1- Monosaccharides: mainly glucose & fructose
ABORBED with NO DIGESTION
2- Disaccharides:
Sucrose, lactose & maltose
DIGESTED into monosaccharides
3-Polysaccharides:
Starch (plant source e.g. rice, potato, flour)
& glycogen (animal source)
DIGESTED into monosaccharaides
Cellulose (fibers of vegetables & fruits)
NOT DIGESTED

The major dietary polysaccharides are of plant (starch, composed of amylose & amylopectin)
& animal (glycogen) origin.
During mastication, the enzyme salivary a
-amylase acts on dietary starch and glycogen hydrolysing some a
(1-4) bonds to give dexrtin
N.B. humans do not have bamylase, so they can not digest cellulose, which is a carbohydate of plant origin containing b
(1-4) glycosidic bonds between glucose molecules.
Salivary a
-amylase action on carbohydrates stops in the stomach as the media is strongly acidic.

2- In the Lumen of small intestine
Pancreatic bicarbonate neutralizes the acidic juice of stomach.
pancreatic a
-amylase continues the process of starch and glycogen digestion
Dextrin is cleaved into oligosachharides and disaccharides.

3- At the Mucosal Lining of Small Intestine
Mucosa of small intestine secretes two types of enzymes:
1- Intestinal oligosaccharidases: digest oligosaccharides into disaccharides & monosaccharaides .
2- intestinal disaccharidases : digest disaccharides into monosaccharides.
Disaccharidases are:
Sucrase: cleaves sucrose into glucose and fructose
Maltase: cleaves maltose into glucose and glucose
Lactase: cleaves lactose into glucose and galactose
Finally, most carbohydrates of diet (polysaccharides & disaccharides) are hydrolysed (digested) into monosaccarides (mainly glucose, fructose & galactose).
Only monosaccharides are absorbed ---- to blood
Cellulose of diet (in fibers of vegetables & fruits) are not digested.

Overview of Digestion of Carbohydrates of Diet

1- From lumen to inside cells:
Only monosaccharaides are absorbed in the small intestine
- The duodenum and upper jejunum absorb the bulk of the dietary sugars
- Insulin hormone is not required for uptake of glucose by intestinal cells.
iGalactose & glucose are transported into the mucosal cells by an active energy requiring process that requires the concurrent uptake of sodium ions.
The transport protein is the sodium dependent glucose cotransporter-1
Ii- Frucose absorption requires a sodium-independent transporter (GLUG-5) for its absorption (energy is not required)
2- From inside cells into blood:
Glucose, galactose & fructose are transported from intestinal mucosal cells into the portal circulation (blood) by GLUT-2 transporter.
(energy is not required)

Deficiency of a disaccharidase of the intestinal mucosa causes:
1- The disaccharide is not digested to monosaccharaide.
2- The undigested disaccharide passes into the large intestine
3- In large intestine, disaccharides which are osmotically active draw water from the mucosa into the large intestine lumen causing osmotic diarrhea.
4- Diarrhea is increased by the fermentation of the remaining carbohydrates to two- and three-carbon compounds which are also, osmotically active.
5- Large volumes of CO2 and H2 gases cause
abdominal cramps and flatulence.

cont.
Causes of deficiency of enzymes:
1- Hereditary deficiencies of a disaccharidase deficiency
For example:
Lactose intolerance:
Inability to digest lactose of milk due to deficiency of lactase enzyme
So, diarrhea will occur on ingestion of milk or milk products
For infants (up to two years old): are treated by lactose-free milk
2- Intestinal diseases or drugs that injure the mucosa of the small intestine

Proteins must be digested to yield amino acids which can be absorbed
1- In the Stomach
Digestion by gastric secretion
The gastric juice contains hydrochloric acid (HCL) & pepsinogen
• Hydrochloric acid:
- Denatures proteins to make them more susceptible to hydrolysis by enzymes
- kills some bacteria.
• Pepsin:
- An acid-stable endopeptidase secreted by stomach cells as inactive pepsinogen
- Pepsinogen is activated to pepsin either by HCL or by other pepsin molecules
- Action of pepsin: digests polypeptides into smaller polypeptides.

Secreted inactive
(Zymogen) = pepsinogen & needs
HCL for starting activation
HCL pH 2
Attacks peptide bonds formed by

cont.
2- In the Lumen of Small Intestine
Digestion by pancreatic enzymes
On entering the small intestine,
• Polypeptides produced in the stomach by the action of pepsin are further cleaved to
oligopeptides by pancreatic proteases :
Trypsin, chymotrypsin, elastase & carboxypeptidase A&B
• These proteases are released from the pancreas as zymogens (inactive forms).
• Release of zymogens is mediated by cholecystokinin & secretin (hormones of GIT)
• Activation of zymogens is mediated by the enzyme enteropeptidase i.e. Trypsinogen (zymogen) is converted to trypsin (active enzyme).

cholecystokinin & Secretin
(Hormones from intestinal Mucosa)

PH 7-8
Enterokinase
Secreted inactive
(zymogen)
& needs enterokinase for activation
Attacks peptide bonds formed by

Secreted as inactive
(zymogen) & needs trypsin for activation
PH 7-8
Attacks peptide bonds formed by

Is an endopeptidase which acts on elastic fibers.
It is secreted as an inactive form (proelastase) & activated by trypsin.
Carboxypeptidase
It is an exopeptidase attacking the peptide chain at its carboxylic end liberating amino acids.
secreted as an inactive procarboxypeptidase activated by trypsin.

cont.
3- On the mucosa of Small Intestine digestion by intestinal aminopeptidases
Aminopeptidase is available on the luminal surface of the intestine cleaves the N-terminal amino acids from oligopeptides to produce smaller oligopeptide & free amino acids

• Free amino acids are taken up into the small intestinal cells by sodium-dependent transport system .
• Amino acids are taken via blood to the liver

In individuals with a deficiency in pancreatic secretion (for example, due to chronic pancreatitis, cystic fibrosis or surgical removal of the pancreas
Incomplete digestion & absorption of fat & protein abnormal increase of lipids (steatorrhea) and undigested protein in the feces