- If lactase is lacking, then ingestion of milk will give disaccharidase deficiency symptoms
Why do symptoms of disaccharidase symmptoms occur in lactose intoerance
- 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
How can the symptoms of lactose intolerance be avoided?
- Avoiding milk products
- Using milk products treated with fungal lactase
- Supplementing diet with lactase
What happens to glucose after it is absorbed?
- 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
What are the enzymes catalyst involved in the phosphorylation of glucose to G-6-P?
- Gluokinase (liver)
- Hexokinase (other tissues
What does high Vmax mean?
Efficient enzyme
What does low Km mean?
High affinity for substrate
What happens when blood Glc is normal?
The liver doesn’t (grab) all of the glucose so other tissue have it
What happens when blood Glc is high?
-Liver ‘grabs’ the Glc
What does high glucokinase Vmax mean?
It can phosphorylate all the Glc quickly thus most absorbed Glc is trapped by the liver
What does hexokinase low Km mean?
Even al tow [Glc] tissues can grab Glc effectively
What does hexokinase low Vmax mean?
Tissues are easily satisfied so don’t keep grabbing Glc
What are the fates of G-6-P?
-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
Where is glycogen mainly found?
90% is in the liver and skeletal muscle
What happens in the liver if [blood Glc] falls?
Glycogen is converted to G-6-P then transported as glucose in the blood
What happens in skeletal muscle to glycogen?
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
How is glycogen synthesise?
- 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
How does the degradation of glycogen begin?
Glc monomers are removed one at a time from the non-reducing ends as G-1-P
What happens after terminal Glc residues are removed to release G-1-P by glycogen phosphorylase from glycogen?
Glc near the branch is removed in a 2 step process by debranching enzyme.
What roles does transferase play 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 (a1-4) bond
What role does glucosidase play in the degradation of glycogen?
Glucosidase activity then removes the final Gls by breaking a (a1-6) linkage to release free Glc.
What is the end product of the degradation of glycogen?
An unbranched chain which can be further degraded or built upon as needed
What is Von Gierke’s disease?
Liver (kidney and intestine) Glucose-6-Phosphatase deficiency
What are the symptoms of Von Gierkes’s disease?
- 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
What is the treatmernt for Von Gierke’s disease?
Regular carbohydrate feeding- little and often
What is McArdle’s disease?
Skeletal muscle phosphorylase deficiency
What are the symptoms of McArdle’s disease?
-High [muscle glycogen]-maintains its correct structure
-Weakness and cramps after exercise
No increase in [blood Glc] after excercise
What is the treatment for McArdle’s dsease?
- Avoid strenuous activity
- Exercise briefly wait for the pain to subside, continue to excercise
